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

To gain further insight into the genetic determinants of diabetic small vessel disease, we studied 22 HLA antigens in 110 juvenile-onset, insulin-dependent diabetics with terminal glomerulosclerosis and retinopathy, who were being prepared for kidney transplant. HLA antigens were comtemporarily determined in non-diabetic kidney transplant recipients and healthy controls. The frequency of antigens A1 and B8 were significantly higher in diabetics than in controls (P less than .02 and .011), but the frequency of BW15 was normal. The data are compatible with the concept that juvenile diabetes with microangiopathy is one of the HLA-B8 associated disorders.
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PMID:Histocompatibility (HLA) antigens and diabetic microangiopathy. 5 63

A series of in vivo and in vitro investigations was performed to examine the localisation of sorbitol pathway activity in the rat renal cortex and to investigate the possible relation that the acculumation of sorbitol pathway intermediates in renal cortical tissue may have to the pathogenesis of renal complications in diabetes mellitus. Neither of the sorbitol pathway intermediates, sorbitol or fructose, were detected either in intact glomeruli which had been isolated from rats rendered chronically diabetic with streptozotocin, or in metabolically active glomeruli which had been incubated in vitro in high glucose media. Such data agreed with previously published observations that the enzyme aldose reductase is not present in renal glomeruli, and suggested that changes in sorbitol pathway activity cannot be directly related to the pathogenesis of diabetic glomerulosclerosis. Sorbitol was detected in low concentrations (3.1 mu-mol/g protein) in cortical tubules which had been isolated from the renal cortex of rats rendered chronically diabetic with streptozotocin. This concentration of sorbitol was higher than that in the intact renal cortex of the diabetic animal (0.3 mu-mol/g protein) or in the cortical tubules of non-diabetic animals (0.5 mu-mol/g protein). It is apparent that the renal cortical tubule is a major site of sorbitol pathway activity in the renal cortex. However, there is presently no obvious causal relationship between the accumulation of such relatively low concentrations of sorbitol in the renal cortical tubule and the pathogenesis of glomerulosclerosis or cortical tubular lesions in diabetes.
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PMID:The localisation of sorbitol pathway activity in the rat renal cortex and its relationship to the pathogenesis of the renal complications of diabetes mellitus. 12 79

The precise etiology and pathogenesis of diabetic glomerulosclerosis still remain obscure. The aim of the present study was 1. to evaluate the morphologic and functional alterations of mesangial cells in long term diabetic rats and 2. to study the effect of islet transplantation on these lesions. Diabetes was induced in inbred Lewis rats with streptozotocin (65 mg per kg). 7 month later glomeruli of diabetic rats showed hyaline nodular deposits, exsudative lesions and glomerular aneurysms. The thickening of the mesangium measured by point counting method was statistically significant compared with age matched controls. Large quantities of IgG, beta 1c and fibrinogen in a predominantly mesangial pattern could be demonstrated by fluorescence microscopy. After injection of aggregated immunoglobulin the uptake of IgG by the mesangial cells was delayed in the diabetics compared with normal controls. Islet transplantation resulted in a marked reduction of the light microscopic and immunohistological glomerular lesions and restored the phagocytic capacity of the mesangial cells almost completely. From these results it is concluded, that the fundamental defect in diabetic glomerulosclerosis is a metabolically induced functional defect of the mesangial cells.
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PMID:[Regression of diabetic glomerular changes following islet transplantation. A study of rats with streptozotocin diabetes]. 15 38

Current information on the nature, pathogenesis and treatment of diabetic glomerulosclerosis is reviewed. The fundamental lesion is one of the glomerular basement membrane, a complex layer of collage-like and other peptides; thickening of this membrane, seen microscopically, is due to the presence of an increased amount of membrane material of normal composition. There is little reliable evidence relating the frequency of glomerulosclerosis to the quality of control of the diabetic state, but indirect evidence from patients with secondary diabetes and from a variety of studies in animals indicates strongly that the glomerular lesion is a consequence of the abnormal metabolic state and can be prevented by adequate treatment of the diabetes. A concept of the pathogenesis of the glomerular lesions and renal failure is presented, but there remain large gaps in knowledge of the mechanisms involved. Treatment of chronic renal failure by maintenance renal dialysis and renal transplantation is not as successful in persons with diabetes as in those without this condition; however, the results appear to be improving, and transplantation particularly holds much promise.
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PMID:Diabetic glomerulosclerosis: current status. 35 65

Renal disease, particularly glomerulosclerosis, is a major cause of morbidity and mortality in patients with juvenile-onset diabetes mellitus. Signaled by the onset of proteinuria after 15 or more years of insulin therapy, progressive renal insufficiency due to glomerulosclerosis terminates in uremia within five years. Although some patients have benefited from chronic dialysis programs, the outcome in uremic diabetics has been considerably better if successful renal transplantation can be accomplished. Extrarenal complications of diabetes mellitus and recurrence of diabetic lesions in transplanted kidneys have hampered the recovery and rehabilitation of transplant recipients. Other renal diseases encountered in juvenile diabetics are reviewed.
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PMID:Grand rounds: Nashville VA Hospital--Vanderbilt University. Saturday conference: renal disease in the juvenile diabetic. 37 Oct 5

Diabetic glomerulosclerosis must be either a primary manifestation or a secondary consequence of the metabolic abnormalities of diabetes. Several earlier reports have attempted to support the former hypothesis by describing cases of pathognomonic renal lesions in nondiabetic subjects; however, the clinical and pathologic data in these reports are inconclusive. We have reviewed our experience at the University of Virginia Hospital with 447 percutaneous renal biopsies performed over a period of four years from July 1973 through July 1977. Of these cases, only two appeared to represent diabetic glomerulosclerosis occurring in nondiabetic subjects. Upon further investigation, one case provided to be light chain disease demonstrated by immunofluorescence staining. The other case, on repeat renal biopsy, proved to be membranoproliferative glomerulonephritis. We conclude that a diagnosis of diabetic glomerulosclerosis must be viewed with suspicion in nondiabetic subjects. Suspected cases should be labeled pseudodiabetic glomerulosclerosis and investigated further.
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PMID:An evaluation of diabetic and pseudodiabetic glomerulosclerosis. 37 61

Marked weight loss with cachexia together with severe depression and pain from symmetrical peripheral neuropathy were noted in a 66-year-old man, known to have had diabetes for six years, which required insulin on admission to hospital. The patient died of bronchopneumonia after one year. The severe neuropathy was proven both neurophysiologically and at necropsy. There was no diabetic retinopathy and no histological evidence of renal glomerulosclerosis. There was no evidence of a malignant tumour either clinically or at necropsy.
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PMID:[Diabetic neuropathic cachexia (author's transl)]. 44 96

Recent evidence has suggested a role for the polyol pathway in pathogenesis of cell damage in diabetes Glucose may be phosphorylated to glucose-6-phosphate via hexokinase and enter glycolysis or reduced to sorbitol via aldose reductase to enter the polyol pathway. The poorly diffusible sorbitol is converted via sorbitol dehydrogenase to fructose. Hexokinase, aldose reductase and sorbitol dehydrogenase activities were measured in glomeruli (G) and small arteries (SA) taken from normal and diabetic human kidneys, Hexokinase in diabetic G was 1688, which was significantly decreased from normal, 3147 mmoles/kg-1/h-1. Alodse reductase was significantly elevated in diabetic G,56-6, compared to normal G,10-8 mmoles/kg-1/h-1. In contrast, sorbitol dehydrogenase was significantly depressed in diabetic G, 3-7 VERSUs 10-9 mmoles/kg-1/h-1. The enzymatic changes observed in diabetic G would facilitate accumulation of sorbitol and therefore could contribute to the progression of glomerulosclerosis. The activity of hexokinase was also significantly reduced in SA, whereas aldose reductase and sorbitol dehydrogenase were unchanged.
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PMID:Quantitative histochemistry of the sorbitol pathway in glomeruli and small arteries of human diabetic kidney. 48 51

Diabetic nephropathy have only rarely been described in patients who have minimal or no glucose intolerance. We herein report the case of a 59-yr-old man who presented with nephrotic syndrome and minimal glucose intolerance whose renal biopsy showed the nodular (Kimmelsteil-Wilson) and diffuse glomerulosclerosis lesions characteristic of diabetes. We critically review the literature on this subject, pointing out the pitfalls in diagnosis and establishing strict criteria for the diagnosis of diabetic nephropathy in patients wihout overt clinical diabetes.
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PMID:Diabetic nephropathy as the mode of presentation of diabetes mellitus. 49 59

A histological study (hematoxylin-eosin staining, and PAS-reaction) of the kidneys was carried out in 5 pubertal rats with diabetic test for glucose tolerance from the progeny of a female with alloxan diabetes and intact male. Changes of the type of diabetic intracapillary glomerulosclerosis were revealed. There were no changes in the kidneys of pubertal rats from the progeny of intact female and male, and an intact female and a male rat with alloxan diabetes.
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PMID:[Histopathological changes in the kidneys of the progeny of rats with aloxan diabetes]. 52 42


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