Diabetic Nephropathy After Renal Transplantation

Abstract

The histologic diagnosis of diabetic glomerulosclerosis was made in 14 renal transplant recipients. All 14 had insulin-dependent diabetes mellitus, which was the original cause of end-stage renal disease in 12; one patient had membranoproliferative glomerulonephritis and another patient had membranous nephropathy as the cause of end-stage renal disease. Insulin-dependent diabetes mellitus was diagnosed at an average age of 18.5 years (range, 8-41 years), and the mean duration of diabetes prior to transplantation was 15 years (range, 2-25 years). All patients were recipients of first kidney transplants (six living related donors and eight cadavers). The histologic diagnosis of diabetic glomerulosclerosis was made on average, 97 months after transplantation (range 41-154 months). All 14 patients had proteinuria (mean 5.3 g/24 hr; range 1.1-12 g/24 hr) and renal dysfunction (mean serum creatinine level, 2.8 mg/dl). Patient and graft survival rates at 1 year, 5 years, and 10 years after transplantation were 100%, 92%, and 59%, and 100%, 92%, and 34%, respectively. Graft failure was due to diabetic nephropathy in seven patients, diabetic nephropathy and membranous nephropathy in one patient, and death due to a cerebrovascular accident in one patient. A total of five patients are alive with a functioning kidney. Of the eight patients who returned to dialysis, four are alive, three remain on dialysis, and 1 had a combined kidney and pancreas transplant. Histologic findings were as follows: 9/14 had moderate or severe diffuse glomerular basement membrane thickening and 2/14 had nodular glomerulosclerosis. Arteriolar lesions were prominent in all cases and was graded moderate or severe in 11 cases. The development of allograft diabetic nephropathy is associated with a high rate of allograft failure.

Visceral Leishmaniasis in a Renal Transplant Recipient: Diagnostic and Therapeutic Problems

“…Coexistence of other infections and a low index of suspicion could also contrib ute to such a diagnostic delay. Our patient was initially given empirically antitubercular treatment, since post transplant tuberculosis is a common problem in India [13], and this patient showed retroperitoneal lymphadenopathy. In the present case, it is difficult to be sure whether visceral leishmaniasis was a fresh infection after transplantation or was a result of reactivation of a pre existing infection.…”

Recurrence of Secondary Glomerular Disease after Renal Transplantation

“…Recurrence of DN accounted for only 1.8% of graft losses in one of the largest series of renal transplants in diabetic recipients (86). This low risk may depend on the short duration of follow-up because the mean interval between the onset of insulindependent diabetes and the development of overt nephropathy in renal transplant recipients requires several years (87). A more recent series demonstrated a histologic recurrence in almost 40% of diabetic patients in a mean of 6.7 years after transplantation (88).…”

“…Microalbuminuria heralds the presence of DN, whereas overt proteinuria and nephrotic syndrome develop later, preceding the onset of progressive renal failure. In transplanted patients with DM who develop overt proteinuria and renal insufficiency, the typical nodular intercapillary glomerulosclerosis (Kimmelstiel-Wilson lesion) is infrequent, whereas vascular changes are prominent (87). The progression of histologic, diabetes-related lesions in the transplanted kidney is slow, but more rapid than in the original disease, perhaps because of the lower nephron mass, the use of nephrotoxic calcineurin inhibitors, and glucocorticoid therapy, and the frequency of concomitant hypertension.…”

Outcomes of De Novo Allograft Diabetic Nephropathy in Renal Allograft Recipients

“…16 However, the recurrence of allograft diabetic nephropathy can occur after 8 years of transplant in almost 100% of transplanted diabetic patients, and is associated with increased risk of graft failure. [16][17][18] These events suggest the role of metabolic abnormalities in the pathogenesis of diabetic nephropathy.…”