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

Glomerular hyperplasia and thickening of the glomerular basement membrane increase with age in humans and animals. This glomerulopathy can be enhanced by hyperglycemic conditions such as diabetes mellitus. When diabetic guinea pigs were examined by fluorescent microscopy, deposits of a substance similar to immunoglobulin G (IgG) were seen. Comparison with nondiabetic age-matched control animals suggest that glomerulopathy is related to aging, and can be further enhanced by hyperglycemia.
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PMID:Glomerular basement membrane changes in aging nondiabetic and diabetic guinea pigs. 702 53

Two patients with long-standing diabetes mellitus and diabetic retinopathy were evaluated for declining renal function and heavy albuminuria. Initially, diabetic glomerulosclerosis was suspected as the cause of progressive glomerulopathy. However, in both patients the rate of loss of glomerular filtration rate was greater than that usually seen in diabetic glomerulosclerosis, and the urine sediment contained many RBC casts. These findings led to renal biopsy, which demonstrated crescentic glomerulonephritis superimposed on diabetic glomerulopathy. Both patients were treated with prednisone and cyclophosphamide and both experienced substantial improvement in renal function. These experiences demonstrate the importance of searching for evidence of a superimposed treatable glomerulopathy in the diabetic patient with glomerulopathy and advancing renal insufficiency.
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PMID:Rapidly progressive glomerulonephritis superimposed on diabetic glomerulosclerosis. Recognition and treatment. 705 37

Thirteen children with abnormal mitochondria in muscle tissue, and a progressive neurological disorder that affected the cerebrum, cerebellum, extrapyramidal system, vestibular system, retina, upper motor neuron, lower motor neuron, and musculature, are reported. Other signs and symptoms were short stature, diabetes mellitus, cardiopathy, hypoplastic anaemia, glomerulopathy, and renal tubular dysfunction. These symptoms may occur singly or in various combinations and the manifestation may differ even within the same family. The most common clinical picture was that of "ophthalmoplegia plus'. Occurrence in relatives varied from isolated symptoms to the complete syndrome with "ragged red fibres' and is not inconsistent with an autosomal dominant mode of inheritance with variable expressivity. Theories for the pathophysiological basis of this syndrome are discussed and the literature reviewed.
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PMID:Mitochondrial cytopathy. A multisystem disorder with ragged red fibres on muscle biopsy. 730 11

Chronic uremia caused by diabetic glomerulopathy accounts for about 25 percent of new patients treated by maintenance hemodialysis. At the onset of glucose intolerance, insulin dependent diabetics have larger than normal kidneys, with a markedly increased glomerular filtration rate. During the subsequent 15 to 20 years of insulin use, glomerulosclerosis progresses silently, until a clinically overt nephrotic syndrome becomes evident. Thereafter, the clinical manifestations of nephropathy appear rapidly with an exponential decline in creatinine clearance to less than 5 ml/min within one to five years. Putting together a life plan for a nephrotic and azotemic diabetic involves awareness, and coordinated management of not only renal but extrarenal vasculopathic complications of diabetes, especially proliferative retinopathy. Carefully made preparations for hemodialysis and/or renal transplantation with increase changes for at least a short-term favorable outcome, which can now be anticipated in a growing proportion of patients.
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PMID:Uremia in diabetics: the prognosis improves. 745 92

It has recently been suggested that immunotactoid glomerulopathy be separated from much more common fibrillary glomerulonephritis by ultrastructural features of highly organized immune deposits containing tubules of more than 30 nm in diameter. We report and discuss the results of a light, immunofluorescence and electron microscopic study of a needle renal biopsy from a 75-year-old, non-insulin dependant diabetic female presented with nephrotic syndrome, hypertension and a progressive renal failure. A unique coexistence of nodular glomerulosclerosis, as traditionally ascribed to diabetes with a peculiar type of immunotactoid glomerulopathy was confirmed by the exclusion of amyloidosis, monoclonal gammopathies, systemic autoimmune diseases and cryoglobulinemia. Mesangial, scattered subepithelial and segmentally prominent subendothelial immune deposits were found highly organized in mostly parallel arrays of 40 to 91 nm thick tubules. The average thickness of 67 nm exceeds the average diameter of tubules in all other 11 published cases of immunotactoid glomerulopathy to date. By immunofluorescence, predominantly capillary wall, thick, ribbon-like glomerular deposits contained IgG, IgM, kappa and lambda light chains of equal intensity, C3, C4 and fibrin related antigens. Mild to moderate glomerular cell proliferation associated with nodular sclerosis has been assumed to be causally related to immunotactoid deposits.
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PMID:Immunotactoid glomerulopathy with unusually thick extracellular microtubules and nodular glomerulosclerosis in a diabetic patient. 747 81

We have previously reported that the mRNA levels of extracellular matrix (ECM) components including alpha 1(I), alpha 1(III), and alpha 1(IV) collagen chains, laminin B1 and B2 chains, and growth factors including tumor necrosis factor (TNF)-alpha, platelet-derived growth factor (PDGF)-B chain, transforming growth factor (TGF)-beta, and basic fibroblast growth factor (FGF) all increase with age in diabetic glomeruli. The present study was designed to assess whether glomerular expression of these mRNAs in rat diabetic glomeruli is affected by a specific endothelin receptor A antagonist, FR139317. Diabetes was produced by streptozotocin injection, and animals were divided into four groups: untreated diabetic rats, FR139317-treated diabetic rats, control nondiabetic rats, and FR139317-treated control rats. FR139317 treatment was continued for 24 weeks. FR139317 attenuated the rise in creatinine clearance (P < 0.01) and reduced urinary protein excretion (P < 0.01) in diabetic rats, but did not affect blood pressure. FR139317 attenuated the increases in glomerular mRNA levels of alpha 1(I) (P < 0.01), alpha 1(III) (P < 0.01), and alpha 1(IV) (P < 0.01) collagen chains, laminin B1 (P < 0.01) and B2 (P < 0.01) chains, TNF-alpha (P < 0.01), PDGF-B (P < 0.01), TGF-beta (P < 0.001) and basic FGF (P < 0.01) in diabetic rats. However, FR139317 did not affect these mRNA levels in glomeruli of control rats. These findings suggest that FR139317 may be useful in the treatment of diabetic glomerulopathy by reducing mRNA levels of ECM components and growth factors.
Diabetes 1995 Aug
PMID:Effect of a specific endothelin receptor A antagonist on mRNA levels for extracellular matrix components and growth factors in diabetic glomeruli. 762 93

Altered proteoglycan metabolism may play a role in the development of diabetic glomerulopathy. This study was conducted to examine the effects of glucose on the production and physical characteristics of proteoglycans generated by rat mesangial cells in culture. Rat mesangial cells were exposed to elevated glucose media (500 mg/dl) or standard glucose media (200 mg/dl) for 8-10 days, and proteoglycan synthesis was determined using 35S-labeling in conjunction with anion exchange and sizing chromatography. Rat mesangial cells generated predominantly chondroitin/dermatan sulfate proteoglycans, with small amounts of heparan sulfate proteoglycans. High glucose did not alter the number of rat mesangial cells after 24 h or after 8-10 days, compared with cells grown under standard glucose conditions. The total amount of glycosaminoglycan generated and the sizes of the major proteoglycans were not different between cultures grown in standard and elevated glucose medium. Levels of mRNA for the proteoglycan, biglycan (as assessed by Northern blot analysis), also were comparable between the standard and elevated glucose conditions. Exposure to media high in glucose did not change the rate of secretion of proteoglycans from the cell layer to the medium, but did result in a greater quantity of radiolabeled proteoglycan deposited in the extracellular matrix. The cell, extracellular matrix and medium proteoglycans isolated from the elevated glucose cultures, consistently eluted from the anion exchange column at a lower [NaCl] compared with those generated under standard glucose conditions, indicating a loss of anionic charges.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1993 Dec
PMID:The effect of glucose on proteoglycans produced by cultured mesangial cells. 769 80

The histopathological characteristics of the kidney using light microscopy and immunofluorescence studies in samples obtained by renal percutaneous biopsy in 19 women and 7 men with non-insulin dependent diabetes mellitus (NIDDM) (mean of age: 55.07 +/- 9.04 yr and mean of "known" diabetes duration: 7.50 +/- 6.87 yr) were studied. The relationship with age, blood pressure, diabetic retinopathy and other complementary diagnostic methods such as serum creatinine (Cr), creatinine clearance (CrC), renal plasma flow (RPF), proteinuria and filtration fraction (FF) were also determined. Light microscopy studies detected 92.3% of patients with renal lesions of different degrees of severity. The presence and severity of glomerulopathy and arteriolopathy were related to diabetes duration (r: 0.764) and they were related to each other (rs: 0.773). In 2 patients, lesions were not observed and in 11 out of 14 patients with less than 5 yr of diabetes duration, mild lesions were detected. However, the histological changes became worse after that period. The glomerulopathy was also statistically correlated with Cr, CrC, RPF, proteinuria and FF. By immunofluorescence, fibrinogen, IgA and C3 were the most frequent and intense precipitates observed. They increased with diabetes duration and were located predominantly in the wall and the periphery of the glomerules and in renal tubules, suggesting that they originated by trapping. There were no precipitates in the mesenchyma, they were scarce in the interstice, Bowman's capsule and arterioles. Statistical correlation between diabetic histopathological renal changes and retinopathy was found. These results confirm that lesions in the kidney and retina in non-insulin dependent diabetic patients generally appear and evolve in a similar manner. Hypertension was diagnosed in 80.76% of patients, without statistical correlation between blood pressure and renal lesions. This suggests that at the onset, in non-insulin dependent diabetic patients hypertension and nephro-pathy are caused by different and independent pathogenic mechanisms. However, at an end stage, it seems that both situations can influence each other in a way that their evolution becomes more severe. Nephropathy in non-insulin dependent diabetes mellitus displayed scarce clinical signs and poor laboratory evidence except when the renal lesions become too severe. The lack of correlation between renal lesions and patients' age and blood pressure suggests the participation of diabetes at the onset of kidney structural impairment.
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PMID:[Histopathological and functional study of the kidney in non-insulin dependent diabetes mellitus]. 771 26

The magnitude of type II diabetic nephropathy dilemma is observable in the growing number of diabetic patients with end-stage renal lesion receiving various modalities of treatment. Progressive glomerulopathy associated with proteinuria and hypertension is strongly causative of renal failure and mortality in diabetic patients. Besides hypertension, diabetes exceeds all other glomerulopathies in causing end-stage renal failure. Alterations in glomerular structure and function observed in diabetic patients are implicated in the development and progression of renal derangement. Diabetic glomerulosclerosis, an aggregate of structural and functional perturbations of the kidney, is indicated by alterations in the accumulation of extracellular matrix components, The pathology, epidemiology, risk factors, and other dependent variables may throw some light in the pathogenetic mechanisms and the prevention, treatment, and management modalities of type II diabetic nephropathy.
J Diabetes Complications
PMID:Type II diabetic nephropathy in perspective. 773 45

Formation of diabetic glomerulosclerosis was followed by the electron microscopy of 21 puncture renal biopsy and 12 incisive pancreatic biopsies from patients with insulin-dependent diabetes mellitus. The influence of the B-cell destruction and the decrease or absence of their activity (the presence of serum C-peptide) on the degree of renal damage and clinical symptoms of the diabetic nephropathy (proteinuria, hypertension) is noted. Dynamics of the diabetic glomerulosclerosis formation is as follows: 1st group--thickening of capillary basal membrane in the glomeruli, mesangial ectopy, formation of nodules at the periphery of loops; 2nd group--increase of the mesangial matrix, doubling of the glomerular capillary basal membrane, hyalin droplets in the capsule membrane. 4 stages in the development of diabetic glomerulopathy are distinguished: diabetic segmentary mesangioproliferative glomerulonephritis, mesangiolysis, two stages of glomerulosclerosis progression. Duration of the disease more than 15 years predetermines the development of diabetic glomerulosclerosis.
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PMID:[Diabetic glomerulosclerosis--a prolonged stage of diabetic glomerulopathy]. 784 6


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