De novo Diabetic Nephropathy with Functional Impairment in a Renal Allograft

Lf, Gimenez; Aj, Watson; Cr, Burrow; Jl, Olson; Dk, Klassen; Cr, Cooke

doi:10.1159/000167196

Cited by 14 publications

(3 citation statements)

References 3 publications

(4 reference statements)

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“…The interval between transplantation and biopsy is about 5 yr (10). Though NODAT develops in about 5-15% of renal transplant recipients, de novo diabetic nephropathy is rare with only 10 cases identified (7,(13)(14)(15)(16)(17)(18). Three of these cases reported had nodular while the others manifested diffuse diabetic glomerulosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Allograft diabetic nephropathy may progress to end‐stage renal disease

Salifu

Nicastri

Markell

et al. 2004

Pediatric Transplantation

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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.

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Section: Discussionmentioning

confidence: 99%

Allograft diabetic nephropathy may progress to end‐stage renal disease

Salifu

Nicastri

Markell

et al. 2004

Pediatric Transplantation

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“…6 There is paucity of data on natural history and clinical course of de novo ADN in patients with new-onset diabetes after transplant (NODAT). The proteinuria, hypertension, and azotemia in these patients are mistaken with the diagnosis of chronic allograft nephropathy (CAN) because only few graft kidney biopsies are performed to establish the diagnosis.…”

Section: Introductionmentioning

confidence: 99%

Outcomes of De Novo Allograft Diabetic Nephropathy in Renal Allograft Recipients

Prasad¹,

Gupta²,

Jain³

et al. 2013

Exp Clin Transplant

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Objectives: Despite increased use of diabetogenic immunosuppressive drugs and increased incidence of new-onset diabetes after transplant in renal allograft recipients, there are few case studies on the subject of de novo allograft diabetic nephropathy and interstitial fibrosis/tubular atrophy without specific glomerular changes. We sought to study the outcomes of allograft diabetic nephropathy and interstitial fibrosis/tubular atrophy without specific glomerular changes in patients with new-onset diabetes after transplant. Conclusions:De novo allograft diabetic nephropathy is a significant cause of graft and patient loss in renal allograft recipients who develop new-onset diabetes after transplant.

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“…Whereas in patients with diabetes mellitus almost all transplants are found to have morphological alterations such as thickening of the basement membrane and capillary hyalinosis after 2-4 years, full-blown nodular glomerulosclerosis and transplant failures have only been reported extremely rarely [6,23]. Sch6nlein-Henoch purpura with mesangial IgA deposits recurs quite rarely after transplants in adults, but very frequently in children [9,16].…”

mentioning

confidence: 99%

Glomerular disease of transplanted kidneys

Frei

1993

Clin Investig

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De novo Diabetic Nephropathy with Functional Impairment in a Renal Allograft

Cited by 14 publications

References 3 publications

Allograft diabetic nephropathy may progress to end‐stage renal disease

Allograft diabetic nephropathy may progress to end‐stage renal disease

Outcomes of De Novo Allograft Diabetic Nephropathy in Renal Allograft Recipients

Glomerular disease of transplanted kidneys

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