Diabetic glomerulosclerosis without glucose intolerance

Nash, Daniel A.; Rogers, Philip W.; Langlinais, Paulette C.; Bunn, S. M.

doi:10.1016/0002-9343(75)90353-8

Cited by 37 publications

(15 citation statements)

References 21 publications

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“…In 3 of our patients, renal biopsy either by light or electron-microscopy disclosed a mild thickening of the GBM [21]. In none of these patients was there any clinical or laboratory evidence of diabetes mellitus.…”

Section: Discussionmentioning

confidence: 59%

Renal Lesions in Chronic Pancreatitis

Salomon¹,

Silva²,

Tchertkoff³

et al. 1978

Nephron

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Many patients with chronic pancreatitis (CP), even in the absence of intrinsic renal disease, are found to have abnormal urine, with persistent proteinuria, cylindruria, micro-hematuria and leukocyturia. The kidneys of 12 necropsy cases with CP showed mild to moderate arterial and arteriolar nephrosclerosis and no other significant changes. Renal biopsies were performed in 10 patients with CP without evidence of systemic disease or intrinsic renal disease, but with persistent urinary abnormalities. By light microscopy, mild arterial and arteriolar nephrosclerosis was present in 5 instances. In 1 patient, evidence of the reparative phase of acute tubular necrosis was noted. In 5 biopsies, electron microscopy revealed minimal to mild increase in mesangial matrix. Mild thickening of the glomerular basement membrane (GBM) was found in three instances but there was no clear-cut evidence of diabetic glomerulosclerosis. The presence of subendothelial electron-lucent material in 3 cases suggests the possibility of previous sub-clinical episodes of intravascular coagulation. The most consistent finding was the presence of lipid material in the cytoplasm of glomerular and tubular cells. The renal lesions associated with CP are mild, nonspecific and nonprogressive. Various pathogenetic factors can be invoked to account for their presence and for the urinary abnormalities found in patients with CP.

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Section: Discussionmentioning

confidence: 59%

Renal Lesions in Chronic Pancreatitis

Salomon¹,

Silva²,

Tchertkoff³

et al. 1978

Nephron

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“…They concluded that the thickening of the MCBM is a characteristic of genetic diabetes mellitus and that this vascular defect is independent of carbohydrate derangement in diabetes mellitus. Nash et al (1975) also observed a significant thickening of the capillary basement membrane of the skeletal muscle in four patients with prediabetes or suspected diabetes mellitus who presented renal abnormalities but no evidence of carbohydrate intolerance. On the other hand, Kilo et al (1972) reported that the thickening of MCBM was proved as an aging phenomenon both in the normal subjects and in the diabetics.…”

Section: Discussionmentioning

confidence: 73%

Thickening of basement membrane of muscle capillary in spontaneously diabetic KK mice.

Itabashi¹,

Ohneda²,

Iimura

1981

Tohoku J. Exp. Med.

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“…In some cases, diabetes was present, but with minimal alterations in glucose or insulin responses to oral or intravenous glucose challenge, whereas, in others, diabetes was never detected. [4][5][6][7] In the latter scenario, similar lesions can be seen in other glomerulonephritides, such as, light-chain deposition disease, amyloidosis, immunotactoid nephropathy, the membranoproliferative form of diffuse glomerulonephritis, and idiopathic, nodular glomerulosclerosis. 8,9 The purpose of this review is to discuss the pathobiology of these lesions reminiscent of diabetic nephropathy and how to differentiate them from diabetic nephropathy (Table).…”

mentioning

confidence: 79%

Renal Morphologic Lesions Reminiscent of Diabetic Nephropathy

Raparia

Usman

Kanwar

2013

Archives of Pathology &Amp; Laboratory Medicine

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Context.-Nodular, intercapillary glomerulosclerotic lesions resembling Kimmelstiel-Wilson nodules commonly observed in diabetic nephropathy can also be seen in patients without any clinical history or evidence of diabetes.Objectives.-To discuss the pathobiology of lesions reminiscent of diabetes nephropathy, including light-chain deposition disease, amyloidosis, immunotactoid nephropathy, the membranoproliferative form of glomerulonephritis, and idiopathic nodular glomerulosclerosis, and how to differentiate them from diabetic nephropathy.Data Sources.-Published literature and authors' personal experience.Conclusions.-The well-formed, intercapillary, nodular mesangial lesions, along with thickened glomerular basement membranes and tubular basement membranes, and hyaline arteriolosclerosis are virtually pathognomic of diabetic nephropathy. However, the pathologist must exclude lesions reminiscent of diabetic nephropathy by performing special stains on histologic sections, immunofluorescence, and electron microscopic studies.

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Diabetic glomerulosclerosis without glucose intolerance

Cited by 37 publications

References 21 publications

Renal Lesions in Chronic Pancreatitis

Renal Lesions in Chronic Pancreatitis

Thickening of basement membrane of muscle capillary in spontaneously diabetic KK mice.

Renal Morphologic Lesions Reminiscent of Diabetic Nephropathy

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