Transplant glomerulopathy
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Transplant glomerulopathy | |
---|---|
Synonyms | |
Pronounce | N/A |
Specialty | N/A |
Symptoms | Proteinuria, hypertension, edema, renal dysfunction |
Complications | Chronic kidney disease, graft failure |
Onset | Months to years post-kidney transplant |
Duration | Chronic |
Types | N/A |
Causes | Chronic antibody-mediated rejection, endothelial injury |
Risks | HLA mismatch, non-adherence to immunosuppressive therapy |
Diagnosis | Renal biopsy, serology |
Differential diagnosis | Chronic rejection, recurrent glomerulonephritis |
Prevention | Adequate immunosuppression, HLA matching |
Treatment | Immunosuppressive therapy, plasmapheresis, IVIG |
Medication | N/A |
Prognosis | Variable, often poor if untreated |
Frequency | Occurs in 5-20% of kidney transplant recipients |
Deaths | N/A |
Transplant Glomerulopathy
Transplant glomerulopathy is a chronic kidney disease that occurs in the setting of kidney transplantation. It is characterized by specific changes in the glomeruli, the filtering units of the kidney, and is a significant cause of chronic allograft dysfunction.
Pathophysiology
Transplant glomerulopathy is primarily associated with chronic antibody-mediated rejection (AMR). The condition is marked by the presence of double contours of the glomerular basement membrane, which are visible under a microscope. These changes are thought to result from endothelial injury caused by donor-specific antibodies (DSAs) targeting the transplanted kidney.
Clinical Presentation
Patients with transplant glomerulopathy often present with proteinuria, hypertension, and a gradual decline in renal function. The condition is usually detected during routine follow-up of kidney transplant recipients, often through a kidney biopsy.
Diagnosis
The diagnosis of transplant glomerulopathy is confirmed by histopathological examination of a kidney biopsy. The key histological feature is the presence of double contours of the glomerular basement membrane, which can be identified using special stains such as silver stain or periodic acid-Schiff stain.
Treatment
Management of transplant glomerulopathy involves addressing the underlying cause, which is often chronic antibody-mediated rejection. Treatment strategies may include the use of immunosuppressive therapy to reduce the activity of DSAs. In some cases, plasmapheresis or intravenous immunoglobulin (IVIG) may be used to lower antibody levels.
Prognosis
The prognosis of transplant glomerulopathy varies depending on the severity of the condition and the response to treatment. It is a progressive disease that can lead to graft loss if not adequately managed. Early detection and intervention are crucial to improving outcomes.
See also
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Contributors: Prab R. Tumpati, MD