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

The study was designed to show whether there was any relation between muscle capillary basement membrane thickness, HLA-antigens, anti-insulin antibodies and proliferative retinopathy. Electron microscopic measurements of muscle capillary basement membrane thickness were performed on muscle biopsies from 15 insulin-dependent diabetics and severe proliferative retinopathy, 24 insulin-dependent diabetics with minimal retinopathy and 18 age- and sex matched non-diabetics. All the patients had had diabetes for 20 years or more. None had biochemical or clinical evidence of diabetic nephropathy. Basement membrane thickness was measured according to the methods of Siperstein and Williamson. Muscle capillary basement membrane thickening occurred in 32 of 39 diabetics, using the Siperstein method, but patients with proliferative retinopathy did not exhibit thicker basement membranes than patients with no or minimal changes in the retina. There were apparent differences in HLA-antigens between diabetics with and without proliferative retinopathy, but they did not reach statistical significance. There was no correlation between muscle capillary basement membrane thickness and the quantity of insulin antibodies. The results indicate that factors other than basement membrane thickening and genetic factors in the HLA-region, are responsible for the development of proliferative retinopathy.
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PMID:Basement membrane thickness, insulin antibodies and HLA-antigens in long standing insulin dependent diabetics with and without severe retinopathy. 48 71

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

The uptake of 45Ca was measured in slices of kidney cortex from normal rats, streptozotocin-diabetic rats, and streptozotocin-diabetic rats treated early and late with insulin. Insulin therapy was performed such that blood glucose levels were controlled in half the treated diabetic animals but not in the others. Considerably earlier than evidence of nephropathy (i.e., proteinuria and increased BUN levels) in streptozotocin-diabetic rats, there was a significant decrease in active uptake of calcium by the kidney. Insulin therapy, begun immediately upon diagnosis of diabetes, maintained normal calcium transport even when blood glucose levels were not controlled. On the other hand, insulin therapy, begun 1 mo after diabetes was confirmed but before evidence of nephropathy, did not restore calcium transport to normal whether or not blood glucose was controlled. We conclude that this biochemical mechanism, which possibly may be implicated in the pathophysiology of diabetic nephropathy, is clearly influenced by duration of insulin deficiency and not by the degree in hyperglycemia.
Diabetes 1979 Dec
PMID:Effectiveness of insulin therapy on altered renal calcium transport in diabetic rats. 51 Aug 5

The paper reports on an adolescent aged 19 1/2 years, in whom a relapse of the idiopathic nephrotic syndrome occurred after a 6 years' remission, when diabetes mellitus had become manifest about 6 months before. Histologically, minimal-changes lesions were found in the kidney at the beginning and also 2 1/2 years after manifestation of the diabetes mellitus; these lesions were of the same type as those which are characteristic for the idiopathic nephrotic syndrome in children. The renal changes in children and adolescents suffering from diabetes mellitus with simultaneous or concurrent onset of nephrotic syndrome, are discussed and contrasted with the lesions observed in adult diabetes. Attention is drawn in this paper to similarity in nature and direction of the biochemical changes of the glomerular basement membrane in the idiopathic nephrotic syndrome and in diabetic nephropathy, as a possible common pathogenetic factor for the occurrence of a marked proteinuria.
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PMID:[Idiopathic nephrotic syndrome and diabetes mellitus (author's transl)]. 56 83

A total of 157 consecutive patients with juvenile diabetes (onset before the 31st birthday), diabetic nephropathy, and impaired renal function were followed up until 1.1.1976. All the patients had been admitted to the Steno Memorial Hospital, Copenhagen, between 1934 and 1972. Independently of the patients' age at onset of diabetes, it was found that persistent proteinuria appeared after an average of 19 years, and that death ensued 5--6 years thereafter. Division of the patients into two groups, according to whether the diabetes had set in before or after 1940, showed no signs of an improved prognosis during the past few decades. Once the serum creatinine has started to rise, the prognosis is very grave. Only 50% were alive 21 months after serum creatinine levels of 2--5 mg/100 ml had been ascertained. Among patients whose serum creatinine exceeded 5 mg/100 ml, 50% succumbed in 9 months. It is concluded that renal transplantation, if it is to be done, should be instituted early.
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PMID:Prognosis for juvenile diabetics with nephropathy and failing renal function. 62 9

Antisera to rat smooth muscle actomyosin (AMY) and myosin localize in the rat glomercular mesangium. The width of mesangial staining for AMY is increased in rats diabetic for four months (p less than 0.01) and seven months (p less than 0.0005) compared with age-matched controls. Mesangial AMY staining of unilaterally nephrectomized control animals was moderately increased after seven months, whereas unilaterally nephrectomized diabetic rats had prominently increased AMY mesangial width at four months, when they were compared with intact diabetic animals (p less than 0.05). Thus, a distinctive alteration that is found in human diabetic nephropathy also occurs in experimental (streptozotocin) diabetes in the rat. Further, this alteration appears to be accelerated by the changes in nephron hemodynamics resulting from unilateral nephrectomy. While the function of mesangial AMY is unknown, it may be related to intrarenal regulation of glomerular ultrafiltration, which appears to be altered in diabetic nephropathy in man.
Diabetes 1978 Jun
PMID:The immunohistopathology of glomerular antigens. III. Increased mesangial actomyosin in experimental diabetes in the rat. 65 8

In order to evaluate a possible relation between cigarette smoking and prevalence of diabetic microangiopathy, a series of 180 consecutive patients suffering from insulin-dependent juvenile-onset diabetes mellitus with different durations of disease (60 patients each with diabetes for 10 to 19 years, 20 to 29 years, and 30 to 39 years, respectively) were examined for clinical signs of retinopathy, nephropathy, and peripheral neuropathy. The results were compared with the patients' previous and actual smoking habits. Cigarette smoking was defined as daily smoking of at least ten cigarettes for one year or more. Smoking habits of the total diabetic sample were not significantly different from those of a nondiabetic control sample. However, a decline in the number of cigarette smokers and a rising number of ex-smokers were noted with increasing duration of diabetes. In comparing smokers and nonsmokers, no difference was found in the prevalence of peripheral neuropathy, background retinopathy, and proliferative retinopathy. However, the prevalence of nephropathy (persistent proteinuria) was significantly higher (p less than 0.05) among these patients who were or had been cigarette smokers. Thus, cigarette smoking might be considered a risk factor for the development of diabetic nephropathy.
Diabetes Care
PMID:Cigarette smoking and prevalence of microangiopathy in juvenile-onset insulin-dependent diabetes mellitus. 72 38

Thirty-two patients with advanced chronic renal insufficiency due to juvenile onset diabetes mellitus were submitted to dialytic treatment, 16 with intermittent haemodialysis and 16 with peritoneal dialysis. Both groups were similar with respect to onset of diabetes, course of renal insufficiency, as well as start and duration of dialysis treatment (382 and 389 patient months respectively). Patients on haemodialysis showed a more rapid progress of retinopathy and neuropathy, whereas the control of hypertension proved to be more difficult with peritoneal dialysis. A reduced peritoneal dialysance of urea, demonstrated in patients with diabetic nephropathy, could be improved by dipyridamole administration, whereas this drug showed no effect on the dialysances of urea and inulin in patients with chronic renal insufficiency of non-diabetic origin. There were no differences between the survival rates of the two groups which were substantially lower than in non-diabetic dialysis patients.
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PMID:Haemo- and peritoneal dialysis treatment of patients with diabetic nephropathy--a comparative study. 74 Jun 64

This study documents the presence of marked immunofluorescence for IgG and albumin in renal extracellular membranes, especially tubular basement membranes (TBM), of patients with severe diabetic nephropathy. A comprehensive immunofluorescent analysis was carried out on kidney tissue from 83 patients--Group I: 24 living normal renal allograft donors and two infants less than one week of age. Group II: 24 patients with severe nephropathy who had juvenile onset of diabetes 16 to 30 years previously and who ranged in age from 20 to 47 years. Group III: 33 patients with severe kidney disease of varied etiologies with an age range of five to 63 years. The sections were assayed for a variety of proteins (immunoglobulins, complement components, and tissue antigens). Kidney sections of all patients with severe diabetic nephropathy were readily distinguished from kidneys of other patients and normals by the intense linear staining of the extracellular membranes, especially the tubular basement membrane for IgG and and albumin. Dual-labeled studies using FITC anti-basement membrane (BM) and tetramethyl rhodamine (TMR) antialbumin demonstrated localization of the albumin predominantly to the outer but also the inner TBM while the BM antisera reacted more intensely with the inner membrane. There is no evidence that an immunologic process is responsible for these findings. These immunofluorescent findings are specific for severe diabetic nephropathy and may reflect structural changes in the renal extracellular membranes that permit entrapment of serum proteins, possibly due to changes in permeability.
Diabetes 1976 Aug
PMID:Immunopathology of renal extracellular membranes in diabetes mellitus. Specificity of tubular basement-membrane immunofluorescence. 78 82

Kidneys of patients with severe diabetic nephropathy demonstrate marked linear immunofluorescent staining of extracellular membranes, including the tubular and glomerular basement membranes (TBM and GBM) and Bowman's capsule. Immunofluorescent studies were carried out on kidney tissue obtained from 12 diabetic and 17 nondiabetic patients from two to 12 years following renal transplantation. The frequency and intensity of SgG and albumin staining of these membranes were significantly greater in the diabetic than in the nondiabetic patients (P less than 0.0005). TBM, GBM, and Bowman's capsule staining did not occur in any of the seven kidneys studies at the time of their transplantation into diabetic recipients. Thus, the abnormalities leading to the deposition or trapping of proteins in renal extracellular membranes occur early after the placement of normal kidneys into the abnormal metabolic environment of the diabetic transplant recipient. The present study supports the concept that basement membrane alterations in diabetes are a consequence of the biochemical perturbations of diabetes rather than a separately inherited genetically linked disorder.
Diabetes 1976 Aug
PMID:Immunopathology of renal extracellular membranes in kidneys transplanted into patients with diabetes mellitus. 78 83


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