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

This report considers the pathophysiologic significance of capillary basement-membrane thickening in diabetic nephropathy and retinopathy and the relationship of capillary basement-membrane thickening to increased susceptibility to infections and to increased vascular permeability in diabetes. The evidence available (1) indicates that basement-membrane thickening affects most if not all capillaries of the diabetic and may contribute to increased susceptibility to infection and (2) suggests that increased capillary permeability in diabetes need not be attributed to basement-membrane changes per se, but rather may be due to changes in the cellular elements of the capillary wall.
Diabetes 1976
PMID:Basement-membrane thickening and diabetic microangiopathy. 78 63

From 1969 to 1974 on 38 diabetic patients with terminal renal insufficiency 1,500 haemodialyses were carried out. Out of them 21 were or are in the prolonged programme of dialysis. The average duration of diabetes up to the terminal renal insufficiency was 20 years. The survival time under dialysis between 50 to 616 days was on the average nearly 248 days. The waste of substances normally contained in the urine and the normalisation of changes of minerals under dialysis is to be compared with that one in non-diabetics. The conduction of the diabetic metabolism in advanced diabetic nephropathy is independent on the form of therapy chosen difficult and undergoes strong variations. For this practical recommendations are given. Dependent on the beginning of the dialysis in 8 cases we succeeded in a temporarily limited full rehabilitation, 5 patients were partially rehabilitated and in 8 patients the general condition could be improved by the treatment without successful rehabilitation. The main complications, which were also dominating causes of death, were seen from the side of the system of coronary circulation. Mediascleroses of the arterial walls partly of a high degree allow the supposition that in these cases additionally a secondary hyperparathyroidism was in question.
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PMID:[Immunological studies on the pancreas]. 81 74

The term diabetic nephropathy includes the Kimmelstiel-Wilson intercapillary glumerulosclerosis (1936), arterio-arteriolosclerotic changes and pyelonephritis. In principle, diabetic nephropathy becomes more frequent with increasing duration of diabetes mellituus. Pyelonephritis is 4 to 5 times more frequent in diabetics than in the general population. Elderly overweight women are particularly at risk. - Only the nodular intercapillary glomerulosclerosis and not the diffuse or exudative form is specific for diabetes mellitus. It is found in 20-40% of all diabetics who have had the disease for 10-15 years. Whether the microangiopathy is typical of diabetes mellitus remains to be seen. Due to the intense cardiovascular changes, possible disorders of brain and liver function and infection, the prognosis of renal insufficiency is considerably worse in diabetics than in non-diabetics.
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PMID:[Diabetic nephropathy (author's transl)]. 81 41

Animal models of diabetes mellitus allow for the manipulation of the metabolic state and the performance of experiments that may shed light on the pathogenesis of diabetic nephropathy. Rats with long-standing chemically induced diabetes develop glomerular mesangial thickening and immunoglobulin and complement deposition. These glomerular changes are reversible on the transplantation of a kidney from a diabetic rat into a normal host and on cure of the diabetic state by pancreatic islet transplantation. Conversely, diabetic renal changes develop in normal kidneys transplanted into diabetic rats (within tow to four months) and humans (within two years). These studies suggest that nephropathy results from the diabetic state. The mesangium is thickened in diabetic rats, mice, and humans. In rats, mesangial function is the processing of macromolecules localized therein is disturbed in areas of mesangial pathology. The finding that glomerulopathy is accelerated in uninephrectomized diabetic rats and is retarded in rat kidneys "protected" by narrowing of the renal artery suggests that alterations in glomerular blood flow are related to the pathogenesis of diabetic glomerular damage. Marked hyperglycemia in animals and man leads to "glycogen nephrosis," which affects the distal tubule at the level of the macula densa of the juxtaglomerular apparatus (JGA). This could lead to disturbance of JGA blood pressure regulation. Disturned mesangial function may result from failure of macula densa cells to process macromolecules that have reached that site from the mesangium.
Diabetes 1976
PMID:Studies of diabetic nephropathy in animals and man. 82 65

A case of acute renal failure after cerebral arteriography with iodinated contrast material in a patient with diabetes and azotemic nephropathy is described. A review of the literature concerning acute renal failure after radiographic contrast material is included. The main risk factors reported in the literature appear to be the presence of diabetic nephropathy and the administration of fairly large doses of iodinated contrast material. Azotemic patients should be kept well hydrated and receive doses of less than 50 cc/m2 of body surface area when studied with such materials. Careful monitoring of urinary output and serum creatinine and ready access to dialytic therapy will aid in the detection and subsequent treatment of this problem.
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PMID:Acute renal failure after cerebral arteriography in a diabetic patient. 84 45

Diabetes mellitus is a systemic disorder that affects many organs in the body. Diabetic nephropathy occurs a number of years after the onset of the disease, and it is usually manifested by the development of the nephrotic syndrome. However, the sudden onset of massive proteinuria or the rapid deterioration of renal function in the stable diabetic patient should suggest that an additional pathologic condition is affecting the kidneys. We report three cases of diabetic nephropathy complicated by other superimposed renal diseases.
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PMID:Acute glomerulonephritis complicating diabetic nephropathy. 86 44

Only from the kidney glomerulus can the capillary basement membrane be isolated in quantities sufficient for biochemical analyses. In this study an attempt has been made to obtain a basement membrane as pure as possible, without contamination from cells or mesangium. In diabetic nephropathy, the glomerular basement membrane shows a decreased content of cystine, but hydroxylysine concentrations was only slightly higher than in normal material. The concentration of glucose was significantly increased. Immunofluorescent studies indicated the presence of serum proteins in the diabetic glomerular basement membrane, probably as a result of increased membrane permeability.
Diabetes 1976
PMID:Biochemical alterations of the human glomerular basement membrane in diabetes. 97 95

Plasma renin activity (PRA) was determined in 48 patients with diabetes mellitus in sodium balance on a 10-20 mEq. Na diet. Nine were normotensive (group I), 11 11 were hypertensive without diabetic nephropathy (group III). Results were compared with those in 16 normal subjects and 49 nondiabetic patients with essential hypertension in similar Na balance. Mean supine PRA did not differ significantly among groups I and II, normal subjects, and patients with essential hypertension. Group III diabetics had a supine PRA of 2.4 +/- 0.4 ng./ml./hr. (x +/- S.E.M.), significantly lower than the other diabetic groups (P less than 0.005) and normal subjects (P less than 0.05). Upright PRA was 12.8 +/- 2.2 in group I diabetics, similar to that in normal subjects (13.3 +/- 2.3), and 8.1 +/- 1.4 in group II diabetics, similar to that in essential hypertensives (6.8 +/- 0.8). In group III diabetics, upright PRA was 4.0 +/- 0.5, significantly lower than that in any other group. These results suggest that (1) PRA is normal in normotensive diabetics, (2) upright PRA in diabetics with hypertension but no nephropathy is similar to that in essential hypertension, and (3) patients with diabetes, hypertension, and nephropathy have "low renin hypertension," explaining the virtual absence of malignant hypertension in this group. Although the major mechanism for this low PRA may be volume expansion, indicating the need for potent diuretics, other mechanisms include hyalinization of the afferent arteriole, decreased cathecholamine stimulation of renin release, and inadequate conversion of prorenin to renin.
Diabetes 1976 Oct
PMID:Plasma renin activity and hypertension in diabetes mellitus. 97 6

The pathophysiology of the microangiopathy of diabetes mellitus is poorly understood, and the relevance of carbohydrate intolerance remains uncertain. Four patients are presented with renal abnormalities suggestive of diffuse diabetic glomeruloscierosis. These patients have no evidence of carbohydrate intolerance by standard clinical technics. A familial incidence of diabetes mellitus and delayed insulin response to an oral glucose load support a classification of prediabetes or suspected diabetes mellitus for these patients. Early intercapillary nodule formation was seen in only two of the four patients. In the absence of this infrequent pathognomonic finding, an alternate approach to the diagnosis of diabetic glomerulosclerosis is suggested. Diffuse glomerular capillary basement membrane thickening, consistently present with diabetic glomerulosclerosis, is demonstrated by measurements utilizing the latex microsphere technic. The mean glomerular capillary basement membrane thickness of these patients was 4,403 A, compared with the control value of 3.098 A (P less than 0.001). Other pathologic findings suggestive of diabetic nephropathy include efferent arteriolosclerosis and linear immunofluorescence without electron dense deposits or inflammation. Skeletal muscle capillary basement membranes of all four patients also demonstrated significant thickening. The mean value for the patients was 1,510 A, as compared with a control value of 961 A (P less than 0.001). The importance of this muscle capillary basement membrane thickening to the diagnosis of diabetic microangiopathy is discussed. The pathologic alterations in the renal biopsy specimens and the demonstration of muscle capillary basement membrane thickening strongly suggest that diabetic glomerulosclerosis may occur in the absence of overt clinical carbohydrate intolerance.
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PMID:Diabetic glomerulosclerosis without glucose intolerance. 115 78

Proteinuria has been analysed in 334 maturity-onset diabetics and 80 matched controls. Proteinuria measured in the recumbent position exceeded 100 mug/min in 53% of the diabetic population. The percentage of excessive proteinuria increased with duration of the disease. Sex and age had no influence. Out of 55 first year diabetics, 49% had abnormal quantitative proteinuria; this is in contrast to 76 longterm diabetics (over 12 years) of whom 38% had proteinuria under 100 mug/min. Electrophoresis and immuno-electrophoresis showed a glomerular pattern in 40%, a tubular pattern in 15% and a mixed pattern in 8% of all the diabetics. 32% of the diabetics with quantitatively normal proteinuria were abnormal qualitatively, and this may be the first manifestation of diabetic nephropathy. Thirty-eight other patients had a normal electrophoretic pattern in spite of increased proteinuria. Proteinuria levels were significantly associated with hematuria, bacteriuria and reduced GFR, but not with leukocyturia, insulin dependence and hypertension. Upright position increased the proteinuria to a greater degree amongst the patients with normal proteinuria. We discuss the role of increased filtration pressure and glomerular permeability in modifying proteinuria in diabetes. Sensitive quantitative and qualitative proteinuria determinations are important tools both in early diagnosis of diabetic nephropathy in clinical practice and in epidemiological studies.
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PMID:[Proteinuria in mature diabetic patients. Quantitative and qualitative analysis]. 121 95


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