Idiopathic Membranous Glomerulonephritis in Diabetic Patients

Renal biopsies were obtained from 164 patients with diabetes mellitus. Their histological changes were evaluated together with clinical findings and prognosis. In 36 patients, various types of glomerulonephritis were complicated: mesangial proliferative glomerulonephritis (17 patients), membranous glomerulonephritis (8), endocapillary proliferative glomerulonephritis (5), membranoproliferative glomerulonephritis (4) and minimal change nephrotic syndrome (2). Superimposed glomerulonephritis was suspected in diabetic patients with a short history of less than 5 years, persistent proteinuria, occasional hematuria and no retinopathy. They may, however, produce little effects on the long-term prognosis of diabetic patients except membranoproliferative glomerulonephritis.

Section: Introductionmentioning

confidence: 99%

Glomerulonephritis in Diabetic Patients and Its Effect on the Prognosis

Chihara¹,

Takebayashi²,

Taguchi³

et al. 1986

“…The coexistence of immune complex-mediated glo merulonephritis and diabetes mellitus has been reported frequently [1][2][3][4][5][6][7]. We reported three patients in whom diabetes mellitus was associated with membranous glo merulonephritis characterized by heavy proteinuria and marked thickening of the glomerular basement membra ne (GBM) [8], All of these patients developed progressive renal failure and subsequently required hemodialysis.…”

Section: Introductionmentioning

confidence: 99%

Autologous Immune Complex Nephritis in Streptozotocin-Induced Diabetic Rats

Okuda¹,

Oh²,

Onoyama³

et al. 1984

In order to investigate the influence of diabetes mellitus on immune complex-mediated nephritis, we produced Heymann nephritis in streptozotocin-induced diabetic rats (DM-HN group) in which the clinical course for 24 weeks and histological changes were examined. Nondiabetic rats with Heymann nephritis (HN group) and diabetic rats (DM group) were also examined as controls. The degree of proteinuria, hypoproteinemia, hyperlipidemia and anemia were more pronounced and the mortality rate was higher in the DM-HN group than in the HN group or in the DM group. Histologically, larger and more subepithelial or intramembranous electron-dense deposits as well as a more markedly thickened glomerular basement membrane (GBM) were observed in the DM-HN group than in the HN group. In conclusion, the nephrotic manifestations and histological changes in the GBM in Heymann nephritis were augmented by the association with diabetes mellitus.

“…From a review of the relevant literature, most of which consists of isolated case reports, a wide spectrum of nondiabetic renal lesions can occur in patients with diabetes [1][2][3][4], Although proteinuria is frequently the initial urinary abnormality observed in diabetic ne phropathy, the nephrotic syndrome is rarely seen in diabetic children [1.5, 6], Here, we report the case of an adolescent with insulindependent diabetes mellitus (IDDM) who developed membranoproliferative glomeru lonephritis (MPGN) 3 years after the diagno sis of diabetes. To the best of our knowledge.…”

mentioning

confidence: 99%

Membranoproliferative Glomerulonephritis Associated with Insulin-Dependent Diabetes mellitus

1996

Dear Sir, The prevalence of nondiabctic renal dis ease in diabetic patients is not known. From a review of the relevant literature, most of which consists of isolated case reports, a wide spectrum of nondiabetic renal lesions can occur in patients with diabetes [1-4], Although proteinuria is frequently the initial urinary abnormality observed in diabetic ne phropathy, the nephrotic syndrome is rarely seen in diabetic children [1.5, 6], Here, we report the case of an adolescent with insulindependent diabetes mellitus (IDDM) who developed membranoproliferative glomeru lonephritis (MPGN) 3 years after the diagno sis of diabetes. To the best of our knowledge. IDDM and MPGN have never been re ported in children.A 14-year-old girl with a 3-year history of IDDM was admitted to hospital because of edema. On admission, blood pressure was 120/80 mm Hg, pulse rate 82/min and pretibial edema was 3+. Fundoscopic examina tion revealed no microaneurysm or exudate. Laboratory' studies showed a normal blood cell count with ESR 60 mm/h. Urinalysis revealed specific gravity 1,025, protein >300 mg/dl, glucose 100 mg/dl and 24-hour protein excretion was 145 mg/m2/h. BUN, serum creatinine, total serum protein and serum albumin were 18 mg/dl, 0.6 mg/dl, 5.6 g/dl and 2.2 g/dl respectively. The blood glucose level was fairly well controlled by dieting and insulin therapy (blood glucose 256 mg/dl. HbA|C 12.7). Cj and C4 were within normal limits. ANA. CRP. and rheu matoid factor were negative. HbsAg, antiHbs, anti-Hbc, anti-delta and anti-HCV were also negative; HAV-IgM was positive. A percutaneous renal biopsy was performed and demonstrated glomerular enlargement and lobulation, mesangial matrix increment and basal membrane thickening. DilTuse de position of lgG and IgM on the glomerular mesangium were revealed immunohistochemically. Prednisolone 60 mg/m2/day, cy clophosphamide 2 mg/kg/day and dipyrida mole 8 mg/kg/day w'ere begun and she con tinued to receive 45 U/day insulin.The patient described in this report had IDDM, and a nephrotic syndrome mani fested by generalized edema. Diabetic ne phropathy is a well-recognized complication of diabetes mellitus but in our case the dura tion of diabetes mellitus was short and did not demonstrate hypertension, diabetic complications such as retinopathy and neu ropathy or high levels of serum creatinine which are usually associated with diabetic nephropathy.