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

This review concerns the present state of accomplishments in the study of SEM of human and experimental renal disease. Critical techniques of specimen preparation reviewed include perfusion fixation, razor tissue sectioning, alcohol cryofracture, microtome sectioning of paraffin or styrene embedded tissue, ultraplaning with glass knives of hard carbowax embedded tissues and glomerular isolation. Gold-palladium coating and heavy metal impregnation with osmium, uranium, and silver are discussed. A compendium of SEM observations of human glomerular, vascular and tubular disease is presented. Techniques for SEM of experimental renal disease are reviewed. These include latex vascular injection, freeze drying, x-ray microanalysis and use of backscattered electron imaging. Experimental models previously investigated by SEM are puromycin aminonucleoside nephrosis, daunomycin nephrosis, and N,N1-Diacetylbenzedine glomerulopathy, nephrotoxic serum nephritis, and protamine perfusion glomerulopathy. Reviewed are acute tubular necrosis caused either by angiotensin, hypotension, norepinephrine, glycerol, mercury, and unilateral renal artery occlusion, also potassium depletion nephropathy, alloxan diabetes and diphenylamine-induced polycystic disease.
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PMID:SEM of human and experimental renal disease. 52 33

Cultured skin fibroblasts from clinically normal offspring of two parents with non-insulin-dependent diabetes have demonstrated premature senescence as a decreased ability of cells to establish colonies when inoculated at low density (plating efficiency). The present study tested the hypothesis that there is an inherent cellular defect affecting viability of diabetic cells in insulin-dependent diabetes. Four insulin-dependent patients, aged 12 to 19 years, included two with joint contracture, skin changes, and growth failure; one with thyroiditis and past history of nephrosis; and one with a family history of insulin dependency. Ten control subjects, aged 10 to 52 years, had negative family histories and normal oral glucose tolerance tests. Number of cells per confluent dish correlated significantly with donor age (p less than 0.001) at 30 and 40 in-vitro generations. The patients' cells' mean confluent density did not differ from that of five age-matched controls. Plating efficiency correlated with donor age at 30 in-vitro generations ( p less than 0.001); plating efficiency of cells from the youngsters with diabetes was virtually identical to that of control cells at 20, 30, and 40 generations. In this small series of two subjects with in-vivo growth failure, one with associated autoimmune disease and another with familial insulin-dependent disease, cultured fibroblasts demonstrated normal viability and the hypothesis of a cellular growth defect was not confirmed.
Diabetes 1978 Mar
PMID:Insulin-dependent childhood diabetes. Normal viability of cultured fibroblasts. 64 Feb 40

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

We describe a method for determining those urinary total phenolic compounds that are tyrosine analogs or metabolites, such as thyroxine and catecholamines. The urine sample, 4-aminoantipyrine in carbonate-bicarbonate buffer, and potassium ferricyanide solution are mixed and the quinoneimine dye that forms is measured at 500 nm. Some cases of hyperthyroidism, diabetes mellitus, nephrosis, obesity, hypertension, or catecholamine-producing tumor showed above-normal values, so that this determination seems useful as a screening test for these disorders.
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PMID:Determination of urinary total phenolic compounds with use of 4-aminoantipyrine: suggested screening test for hyperthyroidism and for catecholamine-producing tumor. 91 84

The exact role of serum pseudocholinesterase (PSCE) is not known. Its main role probably consists in the degradation of butyril-choline, an intermediate of lipid metabolism. Decreased values have been described in liver cirrhosis as an index of diminished proteosynthetic function. An increased activity of this enzyme was reported in obesity, diabetes mellitus, nephrosis, hyperthyroidism and in hyperlipemic subjects without obesity. A significant correlation was found between serum cholesterol, triglycerides and PSCE, as an expression of lipid metabolism. In view of assessing the possible change of this enzyme during fattening, the authors investigated PSCE activity during fattening in pigs (the same breed). The results indicate a statistically significant increase of PSCE during fattening, from 30.4 +/- 1.7 to 43.6 +/- 1.7 (p less than 0.001). These results together with those reported in a previous paper concerning blood lipids and cholesterol, show a positive correlation between these parameters and PSCE during fattening in pigs, which might be due to an adaptative increase of the hepatic synthesis of this enzyme in response to the increased lipid metabolism.
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PMID:Serum pseudocholinesterase activity during experimental fattening. 94 98

A total of 291 urine sediments from 255 patients with various renal or urinary tract diseases have been studied by phase contrast microscopy. Based upon morphological criteria, leucocytes were distinguished from renal epithelial cells and the white blood cells were classified either as mononuclear or polynuclear in 179 patients. The percentage of the different cell types varied considerably between and within the different diseases. The median values for polynuclear granulocytes were higher than 90% in bacterial renal or urinary tract disease and in polycystic kidney disease. In interstitial nephritis, nephrosclerosis and in renal transplanted patients the percentage of polynuclear granulocytes was somewhat lower, 76-85%. In diabetes, amyloidosis, tubular nephrosis (necrosis) glomerulonephritis, lupus nephritis and endemic benign nephropathy there were 14-66% polynuclear granulocytes. 29-33% mononuclear leucocytes were found in lupus nephritis and endemic benign nephropathy. The greatest proportion of renal epithelial cells was found in endemic benign nephropathy, namely 49%. 36% renal epithelial cells were found in tubular nephrosis (necrosis) and in glomerulonephritis. The technique is rapid and inexpensive. It facilitates differential diagnostics of urinary tract disease with pyuria.
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PMID:Differential count of urinary leucocytes and renal epithelial cells by phase contrast microscopy. 110 1

Chronic renal insufficiency is a progressive, self-perpetuating process which is influenced in part by activation of the intrarenal renin-angiotensin system. Oral angiotensin-converting enzyme inhibitors are being studied in animals and humans to determine whether they slow the decline in renal function characteristic of progressive renal disease. In animals that have reduced renal mass, streptozotocin-induced diabetes mellitus, or puromycin aminonucleoside nephrosis, these agents can reduce proteinuria, decrease the frequency of sclerotic glomeruli, and normalize intrarenal hemodynamics. They also may decrease glomerular hypertrophy that occurs after renal ablation. In human trials, angiotensin-converting enzyme inhibitors decrease proteinuria by altering the glomerular capillary permeability. The effect of these agents on progressive disease may be influenced by how soon therapy is begun and how long it is continued.
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PMID:Use of angiotensin-converting enzyme inhibitors in chronic progressive renal disease. 202 23

Angiotensin (Ang) II and prostaglandins, especially prostaglandins E2 and I2, regulate the glomerular filtration of albumin. Albuminuria can be induced by angiotensin II and possibly by prostaglandins. Angiotensin converting enzyme inhibition with captopril, enalapril or lisinopril reduces albuminuria and glomerular injury in experimental and clinical renal diseases, especially diabetes mellitus. Inhibition of prostaglandin synthesis with non-steroidal anti-inflammatory drugs reduces albuminuria in nephrotic patients regardless of the aetiology of the nephrosis. Judicious clinical use of either class of therapy can result in sustained reductions (50-75%) in proteinuria and possible attenuation of the rate of decline of glomerular function.
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PMID:The roles of angiotensin II and prostaglandins in the regulation of the glomerular filtration of albumin. 218 53

Captopril decreases protein excretion in patients with nephrosis. To evaluate whether captopril has an acute antiproteinuric effect and to evaluate the role of changes in renal hemodynamics or glomerular permselectivity on this effect, renal clearance studies were performed in patients without diabetes but with nephrosis. Protein excretion and renal hemodynamics were measured at baseline and after the administration of captopril. To measure the contribution of renal prostaglandins, patients were restudied on a separate day, after the combined administration of captopril and the prostaglandin synthetase inhibitor ibuprofen. Both treatments significantly reduced mean protein excretion, but the change was greater with combined therapy than with captopril alone (40.6% vs 20.0%). Mean glomerular filtration rate (GFR) decreased by 4.8% (not significant) and 16.5% (p less than 0.001), and filtration fraction (FF) decreased by 13.6% (p less than 0.001) and 14.9% (p less than 0.001) after captopril alone and combined therapy, respectively. No significant correlation was found between changes in proteinuria and changes in GFR or FF after treatment with captopril alone. In contrast, the decrease in proteinuria correlated with the change in GFR after combined drug administration (r = 0.68, p = 0.06). The ratio of immunoglobulin G to albumin clearance, an index of glomerular permselectivity, was unaffected by captopril but decreased significantly (by 43%) after combined drug administration. The results suggest that the acute antiproteinuric effect of captopril is not due to changes in FF, GFR, or glomerular perselectivity. The addition of ibuprofen enhances the antiproteinuric effect of captopril by decreasing the GFR as well as by enhancing the permselectivity of the glomerular capillary membrane.
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PMID:Acute effects of captopril and ibuprofen on proteinuria in patients with nephrosis. 221 55

The paper reports on the present knowledge in the diabetic nephrosis (DN) with emphasis on three problems: evolution by stages, possibility of detecting the diabetics with high risk of developing clinic DN, and the prophylactic and therapeutic measures required for a resting or, at least, for slowing down the evolution of this complication. The functional changes, manifested mainly by increasing the glomerular filtration, are detected in many insulin-dependent diabetics even from the diagnosis of the disease and they are predictive elements for the clinic DN; that is the reason why they must be reduced by a correct and prolonged control. Microalbuminuria, defined as a urinary excretion of albumin of less than 250 mg/24 hours (18-74 micrograms/minute) is another characteristic of the precocious stages of the DN. Exceeding the above-mentioned values means the transition to the clinic DN, that subsequently progresses in all cases. The paper also describes the characteristics of the clinic DN and the therapeutic ways both in the incipient and clinic DN, with emphasis on their features in the diabetes mellitus and its complications.
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PMID:[Diabetic nephropathy. I]. 257 30


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