Nephritic Syndrome and Urine Examination

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 nephritic syndrome. In many cases the renal disease is occult and is often detected during the routine physical examination. It is important to understand that acute nephritis, nephrotic syndrome and renal failure 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 hypertension, uremia (elevated level of urea in blood), or anemia may cause occult renal disease.

Hypertension along with mild edema (swelling), apparently as suborbital puffy eyes is characteristic clinical feature of nephritic syndrome. Hematuria (blood in urine) with or without proteinuria (protein in urine), oliguria (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 nephritic syndrome. Microscopic examination of fresh urinary sediment in these patients may reveal very high count of dysmorphic red blood cells (dysmorphic RBCs). The detection of RBCs in the urinary casts signifies that the hematuria comes from the kidneys (renal parenchyma). Proteinuria may vary from 0.3g to 3.0g daily. Urinary sodium level (Na⁺ level) tends to be low due to sodium retention as a result of impaired excretory function by the kidneys. Retention of sodium and water 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 nephritic syndrome need renal biopsy examination and specialized treatment under the supervision of a nephrologist.

Nephrotic Syndrome and its Serious Effects

Urine examination shows critical abnormalities in nephrotic syndrome. 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 nephrotic syndrome is the consequence of prolonged massive proteinuria (excretion of protein in urine). The proteinuria exceeds 3.5 g/24-hours in adults or 50 mg/kg body-weight in children. Nephrotic syndrome is characterized by proteinuria, hematuria (blood in urine), hypertension (high blood pressure), oliguria (low output of urine per day), edema (swelling: apparently suborbital puffy eyes) and diminished renal function. Urine may be brown or red. Sodium (Na⁺) retention, increased circulating blood volume and hypertension (high blood pressure) may lead to cardiomegaly (enlargement of heart). Nephrotic syndrome is usually characterized by insidious onset of massive edema, proteinuria, hypoalbuminemia (low level of albumin in blood) and hyperlipidemia (high level of cholesterol in blood). There could be massive retention of sodium (Na⁺) and a tendency to excessive potassium (K⁺) loss. Serious ill effect of the nephrotic syndrome could be a tendency towards hypercoagulability (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 calcium (Ca⁺⁺) level could be low as this is related to the level of albumin in blood. Dysfunction of proximal tubules of kidneys may cause glycosuria (excretion of glucose/sugar in urine) or aminoaciduria.

Oliguria Or Anuria: Cause May Be Renal Or Non-Renal

The term oliguria means low urine output and anuria stands for no urine output. The oliguria or anuria could be due to renal disease (kidney disease) or non-renal (non kidney) problem. The four possible causes which probably lead to oliguria or anuria are listed below:

1. Obstruction in a kidney: Obstruction in a kidney or lower urinary track may cause oliguria or anuria. Debris of epithelial cell may block the renal tubules. Hemoglobin or myoglobin pigments or crystals of some drugs have also been documented as the possible cause of casts blocking the renal tubules. Interstitial edema (swelling of interstitial tissue in kidney) could also compress tubules thereby leading to impairment of tubular function. Net result of any sort of obstruction in a kidney is the oliguria which could lead to a grave situation i.e. anuria.
2. Dehydration: Continued vomiting, severe diarrhea or profuse sweating may lead to dehydration resulting in oliguria or complete cessation of urine i.e. anuria.
3. Peripheral circulatory collapse: Peripheral circulatory collapse may occur due to post-operative surgical shock leading to reduced renal blood flow and glomerular filtration rate (GFR) resulting in anuria as the tubules reabsorb whatsoever the glomerular filtrate is produced by glomeruli.
4. Degeneration of tubular epithelium: Degeneration of tubular epithelium causes detachment of epithelium from tubular basement membrane (TBM) resulting in massive loss of tubular epithelial cells. The loss of tubular epithelium leads to loss of physiological barrier between glomerular filtrate in tubules and very strong osmotic pull of plasma in the peri-tubular capillaries (PTC), hence any glomerular filtrate present in tubules is sucked out by PTC, leading to anuria. Mercuric chloride poisoning may cause this type of anuria, however, it could be reversible and epithelial lining of tubules be restored within about two weeks. Avoid tasting unknown and unspecified chemicals to save your kidneys and life.

Albumin & Casts in Urine and Associated Renal Lesions

Urine analysis is the cheapest and routine investigation which could be of great help to the clinician to reach at a diagnosis of a complex renal disorder. Albuminuria (excretion of albumin in urine) detected on heat test of the urine and the casts detected on microscopic examination of first morning specimen of urine reveal a lot about the associated renal lesions (pathological changes in kidney). Albuminuria we know definitely to be glomerular origin, although the tubules may also play their part in its production. It seems probable that this is mainly due to the glomerular basement membrane (GBM) which separates the epithelium of the tuft from the endothelium lining the capillaries, with increase of its permeability.

Casts are the microscopic accumulations of cells or coagulated proteins or lipids. Casts if present could be detected on microscopic examination of deposit obtained after centrifugation of urine. The casts must also be traced to the glomerulus, at least the essential hyaline matrix of the cast composed of coagulated albumin. Again the tubules add their contribution in the shape of epithelial cells and fatty and granular detritus which give to the casts their characteristic appearance. Careful examination casts is as informative as blood biochemistry investigations in cases of kidney disease. The cast gives a picture of the degenerative changes in the tubules. A hyaline cast indicates slight glomerular leakage without active tubular degeneration. Cellular casts denote marked activity of the morbid process. Granular casts denote moderate activity. The admixture of red blood cells (RBCs) is a sign of glomerular hemorrhage. We find that the study of casts is of remarkable importance in assessing the prognosis of a renal disorder. As long as there is considerable activity there is a scope for improvement. For such a study to be of value, the urine should be fresh. If the urine is alkaline or has been allowed to stand for long time, the casts may largely disappear. The absence of casts in an alkaline urine has not the same significance as when the urine is acidic. The acidity of the urine assists in the formation of casts. Deposition of casts in the tubules may lead to oliguria (low output of urine) leading to edema.

Reversible Renal Failure

When we come across the term reversible renal failure, it indicates that there was a scope for the repair of renal lesions or complete recovery of renal function. Reversible renal failure is of great importance for the clinician/nephrologist attending to the patient, because he/she could be able to do something for the well being of the patient. Clinical end picture may be same in many renal disorders though the origins are so different. Acute stage is characterized by pain in back, fever and edema, a rise in blood pressure and such urinary changes as oliguria (low output of urine), high specific gravity of urine with high coloration. Presence of albumin, red blood cells (RBCs) and casts have also been observed in urine with low urea content. It has been observed that reversible renal failure is generally extra-glomerular in origin, but it may be nephritic type. Most of the cases with acute glomerulonephritis also make a complete recovery with therapy and dialysis.  Tubular damage may also be repaired, as has been in the cases of mercuric chloride poisoning. Accumulation of nitrogenous waste products in blood is observed in these patients without any renal lesion on blood biochemistry and kidney biopsy evaluation. The condition may also be termed as extra-renal uremia or azotemia without corresponding renal lesion.