tag:blogger.com,1999:blog-63509780141734238502024-03-06T13:05:20.881-07:00Human Anatomy & Physiology and Renal DisordersRenal disorders are associated with altered anatomical and physiological state of kidneys. This altered state of macroanatomy as well as microanatomy of kidneys and their functions is termed as the pathophysiology of renal disorders. This blog would definitely provide an opportunity to the readers to elevate their knowledge about renal disorders or kidney diseases and human anatomy & physiology.Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.comBlogger67125tag:blogger.com,1999:blog-6350978014173423850.post-22315972621364275992023-03-06T09:43:00.001-07:002023-03-06T09:45:30.063-07:00Coagulation Disorders<p><b>Deep Vein Thrombosis</b> (DVT) and <b>Pulmonary Embolism</b> (PE) are
often not optimally diagnosed by many physicians. These are serious but
preventable medical conditions. <b>Deep Vein Thrombosis</b> (DVT) is a medical
condition which occurs when a blood clot forms in deep vein. These clots
usually could develop in the lower leg, thigh, or pelvis. These can also occur
in arm. One should have knowledge about DVT, because it can happen to anybody
and can cause serious illness, disability and morbidity. DVT is preventable and
treatable if detected early.</p><p><o:p></o:p></p>
<p><b>Pulmonary Embolism</b> (PE) is also referred to as complication of DVT.
It happens when part of the clot breaks off and travels through the blood
stream to the lungs, causing a blockage called <b>Pulmonary Embolism</b> (PE).
If the clot is small; with appropriate treatment, people can recover from PE. However,
there could be some damage to the lungs. If the clot is large, it could stop
the blood reaching lungs and can be fatal.<o:p></o:p></p>
<p><b>Risk Factors that could cause DVT<o:p></o:p></b></p>
<p>Anybody can have a DVT. However, the factors listed below could increase the
chance if having DVT. The chance increases for someone who has more than one of
these factors at the same time.<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l4 level1 lfo1; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Hospitalization and some major surgery.<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l4 level1 lfo1; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Being bedridden for long time due to illness.<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l4 level1 lfo1; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Travelling for extended time beyond four hours
in continuity.<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l4 level1 lfo1; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Older age.<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l4 level1 lfo1; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Overweight or obese<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l4 level1 lfo1; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Family history of Venous Thromboembolism (VTE.)<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l4 level1 lfo1; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->During and just after pregnancy.<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l4 level1 lfo1; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Hormonal contraceptive medication (Estrogen
based medication).<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l4 level1 lfo1; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Hormonal Replacement Therapy (HRT).<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l4 level1 lfo1; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Trauma due to injury.<o:p></o:p></p>
<p><b>Preventing tips for DVT</b><o:p></o:p></p>
<p>Following tips could help prevent DVT:<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l2 level1 lfo2; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Move around as soon as possible after having
confined to the bed, after illness, injury, or surgery.<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l2 level1 lfo2; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->If you are at risk of DVT talk to your Physician/Surgeon
for appropriate medication.<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l2 level1 lfo2; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->When sitting for long periods of time such as
travelling for more than 4 hours; get up and walk around after 1 to 2 hours.<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l2 level1 lfo2; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Raising and lowering your heels while keeping
your toes on floor.<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l2 level1 lfo2; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Raising and lowering your toes while keeping
your heels on the floor.<o:p></o:p></p>
<p><b>Symptoms of DVT</b><o:p></o:p></p>
<p>Most of the people with DVT have no symptoms at all. The following are the
most common symptoms of DVT that could occur in affected part of the body:<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l0 level1 lfo3; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Swelling<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l0 level1 lfo3; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Pain<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l0 level1 lfo3; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Redness of the skin<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l0 level1 lfo3; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Tenderness<o:p></o:p></p>
<p>If you have any doubt of having DVT consult your doctor as soon as possible.<o:p></o:p></p>
<p><b>Pulmonary Embolism</b> (PE)<b><o:p></o:p></b></p>
<p>One can have <b>Pulmonary Embolism</b> (PE) without any symptoms of a DVT.
Signs and symptoms of PE could be:<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l1 level1 lfo4; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Difficulty in breathing<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l1 level1 lfo4; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Faster than normal or irregular heartbeat.<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l1 level1 lfo4; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Uneasiness<o:p></o:p></p>
<p><b>Coagulation Mechanisms of our Body<o:p></o:p></b></p>
<p><b>Our blood</b> is a very complex tissue of our body, in the form of a
fluid. It plays a variety of roles for homoeostasis. <b>Our blood</b> has <b>cellular</b>
and <b>noncellular components</b> uniformly suspended in liquid phase. Blood
plays multiple roles in our body for sustain life and longevity. There are three
types of cells in our blood:<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l5 level1 lfo5; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Red Blood Cells (RBCs) or Erythrocytes<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l5 level1 lfo5; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->White Blood Cells (WBCs) or Leucocytes<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l5 level1 lfo5; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Platelets<o:p></o:p></p>
<p><b>Red Blood Cells (RBCs) or Erythrocytes</b> provide red color to our
blood. <b>RBCs</b> carry oxygen from lungs to various organs and parts of our
body. <b>White Blood Cells </b>(WBCs) provide us natural and acquired immunity.
<b>Platelets </b>along with other soluble <b>coagulation factors </b>(CFs) take
part in <b>coagulation of blood</b> to safeguard us from internal of external
bleeding. There are <b>‘XIII’ coagulation factors </b>(CFs) in our blood. We know
the chemistry and role of all the coagulation factors. <b>Coagulation of Blood</b>
occurs through two mechanisms:<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l3 level1 lfo6; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Intrinsic Pathway and<o:p></o:p></p>
<p style="margin-left: 0.5in; mso-list: l3 level1 lfo6; text-indent: -0.25in;"><!--[if !supportLists]--><span style="font-family: Symbol; mso-bidi-font-family: Symbol; mso-fareast-font-family: Symbol;">·<span style="font-family: "Times New Roman"; font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;">
</span></span><!--[endif]-->Extrinsic Pathway<o:p></o:p></p>
<p>Both the coagulation mechanisms involve various coagulation factors and
finally lead to <b>activation of factor ‘X’</b>. Factor <b>‘X’</b> along with
certain factors leads to formation of <b>Thrombin</b> from <b>Prothrombin</b>. <b>Thrombin</b>
is central in clotting process, and it converts <b>Fibrinogen </b>to <b>Fibrin</b>;
activates factor <b>‘V’</b>, <b>‘VIII’</b> and <b>‘XI’, </b>leading to generation
of more <b>Thrombin</b> and stimulation of <b>Platelets</b>. Further by
activating factor <b>‘XIII’,</b> thrombin favors the formation of cross-linked
bonds among <b>Fibrin molecules, </b>thus <b>stabilizing the</b> <b>clot</b>.<o:p></o:p></p>
<p>This determines that <b>direct inhibition of</b> <b>Thrombin</b> is a highly
<b>desirable</b> <b>target</b> for prophylaxis and therapy of various <b>Coagulation
Disorders</b> (CDs). <b>Thrombin </b> has
<b>3-sites</b> for <b>target activation: <o:p></o:p></b></p>
<p><b>Sites 1 and 2 </b>are called <b>Exosites </b>and <b>site-3</b> is called
an <b>active site</b>. <b>Exosite-1</b> is the <b>Fibrin binding site </b>of <b>Thrombin</b>
and <b>Exosite-2</b> serves as the <b>Heparin-Binding Domain</b>. The clotting
pathway has traditionally been <b>inhibited </b>by using <b>Heparin</b> and <b>Warfarin</b>
for treatment and prophylaxis of <b>Coagulation Disorders</b> (CDs).<o:p></o:p></p>
<p><b>Heparin</b> inhibits<b> free Thrombin</b> by binding simultaneously to <b>Exosites</b>
on <b>Thrombin</b> and <b>Antithrombin</b>, forming a <b>Heparin-Thrombin-Antithrombin
Complex</b>. But <b>Heparin </b>cannot inhibit <b>Fibrin bound Thrombin. </b>Heparin
can bind independently to <b>Fibrin </b>and <b>Thrombin</b> to form <b>Fibrin-Heparin-Thrombin</b>
bridge.<o:p></o:p></p>
<p>It has been documented that both <b>unfractionated heparin </b>(UFH) and <b>low
molecular weight heparin </b>(LMWH) are associated with variable <b>anticoagulant
effect</b> and <b>heparin induced thrombocytopenia</b> (HIT) in around 3%
cases. <b>Warfarin</b> acts as a <b>Vitamin-K</b> <b>antagonist</b> to inhibit
formation of clotting factors (II, VII, IX, X). Vitamin-K antagonists have a number
of shortcomings, including a delayed onset of action and interindividual
variability in <b>anticoagulant effect</b>. Other drugs and foods have also
been reported to alter anticoagulant effect of Vitamin-K antagonists. Anticoagulant
treatment requires regular and frequent monitoring.<o:p></o:p></p>
<p>The effectiveness of <b>heparin</b> and <b>warfarin</b> in prophylaxis and
treatment of various <b>thromboembolitic disorders </b>has been well
established.<b> </b> Effective use of
these drugs comes with a steep cost of various side effects and problems like
bleeding tendencies and <b>immune thrombocytopenia</b>. Parenteral administration
needs hospitalization and constant monitoring during therapy.</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-23352356480980198582018-01-01T09:33:00.000-07:002018-01-01T09:33:59.665-07:00Happy New Year - 2018<div dir="ltr" style="text-align: left;" trbidi="on">
<br />
<span style="color: purple;"><br /></span>
<br />
<div class="MsoNormal" style="margin: 0in 0in 0pt;">
<span style="color: purple;"><b style="mso-bidi-font-weight: normal;"><span style="color: #660033;">Dr. CS Rayat wishes his Followers & Friends “A Very Happy & Prosperous New Year-2018”.<o:p></o:p></span></b></span></div>
<span style="color: purple;"><span style="color: black;"></span><br /></span>
<br />
<div class="MsoNormal" style="margin: 0in 0in 0pt;">
<b style="mso-bidi-font-weight: normal;"><span style="color: #660033;">“May every ray of the Sun fill your life with Success and Ultimate Happiness in 2018”<o:p></o:p></span></b></div>
<span style="color: purple;"><span style="color: black;"></span><br /></span>
<br />
<div class="MsoNormal" style="margin: 0in 0in 0pt;">
<div style="margin: 0px;">
<b style="mso-bidi-font-weight: normal;"><span style="color: #660033;">CS Rayat</span></b></div>
</div>
</div>
Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-47675951210740434942014-03-25T11:11:00.001-06:002014-03-25T11:11:47.478-06:00Tuberculosis of Kidneys and Genital Glands<div dir="ltr" style="text-align: left;" trbidi="on">
<br />
<span style="font-family: inherit;">The <b>tuberculosis</b> <b>of kidneys</b>, <b>testicles</b> or <b>ovaries</b>
(<b style="mso-bidi-font-weight: normal;">genital glands</b>) is always <b>secondary</b>
to <b>primary lesion</b> in the<b> lungs, lymph glands</b> or <b>bones</b>. The
<b>tuberculosis</b> <b>of kidneys</b> may occur in early adult life. In the
beginning it is commonly <b>confined to one kidney</b> but can spread to second
kidney if chemotherapy is delayed. If the disease is not detected and treated
well in time<b>, </b>it may <b>spread to urinary bladder</b>. In addition to
low grade fever in the evening, feeling of general weakness and loss of
appetite, it has <b>three additional symptoms:</b> increased <b>frequency o</b><b style="mso-bidi-font-weight: normal;">f <span style="mso-bidi-font-weight: bold;">urination</span></b>,
<b>painless hematuria</b> or <b>passage of red blood cells</b> or <b>blood</b>
in the urine and a feeling of <b>dull pain </b>in the <b>lower back</b> or <b style="mso-bidi-font-weight: normal;">region of loin</b>. The <b>'tubercular toxemia'</b>
is there. The treatment with <b>anti-tubercular drugs is must </b>to avoid
surgical nephrectomy.<o:p></o:p></span><br />
<span style="font-family: inherit;">
</span><br />
<span style="font-family: inherit;">The <b>tuberculosis of testicles or ovaries </b>(<b>genital glands</b>) is
also a serious manifestation of <b>pulmonary tuberculosis</b>. Initially there
is swelling of one testicle in the male patient which can be easily felt. Later
on it may transform into <b>'cold abscess'</b> and a sinus is produced. Such
patients show highly reactive <b>'tuberculin test'</b>. The diagnosis is not
difficult in a case of <b>'tuberculosis of ovary'</b>. The swelling of the
ovary can be palpated by experienced gynaecologist or can be detected by <b>abdominal</b>
<b>ultrasonography</b>. The diagnosis can be confirmed easily by <b>'fine
needle aspiration cytology' </b>(<b>FNAC</b>). The signs and symptoms of <b>'tubercular
toxemia'</b> are there as stated in the case of <b>tuberculosis</b> <b>of
kidneys</b>. The treatment with <b>anti-tubercular drugs is must </b>to avoid
surgical removal of testicle or ovary.<o:p></o:p></span><br />
<span style="font-family: inherit;">
</span><br />
<span style="font-family: inherit;">The treatment begins with active <b>anti-tubercular therapy </b>by the use
of at least three drugs and a longer course of treatment may be required in
these cases. Surgical treatment will be required if the medical treatment alone
is not capable of controlling the disease. If the disease is unilateral in one
kidney or one testicle and there is no arrest of the disease with medical
treatment, these organs would have to be removed surgically with <b>informed
consent of the patient</b>.</span><br />
<o:p><span style="font-family: inherit;"></span></o:p><br />
<span style="font-family: inherit;">
<span style="font-family: "Times New Roman","serif"; font-size: 12pt; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-US;"><span style="font-family: inherit;">To read more about <b style="mso-bidi-font-weight: normal;">‘tuberculosis of lymph glands’ </b>just <b style="mso-bidi-font-weight: normal;">click</b> the following link: </span><a href="http://ntips4u.blogspot.in/2014/03/tuberculosis-of-lymph-glands-common.html"><span style="color: #0563c1; font-family: inherit;">http://ntips4u.blogspot.in/2014/03/tuberculosis-of-lymph-glands-common.html</span></a></span></span></div>
Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com1tag:blogger.com,1999:blog-6350978014173423850.post-2785893953173696992014-02-13T08:05:00.000-07:002014-02-20T07:13:10.060-07:00Dialysis Technology: Application of dialysis in acute renal failure !<div dir="ltr" style="text-align: left;" trbidi="on">
<span lang="EN-US">Our kidneys are destined to perform excretory as well as
regulatory function to maintain a state of homoeostasis in our body. <b>Acute
renal failure </b>(<b>ARF</b>) is a syndrome defined as sudden or rapid loss of
<b>renal function </b>(<b>kidney function</b>) leading to accumulation of <b>urea</b>
and <b>creatinine</b> (<b>nitrogenous waste compounds</b>). If hyperbolic
relationship between <b>plasma creatinine </b>or <b>urea</b> and <b>glomerular
filtration rate </b>(<b>GFR</b>) is observed after investigations, the
diagnosis is established as <b>ARF</b>. The early clinical signs of <b>ARF/uremia</b>
are <b>anorexia</b>, <b>nausea</b>, <b>vomiting</b>, and sometimes <b>pericarditis</b>
also. The <b>ARF</b> is an implication of loss of more than 50% of <b>renal
function</b>. <b>Dialysis</b> should be instituted whenever early signs of
<b>uremia</b> (<b>elevated levels of urea in the blood</b>) are present. Cases
of <b>metabolic acidosis</b> as well as <b>electrolyte and fluid imbalance</b>
also need <b>dialysis</b> for the reversal of <b>hemodyanmics</b> to normal.<o:p></o:p></span><br />
<span lang="EN-US"><br /></span>
<b><span lang="EN-US">Dialysis</span></b><span lang="EN-US"> is a procedure for
artificially purifying the blood of a patient through meticulous surgical
intervention and electromechanical equipment. No specific <b>elevated value</b>
of <b>plasma creatinine</b> or <b>urea</b> could be regarded as critical. The
fluid intake and nutritional requirements are taken into consideration for
deciding the <b>timing</b> and <b>mode of dialysis</b>. Cases of <b>ARF</b>
should be put on <b>dialysis</b> without much delay for the successful recovery
of their <b>renal function</b>. However, cases of <b>chronic renal failure </b>(<b>CRF</b>)
may be kept in waiting. The <b>dialysis procedure </b>is of two types: <b>i)
Hemodialysis</b> (where patient's blood is passed through artificial kidney in
conjunction with dialysis solution) and <b>ii) Peritoneal dialysis</b>
(where dialysis fluid is passed through the abdominal peritoneal cavity of the
patient). The technique of <b>dialysis</b> was established long back in <st1:country-region w:st="on"><st1:place w:st="on">USA</st1:place></st1:country-region> by Dr. Alan
P Kendal, who also patented a <b>'suitcase kidney'</b> in 1978.<o:p></o:p></span><br />
<br />
<b><span lang="EN-US">Conventional</span></b><span lang="EN-US"> <b>hemodialysis
</b>remains the preferred and the best mode of <b>dialysis</b>. The <b>hemodialysis
</b>is ideal for <b>non-hypotensive</b> and <b>hemodynamically</b> <b>stable</b>
patients. <b>Peritoneal dialysis</b> is probably less effective in patients
with <b>hypercatabolic disorder </b>and/or with undiagnosed abdominal disease. <b>Peritoneal
dialysis</b> should be avoided in patients with recent abdominal surgery. The
surgical intervention for hemodialysis can be in the <b>following ways:</b> <b>i)
Continuous arteriovenous hemofiltration </b>(<b>CAVH</b>), <b>ii)
Continuous arteriovenous hemofiltration with/without concomitant dialysis</b>
(<b>CAVHD</b>), <b>iii) Continuous veno-venous filtration</b> (<b>CVVHD</b>).
These <b>hemodialysis techniques</b> are simpler, safe and very effective. The
biochemical recovery is monitored during the dialysis for needful correction of
fluid and electrolytes. After successive dialysis sessions the patient would
return to normal health.<o:p></o:p></span></div>
Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com2tag:blogger.com,1999:blog-6350978014173423850.post-36141031831512146282011-04-07T07:26:00.002-06:002011-04-07T07:37:50.544-06:00How does kidney develop during gestation ?<p>The students of <b>renal pathology</b>, medicine, <b>nephrology</b> and urology would always like to imbibe knowledge about the origin and development of kidney to understand the pathogenesis of developmental kidney diseases. The <b>urogenital system</b> is derived and developed from the intermediate mesoderm and the primitive urogenital sinus of the cloaca. The<b> ureteral bud</b> (<b>UB</b>) develops from the <b>Wolffian duct</b> (<b>WD</b>) at approximately 28 days of gestation. The <b>ureteral bud</b> (<b>UB</b>) initiates the <b>epithelialization/tubulogenesis </b>of the <b>metanephric mesenchyme</b> (<b>MM</b>) while itself undergoes branching to form and <b>adult kidney</b>. Much knowledge about the development of kidney could be gathered from the experimental studies using mouse embryo. In the mouse the <b>ureteral bud</b> (<b>UB</b>) invaginates from the caudal end of the<b> Wolffian duct</b> (<b>WD</b>) and grows out into the adjacent <b>metanephric mesenchyme cells</b>.</p><p>
</p>The <b>metanephric mesenchyme cells </b>comprise of tubule precursors, endothelial precursors and stromal cells. These loose <b>metanephric mesenchyme cells </b>aggregate to<b> </b>form "<b>pre tubular aggregate</b>" which undergoes structural change to form a '<b>tear-drop'</b> like structure called <b>renal vesicle (RV)</b>. The <b>renal vesicle</b> rapidly undergoes<b> mesenchymal-epithelial transformation</b> (<b>MET</b>) to form a <b>comma-shaped structure</b>. The <b>comma-shaped structure</b> formed by the mesenchymal-epithelial<b> transformation</b> of <b>RV</b> undergoes series of tightly controlled transformations and form a very complex <b>S-shaped body</b>. The lower part of the "<b>S</b>" (of S-shaped body) gives rise to <b>podocytes</b> and<b> Bowman's capsule</b>. The upper part of the "<b>S</b>" (of S-shaped body) forms the <b>distal convoluted tubule</b> of the <b>nephron</b>. The middle segment of the "<b>S</b>" (of S-shaped body) gives rise to the proximal<b> convoluted tubule</b> and the <b>loop of Henle</b> of the <b>nephron</b>. Each tip of the <span style="font-weight: bold;">ureteral</span><b> bud</b> gives rise to a <b>nephron</b>. After 20-22 weeks of gestation in humans, the <span style="font-weight: bold;">ureteral</span><b> bud</b> stops branching but the <b>nephron</b> induction continues for other 8 to10 weeks, leading to arcade formation wherein each tip of the <b>ureteral bud</b> has 9-11 <b>nephrons </b>attached to it. The arcade formation is considered as the last step of the <b>nephron induction</b> in humans. However, in mice the process of <b>nephron induction </b>continues for about two weeks after birth. The mouse <b>kidney</b> has single <b>papilla</b> and carries around 35,000 <b>nephrons/kidney</b>. Human <b>kidneys </b>roughly contain 6x10<sup>5</sup> to 1.1x10<sup>6</sup> <b>nephrons/kidney</b>.
<p>The knowledge of developmental stages of kidney is important to understand the pathogenesis of developmental cystic kidney diseases like <b>renal agenesis</b> (no kidney developed), <b>renal hypoplasia</b> (under developed kidneys) and <b>renal dysplasia</b> (abnormally developed kidneys).<b> Renal hypoplasia </b>(reduction in total number of nephrons), <b>renal dysplasia</b> (abnormally developed kidney due to failure of UB to induce formation of nephrons) and <b>segmental hypoplasia</b> are the major <b>developmental cystic kidney diseases</b>. <span style="font-weight: bold;">Simple</span> <b>hypoplasia</b> leads to very small sized kidney called <b>miniature kidney</b>. Miniature kidney would represent reduction in renal calyces with glomerular disarray and reduction of tubules, medulla & cortex. <b>Segmental hypoplasia</b> presents during the late childhood with renal insufficiency associated with hypertension and recurrent urinary tract infection (UTI). Patients with <b>segmental hypoplasia</b> have small sized kidney (s) with a transverse groove on the capsular surface at the upper pole, overlying an area of marked parenchymal thinning. Areas of <b>segmental hypoplasia</b> represented by scarred zones with no glomeruli, atrophic tubules and thick walled blood vessels could be revealed under light microscopy of histological sections.
</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com3tag:blogger.com,1999:blog-6350978014173423850.post-11146184720571257572010-07-27T09:16:00.004-06:002010-07-27T09:30:47.238-06:00Podocytes and Podocytopathies<p>Kidneys play a vital role in excretion and water/fluid volume regulation. <b>Glomeruli</b> are the filtration units of <b>nephrons</b> in the kidneys and these contain cellular and non cellular components in addition to capillary space and urinary space. <b>Podocytes</b> (cells with pedicles or feet) are post-mitotic epithelial cells resting in the urinary space of <b>glomeruli</b>. The number, size and morphology of <b>podocytes</b> are influenced by biochemical, immunological, therapeutic and genetic factors. According to the old classification of renal disorders, the patients having nephrotic syndrome can be grouped into two groups: (1) <b>Non-immune complex mediated nephrotic syndrome</b>, and (2) <b>Immune complex mediated nephrotic syndrome</b>. Now, patients with <b>non-immune complex mediated nephrotic syndrome </b>may have three possible diagnoses:</p><ol><li><b>Minimal change disease: </b>Wherein morphologic evaluation of the <b>renal biopsy </b>(kidney biopsy) by light microscopy does not exhibit any glomerular damage. However, extensive effacement of foot processes of <b>podocytes</b> can be revealed by electron microscopy.</li><li><b>Focal segmental glomerulosclerosis (FSGS):</b> Wherein segmental sclerosis/solidification of the glomerular tuft, along with hyalinosis and adhesion of tuft to the Bowman's capsule is exhibited on the <b>renal biopsy </b>(kidney biopsy) evaluation by light microscopy. In these cases, variable degree of foot process effacement can be revealed by electron microscopy.</li><li><b>Collapsing glomerulopathy: </b>FSGS associated with the rapid deterioration of <b>renal function</b> was described as "<b>Malignant FSGS</b>" in 1978. During HIV pandemic in 1980's the associated nephropathy showing collapse of glomerular capillary wall along with increased cellularity in the urinary space was termed as HIV associated nephropathy (HIV-AN). <b>Collapsing glomerulopathy</b> was first time described in non-HIV patients in 1986 by Weiss and associates. </li></ol><p>Now we know that <b>podocyte number</b> and <b>effacement </b>of their <b>foot processes</b> due to genetic or biological factors are very much associated with the <b>primary nephrotic syndrome </b>or <b>proteinuric renal disorders</b>. The etiology and pathogenic mechanisms are known to influence the morphologic diagnosis of <b>podocytopathies</b>. Podocytopathies are <b>proteinuric renal disorders</b> caused due to intrinsic or extrinsic podocyte injury exhibited by variable degree of foot process effacement and altered genotypic and/or phenotypic expression. <b>Podocytes</b> may reorganize their foot processes (altered cell morphology without change in cell count/number). There may be <b>decreased number of podocytes</b> (podocytopenia) if the injured podocytes die. There may be <b>podocyte developmental arrest</b> as seen in <b>congenital nephrotic syndrome</b> of <b>Finnish type </b>(CNF). <b>Podocytes </b>may <b>dedifferentiate </b>and <b>proliferate </b>under genetic, immunological, viral or therapeutic insult and re-enter the cell cycle despite the fact that podocytes are post-mitotic cells. Two electron micrographs are exhibited below to illustrate the normal (Figure-1) and increased number(Figure-2) podocytes in the urinary space of glomeruli from different cases.</p>
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgRrNDl_oerVuPL7c_WmPrZGNBQ24gIN4NH_koQ6kmxRI4avxLjlDdYrooAoQnyi1n2y1gb69-MriGSh9T2tFgXOctaI_22A3Jj1YUkuVNHsplMRmAt6gq7Fhti5bjXMJe0CwJvm5QtBSo/s1600/Podocyte-1.jpg"><img id="BLOGGER_PHOTO_ID_5498605903948272002" style="WIDTH: 320px; CURSOR: hand; HEIGHT: 316px" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgRrNDl_oerVuPL7c_WmPrZGNBQ24gIN4NH_koQ6kmxRI4avxLjlDdYrooAoQnyi1n2y1gb69-MriGSh9T2tFgXOctaI_22A3Jj1YUkuVNHsplMRmAt6gq7Fhti5bjXMJe0CwJvm5QtBSo/s320/Podocyte-1.jpg" border="0" /></a>
<p><b>Figure-1:</b> Electron micrograph through a portion of glomerulus from a case of minimal change disease showing normal number of podocytes. (GBM: glomerular basement membrane, CL: capillary lumen, EnC: Endothelial cell, US: urinary space and Pc: podocyte)</p>
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiJZrPNZmShVDDHSKuY_FwMFWk9AZoOIkm58yeA5SsMygr4oBnvvVX41RV3RsASsOmv5RxAbExXOcGzWdTTWdoQMLuHVEudZMqQVKrlxosAe5UaUNP9JjfwnlDwTb7Byk42jaSbT82C3fY/s1600/Podocytes-N.jpg"><img id="BLOGGER_PHOTO_ID_5498606526821280370" style="WIDTH: 320px; CURSOR: hand; HEIGHT: 318px" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiJZrPNZmShVDDHSKuY_FwMFWk9AZoOIkm58yeA5SsMygr4oBnvvVX41RV3RsASsOmv5RxAbExXOcGzWdTTWdoQMLuHVEudZMqQVKrlxosAe5UaUNP9JjfwnlDwTb7Byk42jaSbT82C3fY/s320/Podocytes-N.jpg" border="0" /></a>
<p><b>Figure-2:</b> Electron micrograph through a portion of glomerulus from a case of podocytopathy showing increased number of podocytes. (GBM: glomerular basement membrane, CL: capillary lumen, US: urinary space and Pc: podocytes)</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-34019176613144749292010-06-30T09:14:00.002-06:002010-06-30T09:22:22.612-06:00End Stage Renal Disease: Management Issues<p>The patents with <b>end stage renal disease</b> (ESRD) need regular hemodialysis or <b>renal replacement</b> (kidney transplantation) for survival. Both the hemodialysis and kidney transplantation are very costly procedures for the patients and their families. The patients with <b>chronic kidney disease </b>(CKD) are at high risk of developing <b>end stage renal disease</b> (ESRD). <b>Chronic kidney disease</b> (CKD) is diagnosed on the basis of persistently high level of <b>serum creatinine</b> (more than 1.8 mg/dl). As a rough estimate one person in every 150 people may be suffering from CKD and around 3% of CKD cases are sure to develop ESRD. In a country with 500 million population there could be more than 100,000 patients with ESRD and around 3.5 million patients with CKD. Half of the projected figures could be annual incidence. </p>
<p>It has been worked out that the cost of annual dialysis is much more than the <b>renal replacement therapy </b>(RRT). Though the <b>renal transplantation </b>(kidney transplantation) is the more effective and sustainable therapy but the economic factors, availability of kidney and facilities retard its scope. The annual cost of dialysis may range from US$5000 to 10,000 depending on condition of the patient; whereas the one-time cost of <b>renal transplantation</b> at government funded hospitals in most of the developing countries ranges from US$1500 to US$2000 and annual cost of immunosuppressive therapy would be around US$3000 to 4000. As compared to patients on dialysis, the quality of life for the patients of <b>renal transplantation</b> is extremely better. A <b>renal transplantation</b> at an optimum time minimizes the graft maintenance costs and maximizes the graft survival. The patient can return to productive life within a year after <b>renal transplantation</b>. My friend <b>AB</b>, who got <b>renal transplantation</b> around 10 year ago, is living a normal life.</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-87931163568878254012010-06-29T06:20:00.002-06:002010-06-29T06:25:38.113-06:00Kidney Diseases caused by Plasma Cell and B-Cell Disorders<p>A wide spectrum of clinical manifestations may result from the <b>renal involvement</b> with disorders of <b>B-cells</b> (B lymphocytes) and <b>plasma cells</b>. B lymphocytes and plasma cells are responsible cells for providing acquired and active immunity to our body through production of antibodies (immunoglobulins) against infectious organisms. But the disorders related to the function and number of <b>B-cells</b> and <b>plasma cells</b> lead to excessive or incomplete production of immunoglobulin molecules leading to deposition of immunoglobulins or their components in the <b>kidneys</b>. Deposition of immunoglobulins or their light or heavy chains cause a variety of <b>renal disorders</b> affecting glomeruli, extraglomerular blood vessels, tubules and interstitium. Two major classes of such diseases are as under:</p>
<p><b>A) Glomerular</b> <b>and</b> <b>vascular diseases</b></p><p><b>Glomerular</b> and <b>vascular diseases</b> caused by B-cell and plasma cell disorders include <b>amyloidosis</b> (AL, AH and AHL type), light chain deposition disease (LCDD), heavy chain deposition disease (HCDD), light & heavy chain deposition disease (LHCDD), cryoglobulinemic glomerulonephritis (type I & II), monoclonal immunotactoid glomerulopathy and proliferative glomerulonephritis with monoclonal IgG deposits. </p>
<p><b>B) Tubulointerstitial diseases</b></p><p>Cast nephropathy and light chain proximal tubulopathy are the <b>tubulointerstitial diseases </b>caused due to renal involvement in multiple myeloma (<b>Plasma cell disorder</b>).</p>
<p><b>Important Investigations</b></p><p>Routine urine examination along with microscopy, blood biochemistry to ascertain renal functions and kidney biopsy evaluation by light, fluorescence and electron microscopy is required to establish an accurate diagnosis of <b>renal disorder</b> in patients affected by <b>B-cell</b> and <b>plasma cell disorders</b>.</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com1tag:blogger.com,1999:blog-6350978014173423850.post-66608546116067139002010-04-19T07:11:00.003-06:002010-04-19T07:24:52.268-06:00The Role of Lymphatic System in Cellular Nutrition and Immunity<p>Every single cell in our body tissues and organs needs nutrition and clearing away of its waste products for survival and vital functioning. Lymphatic system plays a vital role in the circulation and regulation of interstitial fluid or tissue fluid. As the blood passes through blood capillaries in the tissues; plasma or tissue fluid oozes out through the porous walls of blood capillaries. The tissue fluid or the interstitial fluid fills the spaces or interstices between the cells of different tissues and organs. The blood circulates only through the blood vessels but the tissue fluid circulates through the actual tissue and carries food, oxygen and water from the blood stream to each individual cell and carries away its waste products like carbon dioxide, water and urea and pours out all these in the blood stream for final disposal. Lymphatic system is pump less system and runs parallel to the circulatory system and is comprised of following components.</p><p><b>Components of the Lymphatic System:</b></p><ol type="i"><li><b>Lymphatic capillaries:</b> These are hair like fine vessels in the spaces in the tissues and gather up excess fluid from the tissues. Lymphatic capillaries unite to form lymphatic vessels.</li><li><b>Lymphatic vessels: </b>These are similar to veins in structure but carry lymph instead of blood. They are finer and more in number than the veins and are provided with unidirectional valves, to prevent the back flow of lymph or the tissue fluid. Lymphatic vessels are present in all tissues except the central nervous system. These run in the subcutaneous tissue and pass through one or more lymphatic nodes. </li><li><b>Lymph nodes or lymphatic nodes: </b>Lymph nodes are numerous in number and vary in size from a pinhead to an almond. Lymphatic vessels which bring lymph to them are called afferent vessels. afferent vessels divide up within the node and discharge the lymph into the mesh of the lymph node. The lymph is collected again into a fresh vessel known as efferent vessel, which ultimately empties into a lymph duct. Lymph nodes consist of cells similar to white blood cells and are encapsulated by connective tissue. Lymph nodes filter out bacteria, provide fresh lymphocytes for the circulation and also produce some antibodies and antitoxins and boost up immunity.</li><li><b>Lymphatic ducts: </b>These are major lymph channels. There are two lymphatic ducts,<b> </b>the <b>thoracic duct</b> and the <b>right lymphatic duct</b>. The <b>thoracic duct</b> is larger and all the lymphatic vessels from the lower limbs, and abdominal and pelvic organs empty into it. The thoracic duct empties into the <b>left subclavian vein</b>. The <b>right lymphatic duct</b> is comparatively small vessel formed by union of lymphatic vessels from the right side of the head, thorax and the right upper limb at the root of the neck. The <b>right lymphatic duct</b> is about one centimeter long and empties into the <b>right subclavian vein</b>.</li><li><b>Spleen, the master lymphatic organ:</b> The spleen is the largest nodule of the lymphoid tissue. It is deep purplish red in color and lies high up at the back of the abdomen, on the left side behind the stomach and is enclosed in a capsule of connective tissue. It is composed of fibrous meshwork filled with pulp like material known as splenic pulp. It is a source of fresh lymphocytes for the blood stream, an area for the destruction of worn red blood cells (RBCs) and a legendary organ for fighting out circulatory infections.</li></ol><p><b>Functions of Lymphatic System:</b></p><ol type="i"><li>Restoration of constant stream of fresh interstitial fluid or lymph in the interstitial spaces as depicted in the diagram given below:</li></ol><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjqJI_SOowv9DrcqIguArtpacXMGlhd79aYlwxExzXoCiSgctV0VNHGAX9HaY9YerlYjGXAhWNeCjt5K8m69AAfCle0CSN-xMkdjqt_XHSvX-IkfRRvt0-BCya3w9MxllTFETleQ4K-fd0/s1600/Lymphatic+System_59.JPG"><img id="BLOGGER_PHOTO_ID_5461836431425115714" style="WIDTH: 320px; CURSOR: hand; HEIGHT: 235px" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjqJI_SOowv9DrcqIguArtpacXMGlhd79aYlwxExzXoCiSgctV0VNHGAX9HaY9YerlYjGXAhWNeCjt5K8m69AAfCle0CSN-xMkdjqt_XHSvX-IkfRRvt0-BCya3w9MxllTFETleQ4K-fd0/s320/Lymphatic+System_59.JPG" border="0" /></a>
<ol type="i" start="2"><li>Regulation excess proteins in the tissue fluid and passing that back to the blood stream.</li>
<li>The lymph nodes filter out the bacterial infection and harmful substances from the lymph before pouring it back into the blood stream.</li>
<li>Lymphatic vessels in the abdominal organs assist in the absorption of digested fat.</li>
<li>Lymph nodes also produce fresh lymphocytes for the circulation.</li></ol>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-70199418334092957492010-04-13T07:40:00.002-06:002010-04-13T07:47:58.213-06:00Disseminated Intravascular Coagulation: Pathophysiology and Diagnosis<p><b>Disseminated intravascular coagulation</b> (DIC) should be recognized as consumptive <b>coagulopathy</b> since it is not a primary disease. It is always a complication of an underlying disease that not only triggers it but also fuels it. Disease or trauma associated tissue injury with a release of thromboplastic material into the circulation is the major cause of DIC. The clotting system as well as the fibrinolytic system (bleeding system) are involved in the <b>pathophysiology</b> of <b>disseminated intravascular coagulation</b>. Clinically, coagulopathy could be recognized as acute hemorrhagic DIC and subacute or chronic DIC. A third type of consumptive coagulopathy could be recognized with fibrinolysis. <b>Disseminated intravascular coagulation</b> is an acquired coagulation disorder in which formation of microthrombi, consumption of coagulation factors, activation of fibrinolysis and a bleeding tendency may occur consecutively or simultaneously. In brief, it is a systemic pathologic process characterized by a disseminated (generalized) activation of <b>clotting </b>and/or <b>fibrinolytic</b> <b>systems</b> in the circulatory system of the patient. The common pathway of all inciting causes (independent of etiologies) is the formation of thrombin and plasmin (fibrinolysin).</p><p><b>Thrombin</b> plays a vital role in DIC. The alterations of coagulation system detected in the laboratory during DIC reflect the multiple actions of thrombin. <b>Thrombin</b> cleaves <b>fibrinogen </b>to release <b>fibrinopeptide-A</b> (FPA) and <b>fibrinopeptide-B</b> (FPB). Subsequently the remaining <b>fibrin monomers</b> may combine with fibrinogen and circulate as <b>soluble fibrin monomer complexes</b> (SFMC) or polymerize to form <b>fibrin microthrombi</b>. Thrombin also activates factor XIII (fibrin stabilizing factor) to form factor XIIIa, and the factor XIIIa creates bridges, linking any two adjacent monomers of fibrin. <b>Thrombin</b> activates procoagulant cofactors, factors VIII and V, to participate in the process of its own generation. Thrombin also plays a regulatory role by activating protein-C, which acts as an anticoagulant to inactivate factors VIIIa and Va. In brief, thrombin alone accounts for decreased levels of fibrinogen and factors II, V, VIII & XIII and decreased count of platelets in patients with DIC.</p><p><b>Screening tests for DIC are:</b> Prothrombin time (PT), Partial thromboplastin time (PTT), Fibrinogen assay and Platelet count. Platelet count, PT, Fibrinogen assay and Determination of Antithrombin-III (AT-III) should always be done to diagnose consumptive DIC. </p><p><b>Confirmatory tests for DIC are:</b> Fibrin monomer assay (it measures thrombin cleaved fibrinogen), Detection of fibrin split products (i.e. detection of plasmin-cleaved fibrinogen or fibrin) and Detection of D-dimer (i.e. detection of plasmin-cleaved cross-linked fibrin). Activation of coagulation could be assessed by the detection of <b>soluble fibrin monomer complexes</b>(SFMC). Detection of <b>fibrinogen degradation products</b> (FDPs) is indicative of reactive fibrinolysis.</p><p><b>Medical conditions which may lead to 'Acute Hemorrhagic DIC':</b></p><ul><li><b>Infections:</b> Typhoid fever, Gram-positive and Gram-negative septicemia, viremia, parasites etc.</li><li><b>Tissue injury: </b>Renal allograft rejection, snake bite, heat stroke, brain injury, crush injury, necrotizing enterocolitis, hemolytic transfusion reaction etc.</li><li><b>Malignancy: </b>Acute promyelocytic leukemia.</li><li><b>Obstetric:</b> Amniotic fluid embolism, eclampsia, abruptio placentae, hypertonic saline abortion.</li><li><b>Other causes: </b>Severe liver disease.</li>
</ul><p><b>Medical conditions which may lead to 'Subacute Chronic DIC':</b></p><ul><li><b>Vascular:</b> Chronic renal disease, connective tissue disorders, venous thrombosis, arterial embolization, pulmonary embolus etc</li><li><b>Obstetric:</b> Retained dead fetus.</li><li><b>Malignancy:</b> Mucin-producing adenocarcinomas.</li></ul>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-86398870583079691512010-02-28T23:18:00.002-07:002010-02-28T23:24:51.666-07:00Nephritic Syndrome and Urine Examination<p>Examination of fresh urine as part of routine physical examination may show the presence of protein, blood or pus cells in the patients affected by <b>nephritic syndrome</b>. In many cases the renal disease is occult and is often detected during the routine physical examination. It is important to understand that acute <b>nephritis</b>, <b>nephrotic syndrome</b> and <b>renal failure</b> may occur either as a result of intrinsic disease of the kidneys or in association with a systemic disease. Metabolic and functional disturbances such as <b>hypertension</b>, <b>uremia</b> (elevated level of urea in blood), or <b>anemia</b> may cause occult renal disease.</p><p>Hypertension along with mild <b>edema</b> (swelling), apparently as suborbital puffy eyes is characteristic clinical feature of <b>nephritic syndrome</b>. <b>Hematuria</b> (blood in urine) with or without <b>proteinuria</b> (protein in urine), <b>oliguria </b>(low urinary output) and impaired excretory function are other characteristic features. The urine may be red or brownish to smoky brown in color in patients affected by <b>nephritic syndrome</b>. Microscopic examination of fresh urinary sediment in these patients may reveal very high count of <b>dysmorphic red blood cells</b> (dysmorphic RBCs). The detection of RBCs in the urinary casts signifies that the <b>hematuria</b> comes from the kidneys (renal parenchyma). <b>Proteinuria</b> may vary from 0.3g to 3.0g daily. <b>Urinary</b> <b>sodium level </b>(Na<sup>+</sup> level) tends to be low due to <b>sodium retention</b> as a result of
impaired excretory function by the kidneys. Retention of <b>sodium</b> <b>and water</b> in these patients lead to increased circulatory blood volume and cause hypertension. The uncontrolled hypertension may lead to cardiomegaly along with mild renal pain. Patients affected by <b>nephritic syndrome</b> need <b>renal biopsy </b><b>examination</b> and specialized treatment under the supervision of a nephrologist.</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-76655566493211173602010-02-24T05:37:00.002-07:002010-02-24T05:48:46.276-07:00Diagnosis and Type of Kidney Disease – Investigations and interpretations<p>Correlation of clinical and laboratory features is must for an accurate diagnosis and type of a kidney disease (<b>renal disease</b>) or <b>glomerulonephritis</b>. An experienced nephrologist can make a diagnosis of <b>glomerulonephritis</b> from thorough history, physical examination, urine examination and microscopy of urinary sediment. The assessment of presenting features of the patient, such as <b>nephritic</b> or <b>nephrotic syndrome</b> is important. However, the decision on the type of <b>glomerulonephritis</b> can not be based on the clinical and laboratory features; as the <b>nephrotic syndrome</b> may occur with any <b>histological glomerulonephritis</b>, and <b>nephritic syndrome</b> is the outcome of <b>proliferative glomerulonephritis</b>. So the ultimate diagnostic tool is <b>renal biopsy </b>and its <b>light and fluorescent microscopy</b> as well as <b>ultrastructural study</b> by <b>electron microscope</b>.</p><p>The interpretation of clinical features in the light of histological diagnosis of <b>renal biopsy</b> helps the clinician to detect any systemic disease associated with the <b>renal disease</b> (kidney disease). Majority of the patients with suspected <b>glomerulonephritis</b> need <b>renal biopsy evaluation</b>. However, in children with <b>nephrotic syndrome;</b> if there is no <b>microscopic hematuria</b> (blood in urine) and red cells' or granular casts, <b>renal biopsy procedure</b> may be avoided initially. In patients, who do not respond to steroid therapy; <b>renal biopsy</b> investigation is must. There are around one million glomeruli (1x10<sup>6</sup> glomeruli) in each kidney and at least 5 glomeruli should be included in the <b>renal biopsy </b>evaluated histologically to achieve a diagnosis of <b>glomerulonephritis</b>.</p><p><b>Radiological and laboratory investigations in glomerulonephritis:</b></p><p>The clinical presentation, urine-analysis and microscopy findings, and presence of a normal upper & lower urinary tract on intravenous pyelography (IVP: a radiological investigation) or ultrasonography without any renal scarring could be indicative of <b>glomerulonephritis</b>, but there could be a need for <b>renal biopsy</b>. </p><p><b>Immune system associated investigations:</b></p><p>Our body is equipped with a multitasking immune system composed on lymphocytes, antibodies and complement system. The immune system always defends our body internally against a variety of infections and pathological conditions; and assessment of its components and abnormal products produced by it helps in diagnostic conclusions. Complement system of our body is composed of 9-components and boosts the body defense in association with cellular components. The blood level of complement components C3, C4 and C1q may be reduced or normal in some renal diseases. Low total serum complement, C3, C4 and C1q levels are observed in <b>glomerulonephritis</b> associated with circulatory immune complex disorders like systemic-lupus erythematosis (SLE), bacterial endocarditis and serum sickness. Normal levels of C4 and C1q but decreased level of C3 is generally observed in <b>membranoproliferative glomerulonephritis </b>(MPGN) and dense deposit disease of the kidney.</p><p>Following investigations are considered important to ascertain the <b>diagnosis and type of glomerulonephritis:</b></p><p><b>Investigations for likely diagnosis of glomerulonephritis:</b></p><ul><li>Clinical presentation</li><li>Urine analysis (proteinuria, hematuria and electrophoresis)</li><li>Microscopy of urinary sediment</li><li>Intravenous pyelography (IVP: Radiological investigation)</li><li>Abdominal ultrasonography.</li>
</ul><p><b>Investigations for likely type of glomerulonephritis:</b></p><ul><li>Estimation of serum complement components' level</li><li>Detection of circulating immune complexes</li><li>Detection of auto-antibodies such as anti-nuclear antibodies (ANA), anti-DNA antibodies and anti-glomerular basement membrane antibodies (anti-GBM antibodies)</li><li>Renal biopsy</li></ul><p><b>Investigations for assessing the implications of glomerulonephritis and monitoring the effect of therapy:</b></p><ul><li>Determination of 24 hour urinary protein</li><li>Determination of level of serum proteins</li><li>Determination of serum cholesterol and/or lipid profile</li><li>Determination of serum creatinine, blood urea and serum electrolytes.
</li></ul>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-36572098322035572632010-01-27T06:28:00.004-07:002010-01-27T06:53:34.107-07:00Diabetic Renal Disease<p><b>Diabetes</b> is a multidisciplinary disease, as many systems may need medical care. Optimal control of blood glucose level is essential to prevent <b>diabetic complications</b> like neuropathy, <b>diabetic renal disease </b>(diabetic nephropathy) and diabetic disease of eyes (diabetic retinopathy). There may also vascular and cardiac complications associated with <b>diabetes</b> in some patients. <b>Diabetes </b>may be <b>insulin dependent</b> (type-I) or <b>non-insulin dependent diabetes mellitus</b> (NIDDM or type-II diabetes). Diabetic patients develop progressive thickening of glomerular basement membrane (GBM) of glomerular capillaries along with widening of mesangium in majority of glomeruli of their kidneys. The unusual thickening of GBM and widening of mesangial area of the bundles of glomerular capillaries lead to narrowing down of functional lumen of these capillaries, there by causing pathophysiological change in the glomerular function affecting the glomerular filtration rate (GFR). Ultrastructural features of glomerulus affected by diabetes have been illustrated in Figure-1b below in comparison to normal features depicted in Figure-1a at the same magnification.</p>
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhFc7h02UbJpMxNvs_JNZfE2ReM6DlJ_C3TYWt78mkjlFI8_cBjPsMJOMsVNTkQLwTYKJ-00Aho9nx3_Udfn5s6WrkZCGZIZ0q23pcshRJo5I0eZ7bFbD9bc2nMf9B5eOCjkrQQv76oja8/s1600-h/Normal+Kidney.JPG"><img id="BLOGGER_PHOTO_ID_5431413742283928418" style="WIDTH: 320px; CURSOR: hand; HEIGHT: 318px" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhFc7h02UbJpMxNvs_JNZfE2ReM6DlJ_C3TYWt78mkjlFI8_cBjPsMJOMsVNTkQLwTYKJ-00Aho9nx3_Udfn5s6WrkZCGZIZ0q23pcshRJo5I0eZ7bFbD9bc2nMf9B5eOCjkrQQv76oja8/s320/Normal+Kidney.JPG" border="0" /></a>
<p><b>Figure-1a: </b>Electron micrograph of a portion of the tuft of a normal glomerulus depicting normal GBM: glomerular basement membrane, Mes: mesangial area, EpC: epithelial cells or podocytes, CL: capillary lumen and US: urinary space.</p>
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh5zsxU23qOJ7EsGqFtk9zE5VnOMgGrZWi7z59iUgt2YrcR4aKIXs3yPw743FTGFVqnPjv5Qy3KYjpEckgd0MYs4D-WarvpX1M_dToA7wfG_qQE6N2YUAOA0a18JawoRLisRWlJYZZ0ycw/s1600-h/Diabetic+Kidney.jpg"><img id="BLOGGER_PHOTO_ID_5431414800416469122" style="WIDTH: 320px; CURSOR: hand; HEIGHT: 319px" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh5zsxU23qOJ7EsGqFtk9zE5VnOMgGrZWi7z59iUgt2YrcR4aKIXs3yPw743FTGFVqnPjv5Qy3KYjpEckgd0MYs4D-WarvpX1M_dToA7wfG_qQE6N2YUAOA0a18JawoRLisRWlJYZZ0ycw/s320/Diabetic+Kidney.jpg" border="0" /></a>
<p><b>Figure-1b: </b>Electron micrograph of a portion of the tuft of a glomerulus affected by diabetes, depicting thickened GBM: glomerular basement membrane, Mes: mesangial area (widened), EpC: epithelial cell or podocyte, CL: capillary lumen (narrowed down) and US: urinary space. <b>Note:</b> Just compare the feature with the electron micrograph shown in figure-1a.</p><p>Uncontrolled <b>diabetes </b>may lead to global sclerosis of glomeruli resulting in '<b>end stage renal disease</b>' (ESRD) or <b>renal failure</b>. Retinopathy, neuropathy and vascular and/or cardiac disease accompanying ESRD may complicate the management of prospective patients. So, <b>diabetic patients</b> are advised to comply sincerely with the advice of general physician or diabetologist to avoid diabetes associated complications, otherwise they may require the consultation of a nephrologist, ophthalmologist and cardiologist to manage the complications. The treatment of <strong>diabetes associated</strong> <b>renal disease</b> should ideally be introduced when '<b>traces of albumin in urine</b>' (microalbuminuria) and <strong>polyuria</strong> (increased urine output) are detected in <b>diabetic patients</b>. Optimal control of <b>diabetes </b>by insulin and/or diet and exercise is must to avoid complications. Once massive proteinuria (excretion of >3.5 g protein per 24 hours) is developed in <b>diabetic patients</b>, the cost of reversal of complications may be many times higher. Just be health conscious and stay healthy & live-long.</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-64837144008325084342009-11-27T05:21:00.002-07:002009-11-27T05:26:02.181-07:00Various Causes of Acute Renal Failure<p>The cause and/or precipitating factor of <b>acute renal failure</b> (<b>ARF</b>) is always responsible for the effectiveness of therapy and supportive care techniques including hemodialysis. A rapid loss of renal function is exhibited through elevated levels of <b>serum creatinine</b> and <b>blood urea</b> due to fall in the clearance of these nitrogenous wastes by the kidneys in all cases of ARF. It has been observed that a loss of 50% of <b>glomerular filtration rate </b>(<b>GFR</b>) leads to significant elevation of the level of <b>creatinine</b> in the blood with a decrease in the urine output (oliguria). There could be three types of causes and implicating factors of<b> acute renal failure</b>: 1) Pre-renal, 2) Renal and 3) Post-renal. In <b>pre-renal type ARF</b> causes are the physiological factors or conditions which lead to poor renal perfusion and severe impairment of renal function. Hemorrhage in gastrointestinal tract (stomach and intestines) and other internal spaces, sepsis, hepatic failure (liver failure), over compliance of antihypertensive drugs or non-steroidal anti-inflammatory drugs (NSAID), arterial or venous thrombosis and intra-vascular hemolysis due to transfusion reactions, are the major <b>pre-renal causes</b> of <b>ARF</b>. </p><p>Acute tubular necrosis (<b>ATN</b>), rapidly progressive glomerulonephritis (<b>RPGN</b>), post infection glomerulonephritis and <b>interstitial nephritis</b> are some major <b>renal causes</b> of ARF<b>. Pre-renal</b> factors and use of nephrotoxic drugs may also be associated cause of <b>ATN</b>. Some viral
infections, drugs, multiple myeloma, lymphoma and granuloma may cause <b>interstitial nephritis</b> leading to <b>renal type ARF</b>.</p><p><b>Post-renal type ARF</b> is caused by intra-tubular obstruction due to fibrosis, stones or tumors. Every case of <b>acute renal failure</b> needs urgent investigations to establish the cause and efficient mode of supportive care and line of treatment. A comprehensive physical examination is required to look for possible causes of <b>ARF </b>and planning the investigations to classify the type of ARF. By timely diagnosis and treatment, renal function could be restored in majority of cases of <b>pre-renal type </b>acute renal failure.</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-6079922226005569362009-10-30T06:20:00.003-06:002009-10-30T06:30:45.460-06:00Nephrotic Syndrome and its Serious Effects<p>Urine examination shows critical abnormalities in <b>nephrotic syndrome</b>. The urine may froth if passed in a container or if shaken in a test tube. The dipstick test always shows extensive excretion of protein in urine. Total excretion of protein per day should be measured in 24-hour's collection of urine. The <b>nephrotic syndrome</b> is the consequence of prolonged massive <b>proteinuria</b> (excretion of protein in urine). The <b>proteinuria</b> exceeds 3.5 g/24-hours in adults or 50 mg/kg body-weight in children. <b>Nephrotic syndrome</b> is characterized by <b>proteinuria</b>, <b>hematuria</b> (blood in urine), <b>hypertension</b> (high blood pressure), <b>oliguria</b> (low output of urine per day), <b>edema</b> (swelling: apparently suborbital puffy eyes) and diminished renal function. Urine may be brown or red. <b>Sodium</b> (Na<sup>+</sup>) retention, increased circulating blood volume and <b>hypertension</b> (high blood pressure) may lead to <b>cardiomegaly</b> (enlargement of heart). <b>Nephrotic syndrome</b> is usually characterized by insidious onset of massive <b>edema</b>, <b>proteinuria</b>, <b>hypoalbuminemia</b> (low level of albumin in blood) and <b>hyperlipidemia</b> (high level of cholesterol in blood). There could be massive retention of <b>sodium</b> (Na<sup>+</sup>) and a tendency to excessive <b>potassium </b>(K<sup>+</sup>) loss. Serious ill effect of the <b>nephrotic syndrome</b> could be a tendency towards <b>hypercoagulability </b>(blood clotting disorder) which may lead to venous or arterial thrombosis and embolism. Susceptibility to chest (lung) infections may increase due to decreased immunoglobulins' level in blood. Serum <b>calcium</b> (Ca<sup>++</sup>) level could be low as this is related to the level of albumin in blood. Dysfunction of proximal tubules of kidneys may cause <b>glycosuria </b>(excretion of glucose/sugar in urine) or aminoaciduria.</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-29164424821620236002009-10-03T10:20:00.011-06:002009-10-03T10:31:10.721-06:00Amyloidosis: Causes and Detection<p><b>Amyloidosis</b> or deposition of <b>amyloid</b> in vital organs could be labeled as chronic pathological state. <b>Amyloid</b> is an abnormal protein derivative and <b>amyloidosis</b> is characterized by extracellular accumulation of this abnormal protein, which could be detected with Congo-Red staining during histological examination of biopsies/tissues. Genesis of <b>amyloid</b> is associated with B-cell (B Lymphocytes) and Plasma-cell disorders or chronic infections like tuberculosis. Renal (kidney) involvement in <b>amyloidosis </b>may affect all compartments of kidneys. Renal glomeruli, extraglomerular blood vessels, uriniferous tubules and even interstitium could be severely affected leading to impairment of renal function and can cause renal failure. <b>Amyloid</b> could be composed of one or more proteins out of around two dozen different monotypic polypeptides, including immunoglobulin light chains (AL type amyloid), immunoglobulin heavy chains (AH type amyloid), amyloid-A-protein (AA type amyloid), prealbumin, <span style="font-family:Symbol;">b</span>-2 microglobulin, <span style="font-family:Symbol;">b</span>-amyloid protein, islet amyloid polypeptide, procalcitonin, cystatin-C, apolipoprotein A-1 or A-2, gelsolin, lysozymes etc. Immunoglobulin light chains type (AL type) and amyloid-A-protein (AA type) <b>amyloid </b>mostly affect the kidneys. Almost all the patients with <b>amyloidosis</b> of <b>kidneys</b> have proteinuria (excretion of proteins in urine; >3g/day) and around 70% also have diminished <b>renal function</b>. On <b>electron microscopy</b> amyloid could be resolved as approximately 10 nm thick non branching and randomly arranged fibrils as illustrated in Figure-1.</p><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhqxoE5BxW0grIb0gj8FNS9V7ndQ2X0xlPsgOYpLKlPaJuVPO-94oKeuOPSFh8nyttc3gu46l695nMvySO25Wlw9K3VChIEEYu8rbpTO35dwKKyJWTvff1e9kJQN-DIDte1H2kEwPa3TzU/s1600-h/Amyloid-36K.jpg"><img id="BLOGGER_PHOTO_ID_5388410112264783666" style="WIDTH: 318px; CURSOR: hand; HEIGHT: 320px" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhqxoE5BxW0grIb0gj8FNS9V7ndQ2X0xlPsgOYpLKlPaJuVPO-94oKeuOPSFh8nyttc3gu46l695nMvySO25Wlw9K3VChIEEYu8rbpTO35dwKKyJWTvff1e9kJQN-DIDte1H2kEwPa3TzU/s320/Amyloid-36K.jpg" border="0" /></a>
<p><b>Figure-1:</b> Electron micrograph showing randomly arranged non-branching fibrils of amyloid in the mesangial area of a renal glomerulus. Original magnification 36000x.</p><p>Amyloid-A-protein type (AA type) <b>amyloidosis</b> is most often associated with chronic inflammatory diseases like tuberculosis, osteoarthritis, or rheumatoid arthritis. Some viral infections can also boost <b>amyloidosis</b>. Production of amyloidogenic light chains is associated with B-cell lymphoma, multiple myeloma or plasma-cell dyscrasia. <b>AL</b> and <b>AA</b> type <b>amyloid</b>
have identical physicochemical properties. On renal biopsy evaluation we find acidophilic deposits which stain weakly with <b>Periodic acid Schiff's stain </b>or Silver stain. Amyloid stains bright red with <b>Congo-Red stain</b> and shows <b>apple green birefringence</b> by polarized light microscopy. <b>Amyloid</b> deposits could be revealed in the mesangium and peripheral capillary wall of <b>renal glomerulus</b> depending on the chronicity of the disease process. In advanced stages of <b>amyloidosis</b>, the amyloid deposits could be detected in arteries and interstitial tissue of <b>kidneys </b>in addition to <b>glomeruli</b>, by conventional methods and <b>electron microscopy</b>.</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-85071630235111765572009-09-28T11:32:00.005-06:002009-09-28T11:49:12.024-06:00IgA Nephropathy as a cause of End Stage Renal Disease<p>There are a variety of causes of <b>end stage renal disease</b> (<b>ESRD</b>) in teenagers and adults. <b>Immunoglobulin-A</b> (<b>IgA</b>) nephropathy could be a cause of <b>end stage renal disease</b> (<b>ESRD</b>) in around 25% of cases. There are five types of immunoglobulins in our body for protection against microorganisms and IgA provides defence at mucous membranes. Colostrum
and breast milk are rich sources of IgA and protect us during infancy through breast-feeding. However, later in life, chronic mucosal inflammation (inflammation of respiratory, oral, or gastrointestinal mucous membranes) may lead to <b>IgA-nephropathy</b> (<b>IgAN</b>). Viral (including HIV), bacterial, yeast and parasitic infections have been found to be associated with <b>IgAN</b>.
Environmental and food antigens have also been implicated in <b>IgAN</b> as these may mimic molecular structure of microbial antigens and lead to excessive IgA production, aggregation and breakdown of mucosal barrier. Patients affected by <b>IgAN</b> may present with hematuria (blood in urine) and/or proteinuria (protein in urine) with or without rise in serum creatinine. The most common initial symptom in children is <b>microscopic hematuria</b>. Some adults may present with <b>acute </b>or <b>chronic renal failure</b>. </p><p>IgA nephropathy is a common nephropathy, which could be detected on renal (kidney) biopsy evaluation through light and fluorescence microscopy. However, electron microscopic study of renal biopsy acts as a diagnostic adjunct as the location of immune complexes in the renal glomerulus could be pronounced on electron micrographs. Figures 1 and 2 are the electron micrographs from a proven case of <b>IgAN</b>, illustrating mesangial deposits of IgA. </p><p><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjzKsgf19LlDofUnptvIzwtN-Cb1mMexLfb2d-lGCEc96Kt6P7obHmvXbvovf1sO6iKdpTW9tIOT00EgCc4185TRnGYS_TV_SF-l0vmlBnKHVkigtldOFXuBMMOUVOTK90BIrhmoiwNeSo/s1600-h/EM-477-08-IgAN-4600x+copy.jpg"><img id="BLOGGER_PHOTO_ID_5386573022223912370" style="WIDTH: 320px; CURSOR: hand; HEIGHT: 318px" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjzKsgf19LlDofUnptvIzwtN-Cb1mMexLfb2d-lGCEc96Kt6P7obHmvXbvovf1sO6iKdpTW9tIOT00EgCc4185TRnGYS_TV_SF-l0vmlBnKHVkigtldOFXuBMMOUVOTK90BIrhmoiwNeSo/s320/EM-477-08-IgAN-4600x+copy.jpg" border="0" /></a> </p><p><b>Figure-1: </b>Electron micrograph of an area of glomerulus of a case of IgAN showing electron dense deposits (D) in the mesangial (Mes) area. Glomerular basement membrane (GBM), capillary lumen (CL), podocyte or epithelial cell (EpC) and urinary space (US) are also exhibited; Original Magnification 4600x. </p><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjZs1NIQvwl6TszOuNg8PxP46qkoYVV8ciI0DN1GE53Dg5eCPp2VpLSCsWR9cDy1TV2WcIdt3QcbVKV0Mk_6JoLOsYDlFc4BbCw9l4SXeDG_blACxurVt_g9TIS3clF00aJWZ3pUs_uzAw/s1600-h/EM-477-08-IgAN-6K+copy.jpg"><img id="BLOGGER_PHOTO_ID_5386573608443418850" style="WIDTH: 320px; CURSOR: hand; HEIGHT: 305px" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjZs1NIQvwl6TszOuNg8PxP46qkoYVV8ciI0DN1GE53Dg5eCPp2VpLSCsWR9cDy1TV2WcIdt3QcbVKV0Mk_6JoLOsYDlFc4BbCw9l4SXeDG_blACxurVt_g9TIS3clF00aJWZ3pUs_uzAw/s320/EM-477-08-IgAN-6K+copy.jpg" border="0" /></a> <p><b>Figure-2: </b>Electron micrograph of an area of glomerulus of a case of IgAN showing electron dense deposits (D) in the mesangial (Mes) area. Glomerular basement membrane (GBM), capillary lumen (CL), podocyte or epithelial cell (EpC) and urinary space (US) are also exhibited; Original Magnification 6000x.</p><p>The pathology of <b>IgAN</b> may be variable depending on underlying cause. Mesangioproliferative glomerulonephritis is the most common pattern in many renal biopsies; however, glomeruli may appear normal on light microscopy in some of the cases. Renal biopsies in a few cases may also show crescent formation in occasional glomeruli. Diagnosis of <b>IgA nephropathy</b> is established
by direct immunofluorescence technique on renal biopsies and the pattern may be dominant or co-dominant for IgA staining. The incidence of <b>ESRD</b> has been found to be high in patients presenting with >1g/day proteinuria with increased level of serum creatinine as compared to those having proteinuria <1g/day with increased level of serum creatinine. Pathogenesis of <b>IgAN </b>is very complex. A variety of underlying diseases including hepato-biliary disease can be associated with <b>IgA nephropathy</b>. Defective detection and clearance by liver of polymeric immune complexes of IgA (IgA1) due to abnormal galactosylation of O-linked glycans is probably the major cause of <b>IgAN </b>in addition to loss of mucosal barrier and chronic mucosal inflammation. Recurrent tonsillitis may also lead to IgA nephropathy and tonsillectomy may be helpful in these cases to remove the mucosal foci of infection. Optimal treatment of tonsillitis and other <b>oromucosal infections</b> with antibiotics along with conventional treatment of <b>IgAN</b> would be helpful to put brakes on the progression of <b>IgA nephropathy</b>. Patients with <b>acute</b> or <b>chronic renal failure</b> due to advanced stage of <b>IgAN </b>may need <b>hemodialysis </b>or renal transplantation. Use of anti-oxidants and fish oil as food supplements in some cases of <b>IgA nephropathy</b> have been found beneficial.</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-75181290610177471972009-08-22T10:34:00.002-06:002014-04-08T07:51:57.875-06:00Urea Synthesis and Clearing: Role of Liver and Kidneys<div dir="ltr" style="text-align: left;" trbidi="on">
The proteins we eat contain about 20% nitrogen. A person consuming around 100g proteins daily will excrete about 17g of nitrogen daily in the form of urea. In man and other vertebrate animals the major excretory product of protein metabolism is <b>urea</b>, and they are classified as <b>ureotelic animals</b>. Birds and reptiles excrete the <b>waste nitrogen</b> in the form of relatively insoluble <b>uric acid</b> as the end product of nitrogen metabolism and are <span lang="en-us"></span>called<b> uricotelic animals</b>. Urea is synthesized in liver and is released into the blood and cleared by <b>kidneys</b> in the urine.<br />
Urea synthesis in the liver involves five enzymes: (1) Carbamoyl phosphate synthetase 2) Ornithine carbamoyl transferase (3) Argininosuccinate synthetase (4) Argininosuccinate lyase and (5) Arginase. Deficiency in any of these enzymes may lead to <b>metabolic disorder</b>. The sole function of <b>urea cycle </b>is to convert the <b>ammonia </b>to non-toxic compound <b>urea</b>. All <b>metabolic disorders</b> of <b>urea synthesis</b> cause <b>ammonia intoxication</b>. Catabolism of amino acids in the most of cells produces ammonia. Considerable quantity of ammonia is produced by <b>intestinal bacteria</b> from the dietary proteins and from the <b>urea </b>present in cellular fluids secreted into the gastrointestinal tract. The ammonia produced in the intestine is absorbed into the portal venous blood and is promptly removed by the liver, where <b>urea</b> is synthesized from the ammonia. At first step, <b>carbamoyl phosphate</b> is produced by condensation of one molecule each of ammonia, carbon dioxide and phosphate, under the action of <b>intramitochondrial carbamoyl phosphate synthetase-1</b> (<b>CPS-1</b>) in the presence of Mg<sup>++</sup> and N-acetyl glutamate. Now <b>citrulline </b>is formed from the <b>carbamoyl phosphate</b> by union of <b>carbamoyl phosphate</b> and <b>ornithine</b> under the action of another <b>intramitochondrial enzyme</b> called <b>ornithine carbamoyl transferase</b>. The rest of the steps in the <b>urea synthesis </b>take place in <b>cytosol</b>. Citrulline diffuses out from the mitochondrial membrane into the cytosol, where it is linked with <b>aspartate</b> to form <b>argininosuccinate</b> under the action of enzyme <b>argininosuccinate synthetase </b>in the presence of Mg<sup>++</sup> ions and ATP. There after the cleavage of <b>argininosuccinate</b> to <b>arginine</b> and <b>fumarate </b>is catalyzed by <b>argininosuccinate lyase</b>. The final step in the <b>urea synthesis </b>is the hydrolysis of <b>arginine</b> to <b>urea</b> and <b>ornithine</b>. Ornithine from the cytosol enters the mitochondria and is recycled in <b>urea synthesis</b>. Though other body tissues also exhibit the presence of <b>urea synthesis enzymes</b> but the physiologic contribution of <b>extrahepatic urea synthesis</b> is very low. Urea produced by the hepatic cells enters the blood and is excreted in the urine by the kidneys. Low level of blood/plasma urea and respiratory alkalosis are indicative of <b>urea cycle disorders</b>. <a href="http://www.healthline.com/human-body-maps/liver">Free "Human Body Maps"</a></div>
Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-77287615358973843892009-08-03T08:46:00.003-06:002009-08-03T08:53:45.556-06:00Renal Transplantation and Immune Profiling<p>Organ transplantation is analogous to blood transfusion and we need to detect and match the <b>tissue antigens</b> of the <b>donor</b> and the <b>recipient </b>before transplantation of an <b>organ</b>, say <b>kidney</b>. Tissue antigens are known as <b>human leucocyte antigens </b>(<b>HLA</b>). There are four loci called A, B, C and D on the 6th chromosome, which govern these tissue antigens or <b>HLA</b>. We inherit one gene (each gene has sub-genes) each on each locus from our mother and father. There is antigenic polymorphism at each locus (A, B, C, and D). Unless the <b>kidney donor</b> and the <b>recipient</b> (patient) are identical twins, a 100% match of these HLA is not possible. There is 50% match of <b>HLA</b> amongst parents and children, and the siblings. Unrelated <b>donor </b>and <b>recipient </b>may also have 50% matching of <b>tissue antigens</b> or HLA. The participation of immune mechanisms in <b>allogenic kidney transplant</b> begins with the identification and appropriate reaction to the <b>donor organ</b>, by the <b>recipient</b>, depending on the <b>degree of HLA mismatch</b>. Immunosuppressive therapeutic protocols are prescribed for the adoption and survival of<b> grafted/transplanted kidney</b>. There is very complex immune pathway in our body involving antigen presenting cells and T & B cells (Lymphocytes), which get activated and lead to<b> </b>injury of the target cells.<b> </b>The intragraft cell trafficking and their effector mechanisms may have serious implications. Post transplant <b>immune profiling</b> is a way of monitoring the <b>allograft function</b> and to elucidate pathogenic mechanisms and molecular pathways causing <b>tissue injury</b> and disease. </p><p><b>Transplant tolerance</b> could only be achieved through sincere compliance of <b>immunosuppressive therapy</b>. The immune system of the <b>recipient </b>following <b>renal transplantation</b>, though challenged by the exposure to <b>donor antigens </b>to initiate an early <b>sub-clinical</b> or <b>acute </b><b>rejection </b>process, attempts to regulate the inflammatory processes or maintain homoeostasis in the body. The <b>acute rejection</b> may be cell or antibody mediated. The <b>transplant tolerance</b> is defined as maintenance of stable <b>allograft function</b> without clinical evidence of <b>immunosuppression</b>. There are many therapeutic approaches to achieve the <b>transplant tolerance</b>, however, the best one is <b>donor specific transfusion </b>or hematopoietic cell infusion. Almost all the transplant recipients have to depend on a variety of <b>immunosuppressive protocols</b> to ward of any chance of <b>allograft rejection</b>.</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-48100951851121109762009-07-30T21:12:00.001-06:002009-07-30T21:17:29.478-06:00End Stage Renal Disease and Renal Transplantation<p>Chronic glomerulonephritis, diabetic nephropathy, chronic tubulointerstitial disease, benign nephrosclerosis and polycystic kidney disease are the major causes of <b>end stage renal disease</b> (<b>ESRD</b>) and <b>renal failure</b>. Patients with <b>ESRD</b> exhibit a variety of abnormalities in their <b>autonomic functions</b>. Precise mechanisms of evaluating <b>autonomic functions </b>have revealed abnormalities in <b>efferent parasympathetic pathway</b> and <b>baroreceptor sensitivity</b> in patients with <b>end stage renal disease</b>. An increase in expiration-inspiration, lying standing and valsalva ratios, and baroreceptor sensitivity slope have been well documented in <b>ESRD</b>. Uremic patients with <b>ESRD</b> respond poorly to antihypertensive drugs as compared to otherwise healthy controls. Renal involvement in multiple myeloma is an other cause of <b>ESRD </b>and<b> renal failure</b>. <b>Dialysis</b> is an adoptive procedure in patients having <b>end stage renal disease</b> and ultimate surgical measure is <b>renal</b> (<b>kidney</b>) <b>transplantation</b>. Adequate <b>dialysis</b> in patients with <b>ESRD</b> reverses the elevated levels of urea, creatinine and electrolytes in blood.</p><p>Though <b>renal transplantation</b> is must in patients with <b>ESRD</b>, but it needs a lot of medication and <b>post transplantation care</b> for the successful adoption and survival of <b>renal allograft</b>. Systemic fungal infections (cryptococcosis, mucuromycosis, candidiasis, aspergillosis and mixed
infections) have been documented after <b>renal transplantation</b>. Though these infections are treatable but may complicate the post operative care as additional medication will be required in addition to immunosuppressive therapy. High incidence of tuberculosis has also been observed in <b>recipients of renal transplant</b> along with viral infections like <b>BK virus</b> and cytomegalovirus (<b>CMV</b>). Adverse impact of pre-transplant polyoma virus (BK virus) infection on the graft survival has also been documented. Molecular technology has been developed for the early detection and identification of these viruses from the time of <b>renal transplantation</b> onwards by using protocol biopsies from the grafted kidney.</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-5303511137628358842009-07-30T21:05:00.003-06:002009-07-30T21:10:19.226-06:00Acute Renal Failure: Medical and Other Causes<p>If we look at the spectrum of <b>acute renal failure</b> (<b>ARF</b>), we find that in more than 65% of cases <b>medical causes</b> or <b>ailments</b> are associated. Around 20% of cases generally have <b>obstetrical causes</b> and 15% of cases of <b>acute renal failure </b>may have surgical or other causes. Diarrhoea, mismatched blood transfusion, intravenous hemolysis in glucose-6-phosphate dehydrogenate (<b>G-6-PD</b>) deficient patients, <b>hemolytic uremic syndrome</b> (<b>HUS</b>), severe glomerulonephritis, falciparum malaria, snake bite, insect stings, septicemia and copper sulphate, mercuric chloride and zinc phosphide poisoning are some medical conditions in which if effective treatment is delayed may lead to <b>acute renal failure</b>. Intake of nephrotoxic drugs
can also cause acute renal failure. <b>Obstetrical causes</b> include toxemia of pregnancy, postpartum hemorrhage, puerperal sepsis and post abortal sepsis. Major surgery may cause <b>ARF</b> in some cases. Nephrotoxic drugs and sepsis could be compounding factors in cases <b>ARF</b> with surgical cause. </p><p align="left">Acute gastroenteritis, septicemia and <b>HUS</b> may singly or in combination be the major cause of <b>ARF</b> in tropical countries. Rhabdomyolysis has been observed to play a significant role in causing <b>ARF</b> in a variety of conditions including <b>toxemia of pregnancy</b>, status asthmaticus, status epilepticus, hypothermia, burns, dermatomycosis, wasp and hornet strings, and copper sulphate, mercuric chloride and zinc phosphide poisoning. The main causative factors for intravenous hemolysis in <b>G-6-PD</b> deficient patients include the commonly used drugs like aspirin, chloramphenicol, chloroquine, quinine and phenylbutazone. Bilateral <b>mucuromycosis</b> has also been documented to cause <b>ARF</b> even in non-immunocompromized subjects. Sometimes nephrectomy may be required in cases of <b>ARF</b> due to <b>mucuromycosis</b>. The spectrum of <b>community acquired</b> <b>acute renal failure</b> and <b>hospital acquired acute renal failure </b>is almost similar throughout the world. Decreased renal perfusion in cases of hypothermia and hypotension (low blood pressure) may cause <b>ARF</b> if not treated well in time. Timely treatment and <b>hemo-dialysis</b> or <b>peritoneal dialysis</b> can definitely benefit the patient in restoration of renal function and reversal of <b>acute renal failure</b>.</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-18085545551998134372009-06-30T08:13:00.007-06:002009-06-30T08:29:29.563-06:00The Space Within and Outside Our Body<p>The <b>space</b> has a great role in our life. Our body is composed of five basic components: the earth, water, air, fire (heat or temperature) and the sky or space. The <b>space within </b>and <b>outside</b> our body is must for the existence of life. The <b>outer space</b> is composed of air (mixture of gases), vapours, finer particles, microorganisms, radiation, light, cold and heat. The composition of<b> </b>environment<b> </b>influences our breathing, metabolism and physiology. Our body reacts in a variety of ways to the <b>external space</b> and the <b>environment </b>possessed by it. In fact the particles floating in the air or transmitted through it may cause allergic reactions, infections, hot or cold skin burns or even skin cancer. All activities of human beings or animals are space oriented.</p>
<p>Just think of the life without <b>space </b>and you would understand its importance. Our body is like a tube open from both ends. You may appreciate <b>space</b> in your mouth (oral cavity), throat, nostrils, ears and lungs. In addition to these gross pockets of space there are hollow organs like heart (four chambers are there for blood flow regulation), gall bladder, urinary bladder and uterus (in females). Other examples of <b>space within</b> our body are cranial cavity,<b> </b>visceral cavity and cavities around all vital organs. There are <b>micro-spaces</b> in glandular tissues, alveoli of lungs, blood vessels and nephrons (glomeruli have capillary lumen and urinary space) in kidneys. In some of the <b>renal disorders</b> there are ultrastructural alterations in the areas/volumes of these <b>micro-spaces</b> within the kidneys leading to altered <b>renal physiology</b> and <b>renal function</b>. The <b>figure-1</b> below illustrates <b>normal urinary space</b> (<b>US</b>) and <b>capillary lumen</b> (<b>CL</b>) or capillary space in a normal kidney; and <b>figure-2</b> illustrates <b>congestion</b> of <b>capillary lumen</b> (<b>CL</b>) due to deposition of <b>subendothelial deposits</b> (<b>SeD</b>) in a kidney affected by <b>lupus nephritis</b>.</p>
<p><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhIg37uqOG6nu0unHFdF2Jal0gP8P29-sP2P6MLWXuqE_iQtcoV1IJJov_bDOkGHXQoJ8HAP5AEDZXOp_uDFe7TXy1o72av_iiiaI4Ln3r0-9d88wX60eZzRrE-yeYjrd8DdSpA0Jm_KbQ/s1600-h/Normal+GBM_Blog-46.jpg"><img id="BLOGGER_PHOTO_ID_5353124515382592738" style="WIDTH: 320px; CURSOR: hand; HEIGHT: 262px" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhIg37uqOG6nu0unHFdF2Jal0gP8P29-sP2P6MLWXuqE_iQtcoV1IJJov_bDOkGHXQoJ8HAP5AEDZXOp_uDFe7TXy1o72av_iiiaI4Ln3r0-9d88wX60eZzRrE-yeYjrd8DdSpA0Jm_KbQ/s320/Normal+GBM_Blog-46.jpg" border="0" /></a>
<b></b></p><p><b>Figure-1: </b>Ultramicrograph of a capillary loop from a normal human kidney illustrating normal urinary space (US) and capillary lumen (CL) with normal thickening of glomerular basement membrane (GBM); Uranyl acetate and Lead citrate stain.</p>
<p><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjJ_CajpaqgZ7ZXqypz537WPc7enzsankbyJ20w6psxs9S5XnLy9MWfEvqyP1DITNZBAQedsZlw191ch_0Twfq3MNU5XqZ0hOlDL-i-etEZ5x5XOF2pPxEpcXj6CBcEyQY1fpySALJOOBs/s1600-h/LupusNeph-6Kx_Blog-46.jpg"><img id="BLOGGER_PHOTO_ID_5353125047111474290" style="WIDTH: 320px; CURSOR: hand; HEIGHT: 320px" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjJ_CajpaqgZ7ZXqypz537WPc7enzsankbyJ20w6psxs9S5XnLy9MWfEvqyP1DITNZBAQedsZlw191ch_0Twfq3MNU5XqZ0hOlDL-i-etEZ5x5XOF2pPxEpcXj6CBcEyQY1fpySALJOOBs/s320/LupusNeph-6Kx_Blog-46.jpg" border="0" /></a>
<p><b>Figure-2: </b>Ultramicrograph of a capillary loop from human kidney affected by lupus nephritis, illustrating congestion of capillary lumen (CL) due to deposition of subendothelial deposits (SeD) with normal urinary space (US) but irregular thickening of glomerular basement membrane GBM); Uranyl acetate and Lead citrate stain.</p>
<p>In the illustration cited above you have seen the alteration in the <b>space within</b> the <b>renal glomerulus</b>. Abdominal tumors, brain tumors, polyps in the uterus, enlargement of spleen and liver, all these lead to functional as well as physiological changes in the body of a patient due to impact on <b>space </b><b>within</b> the body.</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-74814844727167160512009-06-18T07:37:00.004-06:002009-06-18T07:46:01.606-06:00Therapy and Management of Glomerulonephritis<p>In my other articles you must have got ample information regarding classes or types of <b>glomerulonephritis</b> (<b>GN</b>). Primary glomerulonephritis accounts for about 30% patients requiring dialysis (a medical procedure of purifying blood with by passing through artificial kidney) and hospitalization. The yearly prevalence of<b> primary GN</b> is 0.002% that means 2 new patients per 100,000 population<b> </b>in a year. There are a variety of causes of <b>primary GN</b> with identical histopathological features. It is worth to mention here that there may be many immunopathological reasons in <b>membranous glomerulonephritis</b> (<b>MGN</b>). The character and severity of <b>GN </b>varies with the status of altered immune status of an individual. The understanding of pathogenesis of <b>GN</b> is must before initiating any therapy.</p>
<p>Regular follow-up in a clinic/renal clinic is must for the patient diagnosed of having a <b>renal disease</b> or glomerulonephritis. The follow-up provides an opportunity to the patient to learn about the complications of <b>persistent GN</b> and/or <b>chronic renal failure</b>. It has been observed that hypertension often develops coincidental with progression of <b>renal disease</b>. The hypertension needs to be kept under control in patients affected by <b>persistent GN</b>. The renal function deterioration causes <b>edema</b> in patients with <b>glomerulonephritis</b>. Though <b>restriction</b> in <b>salt </b><b>and</b> <b>water intake</b> may cure the edema to some extent but <b>diuretic drugs</b> are preferred to treat the <b>edema</b>. Dietary management of progression of <b>renal disease</b> demands moderate <b>reduction in protein intake</b> (recommended: 0.8-1.0 g/kg body weight/day, during edema) to reduce the nephrotic overload and correction of <b>proteinuria</b>. Effective measures to reduce <b>proteinuria</b> are must to speed-up healing of renal lesions.</p>
<p>Corticosteroids, cyclophosphamide, chlorambucil and cyclosporin are the drugs of choice for the treatment of <b>GN</b>. About 95% of children generally respond to the first course of <b>steroids</b> within 8 weeks of commencement of treatment, whereas in adults it may take up-to 16 weeks and the percentage responding to the therapy could be around 80%. <b>Oral prednisolone</b> in single daily dose of 1mg/kg body weight is generally administered in adults. In children somewhat higher dose is required with reference to their body weights. Treatment of <b>glomerulonephritis</b> should never be tried as self help protocol as it needs regular follow-up. Parameters like body weight, blood pressure, 24 hour urinary protein, blood cells' count, blood urea and creatinine need to be worked out periodically to taper down the dose of steroids. Remission can also be achieved with cyclophosphamide, chlorambucil, cyclosporin and azathioprine. About 20-25% of patients are permanently cured with single course of treatment and around 50% may have relapse and need a repeat course of steroid treatment in combination with other immunosuppressive drugs. The dietary advice of nephrologist, controlled blood pressure and a treatment regimen for a sufficient time period may help a patient to keep a check on the complications of glomerulonephritis.</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-30387083697189021692009-05-30T11:56:00.001-06:002009-05-30T12:04:12.385-06:00Nephrotic Syndrome and Associated Renal Lesions<p><b>Nephrotic syndrome</b> may occur in any type of <b>primary </b>or <b>secondary </b><b>glomerulonephritis</b>. Around two dozen histopathological categories or subcategories of <b>glomerulonephritis</b> are now recognized and etiological factors are largely determined. However, <b>prevention </b>and<b> treatment </b>of<b> glomerulonephritis </b>needs momentum to curb the development of <b>irreversible renal failure</b>. The main diagnostic feature of <b>nephrotic syndrome</b> is massive <b>proteinuria</b> (excretion of protein in urine) exceeding 3 g/24 hour. The other features of <b>nephrotic syndrome</b>, such as, <b>hypoproteinemia</b> (decreased level of proteins in blood), edema (swelling) and <b>hyperlipidemia</b> (elevated levels of lipids in blood) are consequential due to excretion of proteins in urine. Clinically the patient does not bother to consult a nephrologist or general physician until edema becomes evident. With the fall in the plasma osmotic pressure due to loss of the plasma proteins in urine the fluid from blood would leak into the interstitial space resulting in a reduction in circulating blood volume, but the kidneys try to maintain blood volume by retaining salts and water.</p>
<p>In children around 80% cases of <b>nephrotic syndrome</b> are due to minimal change disease(MCD) and in adults the dominance of MCD<b> </b>is lost. In adults the cause of <b>nephrotic syndrome</b> may be minimal change disease, membranous glomerulonephritis (MGN), focal glomerulosclerosis, mesangial proliferative glomerulonephritis or membranoproliferative glomerulonephritis (MPGN). Metabolic disorders like diabetes mellitus could also be a cause of <b>nephrotic syndrome</b>. Secondary amyloidosis is also known to cause renal lesions associated with <b>nephrotic syndrome</b>. Immunological disorders like systemic lupus erythematosis and vasculitis may also be a cause of <b>glomerulonephritis</b>. Renal biopsy evaluation by light microscopy (LM), immunofluorescence microscopy (IFM) and electron microscopy (EM) is must for an accurate diagnosis of type of <b>glomerulonephritis</b> in a patient of <b>nephrotic syndrome</b>. Minimal change disease, membranous glomerulonephritis (MGN), focal glomerulosclerosis, mesangial proliferative glomerulonephritis, membranoproliferative glomerulonephritis (MPGN) and diffuse endocapillary glomerulonephritis are the common and primary causes of <b>nephrotic syndrome</b>. Focal segmental proliferative glomerulonephritis and diffuse proliferative glomerulonephritis with crescents are considered as uncommon-primary causes of <b>nephrotic syndrome</b>.<b> Glomerulonephritis</b> due to metabolic disorders, immunological disorders, toxemia of pregnancy or malignant conditions of kidney are labeled as secondary causes of<b> nephrotic syndrome</b>.</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com0tag:blogger.com,1999:blog-6350978014173423850.post-17436861454531871162009-05-29T08:39:00.003-06:002009-05-30T11:56:21.243-06:00Bacterial Endocarditis and Associated Kidney Disease<p>There is very strong association between <b>bacterial endocarditis</b> or <b>heart valve infection</b> and <b>kidney disease</b>. Prior to the discovery, development and active use of antibiotics, the majority of the patients developed <b>renal disease</b> (<b>kidney disease</b>) as a consequence of <b>subacute valvular infection</b>. The incidence of clinical <b>renal involvement</b> has dropped significantly with the introduction of effective treatment of <b>bacterial endocarditis</b> with antibiotics. The assessment of <b>renal involvement</b> in <b>bacterial endocarditis</b> is quite difficult as transient changes in urine sediment are generally observed. There may be focal and segmental lesions with normal creatinine clearance. Intravenous drug users are at greater risk of developing <b>bacterial endocarditis</b>.</p>
<p>Staphylococcus aureus infection as the cause of <b>bacterial endocarditis</b> has been reported in majority of the cases that lead to a higher frequency of <b>diffuse glomerular disease</b>. The <b>renal lesions</b> associated with <b>endocarditis</b> involved embolization and infection. The <b>renal lesions</b> could also have immunological basis as immune complex deposits within glomeruli have been detected in majority of the cases. The involvement of complement (an immune response modulator protein in our blood) system during active disease (<b>bacterial endocarditis</b>) in association with immune complexes complicates the severity of<b> intra-glomerular lesions</b>. The two major categories of <b>renal lesions</b> found in patients affected by <b>bacterial endocarditis</b> are: (1) Focal segmental abnormality due to <b>subacute infection</b> and (2) Diffuse glomerular lesions in the patients with <b>acute bacterial endocarditis</b> mimicking the pattern of <b>post-streptococcal glomerulonephritis</b>. The electron micrograph (Fig-1) from the kidney biopsy of a patient with <b>acute glomerulonephritis</b> and <b>acute bacterial endocarditis </b>illustrates the subepithelial immune complex deposits. </p>
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgLIB0Asok5yKJMpA8GPYJ-fMdQ4JTB5pgnHtKeXQu-YuWew1v0eRX0XzIb1uq0xPYdco3EZvjTm5KeISkjwRNtN4xKU4cRHqkRf5_FU-LfCBsfQdOUYdlDYC9325uZsAzwwhVE0vY-PaM/s1600-h/Acute+GN-2.jpg"><img id="BLOGGER_PHOTO_ID_5341675715698648930" style="WIDTH: 320px; CURSOR: hand; HEIGHT: 320px" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgLIB0Asok5yKJMpA8GPYJ-fMdQ4JTB5pgnHtKeXQu-YuWew1v0eRX0XzIb1uq0xPYdco3EZvjTm5KeISkjwRNtN4xKU4cRHqkRf5_FU-LfCBsfQdOUYdlDYC9325uZsAzwwhVE0vY-PaM/s320/Acute+GN-2.jpg" border="0" /></a>
<p><b>Fig-1: </b>Electron micrograph illustrating the hump shaped subepithelial immune complex deposits (D) alongside the glomerular basement membrane (GBM) and urinary space (US), during acute glomerulonephritis. Uranyl acetate and Lead citrate stain.</p>
<p>The assessment of renal involvement in <b>endocarditis</b> may be difficult diagnostic entity as only minor and transient changes are observed in urinary deposit with variable changes in blood biochemistry. The clinician must recognize the status of impaired cardiac output in the first stage and later workout the potential risk of <b>treatment associated antibiotic nephrotoxicity</b>. The assessment of renal function at the time of presentation of case could be helpful to rule out<b> endocarditis associate renal disease</b> or <b>treatment associated antibiotic nephrotoxicity</b>.</p>Dr. CS Rayathttp://www.blogger.com/profile/06457191160876045757noreply@blogger.com1