Showing posts with label MGN. Show all posts
Showing posts with label MGN. Show all posts

Thursday, June 18, 2009

Therapy and Management of Glomerulonephritis

In my other articles you must have got ample information regarding classes or types of glomerulonephritis (GN). 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 primary GN is 0.002% that means 2 new patients per 100,000 population in a year. There are a variety of causes of primary GN with identical histopathological features. It is worth to mention here that there may be many immunopathological reasons in membranous glomerulonephritis (MGN). The character and severity of GN varies with the status of altered immune status of an individual. The understanding of pathogenesis of GN is must before initiating any therapy.

Regular follow-up in a clinic/renal clinic is must for the patient diagnosed of having a renal disease or glomerulonephritis. The follow-up provides an opportunity to the patient to learn about the complications of persistent GN and/or chronic renal failure. It has been observed that hypertension often develops coincidental with progression of renal disease. The hypertension needs to be kept under control in patients affected by persistent GN. The renal function deterioration causes edema in patients with glomerulonephritis. Though restriction in salt and water intake may cure the edema to some extent but diuretic drugs are preferred to treat the edema. Dietary management of progression of renal disease demands moderate reduction in protein intake (recommended: 0.8-1.0 g/kg body weight/day, during edema) to reduce the nephrotic overload and correction of proteinuria. Effective measures to reduce proteinuria are must to speed-up healing of renal lesions.

Corticosteroids, cyclophosphamide, chlorambucil and cyclosporin are the drugs of choice for the treatment of GN. About 95% of children generally respond to the first course of steroids 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%. Oral prednisolone 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 glomerulonephritis 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.

Saturday, May 30, 2009

Nephrotic Syndrome and Associated Renal Lesions

Nephrotic syndrome may occur in any type of primary or secondary glomerulonephritis. Around two dozen histopathological categories or subcategories of glomerulonephritis are now recognized and etiological factors are largely determined. However, prevention and treatment of glomerulonephritis needs momentum to curb the development of irreversible renal failure. The main diagnostic feature of nephrotic syndrome is massive proteinuria (excretion of protein in urine) exceeding 3 g/24 hour. The other features of nephrotic syndrome, such as, hypoproteinemia (decreased level of proteins in blood), edema (swelling) and hyperlipidemia (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.

In children around 80% cases of nephrotic syndrome are due to minimal change disease(MCD) and in adults the dominance of MCD is lost. In adults the cause of nephrotic syndrome 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 nephrotic syndrome. Secondary amyloidosis is also known to cause renal lesions associated with nephrotic syndrome. Immunological disorders like systemic lupus erythematosis and vasculitis may also be a cause of glomerulonephritis. Renal biopsy evaluation by light microscopy (LM), immunofluorescence microscopy (IFM) and electron microscopy (EM) is must for an accurate diagnosis of type of glomerulonephritis in a patient of nephrotic syndrome. 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 nephrotic syndrome. Focal segmental proliferative glomerulonephritis and diffuse proliferative glomerulonephritis with crescents are considered as uncommon-primary causes of nephrotic syndrome. Glomerulonephritis due to metabolic disorders, immunological disorders, toxemia of pregnancy or malignant conditions of kidney are labeled as secondary causes of nephrotic syndrome.