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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kidney biopsy specimens from 15 patients ranging in age from 11 to 19 years with two- to 14-year histories of insulin-dependent diabetes mellitus were evaluated electron microscopically. Although the mean duration of disease was only eight years, the glomerular basement membrane (GBM) in these patients showed a variety of alterations typical of insulin-dependent diabetes mellitus. Saccular glomerular microaneurysms, previously little recognized, were seen in six of the specimens. These lesions, always associated with breaks in the paramesangial BM, were morphologically distinct from the ectatic capillary loops and glomerular capillary aneurysms described previously in diabetic glomerulopathy. All of the patients with such aneurysms also had other severe GBM alterations. Lytic or mechanical injury to the structurally and biochemically altered diabetic GBM may be responsible for the formation of microaneurysms.
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PMID:Glomerular membranopathy in adolescents with insulin-dependent diabetes. 394 44

Thirty-five patients with Type 1 (insulin-dependent) diabetes mellitus and 90 normal subjects had renal size (renal area index) determined by X-ray and also had examination of renal biopsies by light and electron microscopy. Renal area index of 206 +/- 32 cm2/1.73 m2 (mean +/- SD) in the Type 1 diabetic patients exceeded that in the normal subjects (180 +/- 25 cm2/1.73 m2, p less than 0.001). In the diabetic patients, the renal area index correlated with creatinine clearance (r = +0.43, p less than 0.05), but did not correlate with urinary albumin excretion, or the electron microscopic measurements of percentage total mesangium and glomerular basement membrane width. In diabetic patients with clinical nephropathy or severe glomerulopathy on biopsy, the kidneys may remain large. Thus, renal size does not indicate the severity of diabetic renal lesions on biopsy.
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PMID:Relationship of renal size to nephropathy in type 1 (insulin-dependent) diabetes. 397 81

Rats with streptozotocin-induced chronic diabetes mellitus develop a glomerulopathy functionally manifested by proteinuria. The ability of the glomerular capillary wall to retard filtration of macromolecules was examined in 5 chronically diabetic Munich-Wistar rats exhibiting excessive proteinuria (39 +/- 7 mg/24 h, mean +/- SEM) and 5 age-matched normal Munich-Wistar rats without increased proteinuria (4.7 +/- 0.2 mg/24 h). Urinary albumin excretion was not increased in the diabetic rats (2.0 +/- 0.6 mg/24 h vs 1.6 +/- 0.3 mg/24 h) suggesting that the normal net electronegative charge of the glomerular capillary wall was not altered. Fractional clearances of macromolecular neutral dextrans were similar in diabetic and normal rats throughout a wide range of molecular size (18-42 A). Glomerular filtration rate was the same in the two groups of rats (2.77 +/- 0.16 ml/min in diabetics and 2.72 +/- 0.11 ml/min in normals) suggesting that renal haemodynamic factors did not influence fractional clearances of neutral dextrans in diabetic rats. We conclude that the proteinuria exhibited by these chronically diabetic rats is not attributable to alterations of size-selective properties of the glomerular capillary wall, such as increases in the size or the number of pores.
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PMID:Glomerular selective permeability to macromolecular neutral dextrans in experimental diabetes. 616 92

A 51-year-old man with diabetes mellitus and the nephrotic syndrome on renal biopsy was found to have diabetic glomerulosclerosis, amyloidosis and membranous glomerulopathy. The presence of three distinct glomerular diseases in the same patient is unique. Possible factors involved in their pathogenesis are discussed and the literature on concomitant glomerular diseases is reviewed.
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PMID:Concomitant presence of three different glomerular diseases in the same patient. Report of a case and review of the literature. 634 70

The earliest manifestations of clinical diabetic nephropathy, including proteinuria, hypertension, and declining GFR, represent very advanced diabetic glomerulopathy with especially prominent mesangial expansion. Mesangial expansion, by restricting glomerular capillary filtration surface and lumenal volume, stimulates compensatory mechanisms analogous to those resulting from a marked reduction in nephron number. These compensatory mechanisms involve alterations in glomerular hemodynamics designed to maintain glomerular filtration but which ultimately injure the kidney. These hemodynamic perturbations are not specific to diabetes but represent a final common pathway toward endstage renal failure that also characterizes the remnant kidney. This thesis concludes that the onset of clinical diabetic nephropathy augurs inevitable decline in kidney function, and that only studies and interventions exercised before clinical nephropathy develops can influence understanding and outcome of diabetic nephropathy.
Diabetes 1983 May
PMID:Diabetic nephropathy. A perspective. 640 Jun 68

Studies of the glomerular structure in diabetes mellitus have helped to elucidate the basis for some functional abnormalities. The decline in glomerular filtration occurring in many long-term diabetics is a functional disorder of great clinical importance. Quantitative structural studies of the glomeruli in diabetics at different stages of disease are necessary to learn about the development of structural changes leading to the end-stage kidney disease. Preliminary results of a study of glomeruli from long-term diabetics with clinical nephropathy are compared with those obtained in control subjects and in diabetics within the first 5 yr of disease. In the long-term diabetics the peripheral basement membrane thickness was doubled. On the average, mesangial regions occupied nearly 60% of the total tuft volume as compared with 33% in the early stages. A marked accumulation of basement membrane material in the mesengial regions had taken place so that 85% of the total basement membrane material of the tufts (i.e., peripheral basement membrane in the capillary walls plus mesangial basement membrane-like material) was localized within the mesangial regions. In the early stages equal amounts were found at these two different sites. The distribution of the lesions within the kidney is under investigation in a light microscopic study of autopsy material from long-term diabetics with varying degrees of glomerulopathy. The severity of the diabetic glomerulopathy was quantitated separately within the superficial and the deep cortical zones. The results showed that there was no tendency toward increased severity in the deep glomeruli.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1983 May
PMID:Diabetic glomerulopathy. Structural characteristics of the early and advanced stages. 640 Jun 71

Light-chain glomerulopathy occurred in a middle-aged woman with adult-onset diabetes mellitus and IgG-kappa light-chain multiple myeloma. Unusual features of the glomerulopathy included the presence of numerous epithelial crescents and rapid progression to chronic renal failure. The aggressiveness of her disease may be related to her underlying diabetes mellitus and associated abnormalities in glomerular clearance of macromolecules, including immunoglobulin light chains.
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PMID:Crescentic light-chain glomerulopathy. Report of a case. 640 21

The onset of fixed proteinuria and hypertension in insulin-dependent diabetic is generally associated with eventual renal insufficiency due to diabetic nephropathy or with a superimposed glomerulopathy. We report three adolescents with normal renal function who developed fixed proteinuria and hypertension after only 7 to 11 years of insulin-dependent diabetes mellitus. Blood pressure ranged from 130/95 to 165/104 mmHg, urinary protein excretion was 1.31 to 1.37 g/24 hours, and creatinine clearance ranged from 98-133 ml/min/1.73 m2. Renal biopsy revealed changes consistent only with diabetic glomerulosclerosis. Follow-up evaluation for 11 months to 3 1/2 years revealed blood pressure reductions to 125/78-140/85 mmHg as a result of antihypertensive medications. Creatinine clearance increased by 12-20% and urinary protein excretion remained unchanged. We conclude that these patients may represent an unusual subgroup of insulin-dependent diabetics with early development of clinical and pathological diabetic nephropathy in the face of normal renal function.
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PMID:Early onset of clinical diabetic nephropathy in children--a new subgroup? 671 12

The purpose of this study was to determine the use of continuous intraperitoneal insulin infusion over an extended period (in maintaining metabolic control) and to evaluate the benefits of this treatment in reversing the kidney pathology of a chronic diabetic dog with membranous glomerulopathy. Hyperglycemia was eliminated, but reevaluations of the insulin infusion pattern were necessary. An initial kidney biopsy revealed fusion of the foot processes, thickening of the basement membrane, and subendothelial deposition. After 5 months of infusion, there was less fusion of the foot processes and a decrease in the subendothelial deposition. Urinary protein loss decreased from 17.3 g/day to 625 mg/day after 2 months of infusion. The dog gained weight, muscle wasting was reversed, and his stamina returned while on continuous insulin infusion. The reduction of a life-threatening urinary protein loss to a tolerable level and the improvement in the microscopic kidney lesions observed indicate that this treatment with insulin infusion may be beneficial in the management of long-term diabetic dogs, affected with advanced kidney lesions secondary to diabetes.
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PMID:Case study of a diabetic dog with chronic membranous glomerulopathy treated with continuous intraperitoneal insulin infusion. 675 39

Exact parameters for relevant glomerular structures in the course of streptozotocin diabetes in rats with 1 to 18 months' duration were obtained with stereological methods. Renal cortical tissue from diabetic (D) and control animals (C) was processed for light- and electron microscopy and measurements were performed on systematically sampled glomeruli. The thickness of the basement membrane (BM) increased with age in both groups, but the rate of increase was 50% higher in D: 19 +/- 1.2 nm/month (mean +/- SD) vs. 13 +/- 0.9 nm/month, P = 0.0003. The time course of other structural quantities was characterized by the acute changes constituting the glomerular hypertrophy, earlier shown to develop within the first few days of diabetes. All these changes were confirmed in the present study: In the earliest phase the diabetic rats showed an increased total volume of glomeruli, mesangium, and mesangial BM material, as well as an increased surface of the capillary walls. However, none of these differences between the groups showed progression with increasing duration. Mesangial changes corresponding to those of the glomerulopathy in long-term diabetes were not demonstrable within the experimental period. The streptozotocin diabetic rat, therefore, is not useful as a model of advanced diabetic glomerulopathy. But the BM thickness follows the same predictable time course as in human diabetes insofar as moderately advanced cases are concerned. BM thickness is the parameter of choice when a potential effect of different variables on the development of diabetic glomerulopathy is under study.
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PMID:Development of glomerular lesions in experimental long-term diabetes in the rat. 698 Oct 23


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