Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma factors influencing PGI2-like activity in 19 patients with diabetes mellitus /Dm/ and 17 controls were studied through a comparison with the signs of retinal and glomerular angiopathy. The plasma PGI2 supporting activity /PSA/ was lower in 15 Dm cases than in the controls. Inhibitory activity against PGI2 production was detected in 6 patients. In the cases of more serious retinopathy associated with glomerulopathy, a significantly lower level of PSA was observed than in patients with mild retinopathy without glomerular diseases. The plasma concentrations of total and LDL-cholesterol were significantly higher, while the level of HDL-cholesterol was lower than in the controls. There was a positive correlation between PSA and HDL-cholesterol values and a negative correlation between PSA and LDL-cholesterol levels, which relates to an inhibitory effect of LDL and a protective role of HDL in PGI2 synthesis.
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PMID:Plasma factors influencing prostacyclin-like activity in patients with diabetic microangiopathy. 328 94

We quantitated glomerular structure by light microscopy in 19 subjects with non-insulin-dependent diabetes mellitus (NIDDM) and studied the possible connection between morphology and urinary albumin concentration. Autopsy material was collected retrospectively from diabetic subjects in whom urinary albumin concentration had been measured within 1.5 yr. Nineteen consecutive sex- and age-matched nondiabetic subjects were controls. A quantitative study of a random sample of glomeruli was performed blindly on periodic acid-Schiff (PAS)-stained sections. The main parameters obtained were 1) mean volume of open glomeruli, 2) frequency of glomerular occlusion, and 3) volume fraction of red-stained material (PAS-positive substance) in open glomeruli [Vv(R/G)]. There was no increase in glomerular volume in these NIDDM subjects, contrary to the glomerular hypertrophy found early as well as late in insulin-dependent diabetes mellitus. An increase in Vv(R/G) was found in diabetic subjects, demonstrating the presence of glomerulopathy as it is diagnosed by light microscopy. The frequency of glomerular occlusion was not significantly different between the groups. A high urinary albumin concentration did not necessarily reflect more advanced glomerulopathy.
Diabetes 1988 Jan
PMID:Glomerular morphology by light microscopy in non-insulin-dependent diabetes mellitus. Lack of glomerular hypertrophy. 333 76

Differential macromolecule clearances were used to elucidate the mechanism of proteinuria in patients with diabetic glomerulopathy. Uncharged dextrans of graded size, combined with albumin and IgG separated into narrow fractions of varying charge by preparative electrofocusing, were used to probe the filtration barrier. Analysis of the fractional clearance profile of dextrans in the 30- to 60-A interval revealed a small fraction of filtrate volume (0.0023-0.0097) permeating large nonrestrictive glomerular pores and correlating strongly with the fractional clearances of albumin (r = .88, P less than .001) or IgG (r = .91, P less than .001). The fractional clearance of the most anionic species of albumin [isoelectric point (pI) 4.0-4.5] significantly exceeded that of less anionic species (pI 4.5-5.5) at all levels of proteinuria. A corresponding increase in fractional clearance of anionic (pI 4.5-5.0) over neutral (pI 7.0-7.5) IgG species was observed in patients with subnephrotic-range proteinuria. We conclude that a loss of barrier size selectivity underlies proteinuria in diabetic glomerulopathy. In addition, either facilitated filtration of polyanions or preferential tubular reabsorption of polycations can be invoked to explain the final composition of urinary protein. Similar loss of size selectivity combined with enhanced fractional clearance of anionic IgG in a group of nondiabetic patients with nephrotic syndrome indicates that the foregoing abnormality of renal protein handling is not unique to diabetic glomerulopathy.
Diabetes 1988 Sep
PMID:Charge selectivity of proteinuria in diabetic glomerulopathy. 341 Jan 64

Diabetic glomerulopathy is characterized by a very slow development of basement membrane (BM) accumulation, manifested as thickening of the peripheral BM and increased volume of the mesangial BM-like material (BMLM) with mesangial expansion. The initiation of the process is probably at the onset of diabetes since the BM thickening is detectable after a few years. The BM accumulations at the two sites (PBM and BMLM) in the glomerular tuft are considered as two different expressions of a fundamental BM abnormality. The two locations present different conditions for quantitation, may have a different biochemical make-up, and immediate functional implications of the abnormalities may differ as well. In the long run, however, the two in concert lead to the ultimate solidification of the glomerular tuft with loss of capillary surface. The end-stage is glomerular closure, with elimination of glomerular function. A very close correlation has been found between the total remnant surface area of the glomerular capillaries and the level of GFR. Along with the classical changes of the diabetic glomerulopathy, changes in glomerular size are detectable. In early diabetes during the stages of glomerular hyperfunction, hypertrophy develops acutely at the onset of diabetes, leading to an increase in capillary surface corresponding to the increase in filtration rate. In the advanced stages when glomerular closure involves a proportion of the nephrons compensatory hypertrophy develops, thereby probably helping to preserve capillary surface for a period of time. The exact mechanisms that may influence these developments are not known, but underlying them all are the metabolic abnormalities of diabetes.
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PMID:Structural changes in the diabetic kidney. 353 98

The spontaneously diabetic BioBreeding/Worcester (BB/W) rat was used to examine the role of glycemic control in the pathogenesis of diabetic glomerulopathy and proteinuria. Nondiabetic BB/W rats (group 1) were compared with moderately (group 2) and severely (group 3) hyperglycemic diabetic animals of similar age. Urinary protein excretion and morphometric measurements of glomerular basement membrane (GBM) width and mesangial area were performed after 4, 8, and 12 mo of study. At 4 mo, urinary protein excretion both in group 2 (9.3 +/- 0.7 mg/24 h) and group 3 (24.8 +/- 1.98 mg/24 h) exceeded that in group 1 (5.4 +/- 0.6 mg/24 h; P less than .05). Moreover, proteinuria in group 3 was significantly greater than in group 2 (P less than .05). In addition, proteinuria increased in group 3 animals between 4 and 12 mo of study but did not advance in groups 1 or 2. GBM width in both diabetic groups (168.8 +/- 2.4 and 165.7 +/- 2.2 nm, groups 2 and 3, respectively) exceeded that in group 1 (148.3 +/- 3.8 nm; P less than .01) by 4 mo. At 12 mo, severely hyperglycemic group 3 animals had significantly greater GBM thickening than group 2. GBM width increased in all three groups over the course of study, but the rate of growth did not differ between groups 1 and 2. However, the rate of growth in group 3 was greater than in either group 1 or group 2. Urinary protein excretion correlated significantly with GBM width in diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1987 Aug
PMID:Glomerulopathy in spontaneously diabetic rat. Impact of glycemic control. 359 62

The kidney as a target organ for secondary microvascular complications of diabetes mellitus represents a major problem. The pathology of diabetic glomerulopathy is well known. The coexistence of immunocomplex-mediated glomerulonephritis and diabetes mellitus has rarely been reported. The presence of crescents in glomerular disease of diabetes mellitus has been usually ignored in the literature. The present study describes one patient with epithelial crescentic diabetic glomerulopathy with rapidly progressive renal failure.
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PMID:Epithelial crescent in diabetic glomeruli. A case report. 366 43

Loss of renal mass in rats with experimental diabetes mellitus leads to exaggerated hypertrophy of remaining nephrons and accelerated diabetic glomerulopathy. To examine factors responsible for glomerular injury in this setting, rats with preexisting diabetes were subjected to unilateral nephrectomy. Micropuncture studies and evaluation of glomerular morphology were performed 2-3 mo later. Nephrectomized diabetic rats demonstrated significant increases in kidney weight, superficial nephron glomerular filtration rate, and superficial nephron plasma flow compared with two-kidney diabetic rats and nephrectomized nondiabetic controls. Glomerular capillary hydraulic pressure was comparable in two-kidney and nephrectomized diabetic rats and was significantly reduced compared with nephrectomized nondiabetic controls. Nephrectomized diabetic rats demonstrated significant albuminuria, mesangial matrix expansion, and focal glomerulosclerosis, whereas two-kidney diabetic rats and nephrectomized nondiabetic controls showed only minimal alterations in glomerular morphology. It is concluded that diabetic rats can undergo glomerular functional compensation in response to nephron loss. Moreover, accelerated glomerular injury caused by nephron loss in diabetic rats could not be attributed to increased glomerular capillary pressure.
Diabetes 1986 Sep
PMID:Effects of nephron loss on glomerular hemodynamics and morphology in diabetic rats. 374 5

Six groups of Munich-Wistar rats underwent micropuncture study 2-10 weeks and morphologic studies 11-13 months after induction of streptozotocin diabetes or after sham treatment. Diabetic rats received diets containing 6% (group D6), 12% (D12), or 50% protein (D50) and were maintained under similar conditions of moderate hyperglycemia by daily injections of ultralente insulin. Age- and weight-matched normal control rats were also given 6% (Group N6), 12% (N12), or 50% protein (N50). Kidney weight, whole-kidney and single-nephron glomerular filtration rate, glomerular plasma flow, and mean glomerular transcapillary hydraulic pressure difference were higher in D50 rats than in all other groups and predisposed this group to marked and progressive albuminuria. Likewise, histological examination of the kidneys disclosed areas of sclerosis in 19.6% of glomeruli in D50 rats; the frequency of such lesions was less than 2.5% in all other groups. These findings indicate that the metabolic disorder seen in stable, moderately hyperglycemic diabetic rats does not lead to glomerulopathy as long as elevations in glomerular pressures and flows are prevented.
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PMID:Predominance of hemodynamic rather than metabolic factors in the pathogenesis of diabetic glomerulopathy. 386 10

To evaluate the role of glomerular hyperfiltration in the development and progression of diabetic nephropathy, we performed clearance and histopathologic studies in 24 rats with streptozocin-induced diabetes after 3 months of diets with different protein compositions. Calcium phosphate was added to an 8% protein diet in group I (nine rats), and calcium carbonate to a 24% protein diet in group II (nine rats) to equalize calcium and phosphate contents in these diets. Group I and II rats also received small doses of insulin to reduce the excessive hyperglycemia induced by the high sucrose content of the diets. In group III, six rats given an 8% protein diet, no calcium, phosphate, or insulin was added. In groups I and III, low dietary protein significantly reduced glomerular filtration rate and renal plasma flow per gram of kidney weight as compared with rates observed in group II rats with a higher protein intake. Features of diabetic glomerulopathy including mesangial hypercellularity and mesangial matrix expansion were also significantly milder in the groups with a low protein diet. On the other hand, medullary calcification and interstitial changes were most prominent in group I, given calcium phosphate supplement; the increase in the kidney weight was greater in groups I and II, which received insulin, than in group III, which did not. It was concluded that low protein diet significantly ameliorates diabetic glomerulopathy but that supplementation with inorganic phosphate in an amount equal to organic phosphate contained in the higher protein diet causes medullary calcification and interstitial nephritis. Also, administration of suboptimal doses of insulin in diabetic animals greatly enhances renal growth, more than that induced by diabetes alone.
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PMID:Effects of low-protein diet on experimental diabetic nephropathy in the rat. 390 11

The diagnosis of light chain deposition nephropathy is based on the immunohistochemical demonstration of monoclonal light chain deposits within connective tissue matrix and on the presence at the ultrastructural level of electron-dense granular deposits along glomerular and tubular basement membranes. A nodular glomerulopathy characterized by amorphous periodic acid-Schiff-positive and argyrophilic widened mesangium and nodules is described in three patients with light chain deposition nephropathy. Light microscopic examination did not allow discrimination between the glomerular changes found in these specimens and the nodular glomerulosclerosis described in four patients with well-documented diabetes mellitus. Electron microscopic examination revealed microtubular fibrils 10 to 12 nm thick in mesangial areas in both groups. Such microfibrils could be glycoproteins. Immunofluorescence localization of matrix proteins, by staining with affinity-purified antibodies to types I, III, IV, and V (A, B) collagens, fibronectin, laminin, and heparan sulfate-containing proteoglycans, showed similar distributions in the two conditions. The mechanism of this abnormal accumulation of mesangial and glomerular basement membrane matrix proteins in two different conditions remains unknown.
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PMID:Glomerular matrix proteins in nodular glomerulosclerosis in association with light chain deposition disease and diabetes mellitus. 392 52


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