Mesangial expansion and glomerular basement membrane thickening characteristic of
diabetic nephropathy recur in diabetic recipients of renal allografts from non-diabetic donors but progression to
renal failure is minimally documented. Three female renal allograft recipients (aged 40, 62 and 73 yr), who developed
end-stage renal disease (
ESRD) due to recurrent
diabetic nephropathy (two patients) and de novo diabetes (one patient) are reported. Onset of
proteinuria, uncontrolled
hypertension,
azotemia, renal allograft pathologic findings and the need for
hemodialysis were analyzed. None of the kidney donors (one cadaver, two living related) had known diabetes or perturbed
glucose metabolism pre-
transplantation. The three patients presented had different varieties of
diabetes; type 1, type 2 and new onset diabetes after
transplantation (NODAT). In each subject,
proteinuria was detected by dipstick at a mean of 8.3 yr (range 8-9) post-
transplantation and increased to the nephrotic range (3.7-4.8 g/day) inducing
hypoalbuminemia and
azotemia. A histopathologic diagnosis of allograft
diabetic nephropathy was made in a mean of 11.7 yr (range 10-14), based on glomerular basement membrane thickening, nodular and diffuse intercapillary glomerulosclerosis,
arteriolosclerosis, and tubular
atrophy with marked tubular basement membrane thickening characteristic of advanced
diabetic nephropathy. All three patients manifested
uremia and resumed
hemodialysis. Two patients died from
sepsis within 2 months and one patient died 2.5 yr later after resumption of maintenance
hemodialysis. We infer that recurrent or de novo
diabetic nephropathy in renal allografts follows a clinical decade-long course irrespective of diabetes. Reports of
ESRD due to allograft
diabetic nephropathy (ADN) have been limited because of shorter survival of diabetic transplant recipients and few kidney biopsies performed in patients with chronic allograft dysfunction. The occurrence of allograft
diabetic nephropathy in some, but not all patients, however, suggests that individual genetic variability modulates disease expression.