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09.07.04 (3 years ago)
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READ THIS ARTICLE
ACCORDING TO IT I THINK THE ANS IS MEMBRANOPROLIFERATIVE DISEASE
WHAT DO U ALL SAY
AS SUCH MOST COMMON CAUSE OF TRANSPLAN WORLD WIDE IS : DIABETES
Diabetes – 31%
Chronic glomerulonephritis – 28%
Polycystic kidney disease – 12%
Nephrosclerosis (hypertensive) – 9%
Systemic lupus erythematosus (SLE) – 3%
Interstitial nephritis – 3%
Recurrent renal disease in patients who have had kidney transplants accounts for less than 2% of all graft losses, though it affects as many as 10% of transplant recipients. A few diseases have a high risk of renal allograft loss, such as focal segmental glomerulosclerosis, HUS oxalosis, and membranoproliferative glomerulonephritis. Diabetic nephropathy can recur in renal allografts, but the time to onset is similar to that seen in native kidneys and is an uncommon cause of graft loss.
Rejection
Hyperacute rejection of the renal allograft happens within hours of the transplant, and it occurs when circulating, preformed, cytotoxic, antidonor antibodies directed to the ABO blood group antigens or to the donor HLA class I antigens are present. No treatment exists, and nephrectomy is indicated.
Accelerated acute rejection is a very early, rapidly progressive, aggressive rejection reaction. It can occur within the first week of transplantation. Immediate therapy with anti–T-cell antibodies and pulse corticosteroids may reverse the process. Approximately 50% of cases can be salvaged.
Acute tubular interstitial cellular rejection is the most common type of rejection reaction with an incidence of approximately 20-25%. Typically, it occurs between 1-3 months posttransplant. It is T-cell mediated, and injury is directed to the renal tubules. The criterion standard for diagnosis is renal allograft biopsy. Mild rejections may be successfully reversed with corticosteroids alone, whereas moderate or severe rejections may require the use of anti–T-cell antibodies, either polyclonal or monoclonal.
Chronic rejection is a slow and progressive deterioration in renal function characterized by histologic changes involving the renal tubules, capillaries, and interstitium. The precise mechanism of this disease is poorly defined and is an area of intense study. Application of conventional antirejection agents, such as corticosteroids or anti–T-cell antibodies, does not appear to alter the progressive course. Unfortunately, this is a major cause of kidney allograft loss, occurring later than 2 years posttransplant.
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