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

Twelve cats were used to study autolytic changes in glomerular morphology and compare these with lesions of naturally occurring feline renal disease. The 12 cats had normal clinical, urinary, and blood features. One kidney (0-hour control) was excised immediately after a given cat was euthanatized, and portions of it were prepared for light and electron microscopy. The opposite kidney (autolytic) remained in situ for selected postmortem intervals, up to 24 hours, at which time it was similarly processed. Renal tissues from 4 additional cats (3 with proteinuria and 1 with diabetes mellitus) were processed and examined for comparison. Zero-hour control kidneys had the following mean quantitations: renal weight was 9.9 g; glomerular diameter, 83 mum; number of cells per glomerulus in 1-mum section was 63; and diameter of cell nuclei was 6.3 mum for mesangial, 6.7 mum for visceral epithelial, and 6.4 mum for endothelial. In comparison with 0-hour control kidneys, autolytic kidneys had increased weight and glomerular diameter, but the diameter of cell nuclei decreased. Basement membrane thickness and glomerular cell numbers did not differ between 0-hour control and autolytic kidneys. Kidneys from 4 diseased cats had increased glomerular diameter and glomerular basement membrane changes characterized by hyalin thickening and dense deposits. These changes are compatible with a lesion diagnosis of membranous glomerulonephritis.
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PMID:Feline glomeruli: morphologic comparisons in normal, autolytic, and diseased kidneys. 96 8

Membranous nephropathy (MN) accounts for about 20 percent of cases of the nephrotic syndrome. The importance of renal biopsy in establishing the diagnosis is emphasized. In the great majority of MN patients, no etiologic factor can be discerned. In a significant minority, MN appears to be a manifestation of sarcoidosis, diabetes, lupus, syphilis, malaria, or toxicity from heavy metals or drugs. In some cases the "cause" is neoplasia (including lymphoma) or a viral infection. Massive proteinuria, hypoproteinemia and edema are the principal manifestations of MN, finally resulting in renal failure. Treatment consists chiefly of diet and diuretic drugs. In the more pronounced cases, corticosteroids may have a favorable effect and in very resistant cases, cyclophosphamide is indicated. Judicious use of these modalities if often associated with the diminution or disappearance of the clinical signs of MN.
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PMID:Membranous nephropathy: an overview. 120 87

A 64-yr-old man presented with diabetes mellitus, proteinuria, hypertension and moderate renal dysfunction. Renal biopsy revealed diabetic glomerulosclerosis (diffuse lesion), IgA nephropathy and membranous nephropathy (stage 2). Both mesangial IgA and subepithelial IgG deposits were demonstrated by immunofluorescence and immunoelectron microscopy. Electron microscopic studies by immunogold method showed localization of IgA (diameter 15nm gold particles) within mesangial dense deposits and IgG (diameter 15nm gold particles) within subepithelial dense deposits. Overlapping IgA and membranous nephropathy was revealed in the same diabetic glomeruli with functional and biochemical alternations.
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PMID:[A case of superimposed renal lesions of IgA and membranous nephropathy with diabetic nephropathy]. 148 12

The clinicopathological and laboratory findings for 35 diabetic patients who had undergone renal biopsy from 1982 to 1990 were reviewed. Ten of these patients (28.6%) were found to have nondiabetic renal diseases. Five of those patients (14.3%) suffered from nondiabetic renal disease complicated by diabetic nephropathy. Nondiabetic renal diseases included IgA nephropathy, idiopathic membranous nephropathy, membranoproliferative glomerulonephritis (types I and III), minimal change disease, and toxemia of pregnancy. The diagnosis of nondiabetic renal diseases complicated by diabetes is important for the treatment of renal disease. Urinary abnormalities and/or deterioration in renal function inconsistent with the natural history of diabetic nephropathy were suggestive of the presence of nondiabetic renal disease.
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PMID:Nondiabetic renal disease complicating diabetic nephropathy. 177 26

In experimental membranous nephropathy, antibody binding to glomerular epithelial cell membrane antigens results in complement activation and formation of complement C5b-9 membrane attack complexes in glomeruli. During active disease, the C5b-9 complexes are shed into the urine. To test the hypothesis that a similar mechanism might be operative in human membranous nephropathy, we measured urinary excretion of C5b-9 and C5 in 146 proteinuric patients with biopsy-proven glomerular diseases or diabetes mellitus. Urinary excretion of C5b-9 relative to C5 excretion was higher in 40 patients with membranous nephropathy than in 106 patients with proteinuria due to non-membranous glomerulonephritis when analyzed by covariance analysis (P less than 0.0002). Urinary C5b-9 excretion was higher in membranous nephropathy than in membranoproliferative glomerulonephritis (N = 13, P less than 0.05), minimal change-focal sclerosis (N = 33, P less than 0.001), mesangial proliferative glomerulonephritis (N = 9, P less than 0.02) and IgA nephropathy (N = 7, P less than 0.025). Urinary C5b-9 excretion was also higher in patients with lupus nephritis (N = 18, P less than 0.02) compared to those with non-membranous glomerulonephritis. The lupus patients with the highest excretion had clinical or pathological features of membranous nephropathy. Nine patients with membranous nephropathy and elevated urinary C5b-9 excretion had a shorter duration of disease (P less than 0.05), lower serum creatinine levels (P less than 0.05) and more proteinuria (P less than 0.02) than the 31 membranous nephropathy patients with normal values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elevated urinary excretion of the C5b-9 complex in membranous nephropathy. 178 50

The demonstration of circulating anti-glomerular basement membrane (GBM) antibodies is almost diagnostic for anti-GBM disease and Goodpasture's syndrome. These antibodies are, however, occasionally present in SLE and diabetes, in association with IgA disease and membranous nephropathy and after transplantation in Alport's syndrome. In addition, we describe circulating anti-GBM antibodies in a research worker who handled GBM and in whom coeliec disease later developed, and in an individual with epidermolysis bullosa acquisita. Neither patient had impaired renal function nor an abnormal urinary sediment, suggesting either that these antibodies were of low affinity, or that additional factors are required for the pathogenesis of an aggressive glomerular lesion when circulating anti-GBM antibodies are present. In at least one of these individuals anti-GBM antibodies may have developed after the exposure of basement membrane collagen type IV to activated immunological mediators and cells.
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PMID:Circulating anti-glomerular basement membrane antibodies in coeliac disease and epidermolysis bullosa acquisita. 181 46

We have investigated the distribution of genotypes of a restriction fragment length polymorphism of the T-cell receptor beta-subunit gene in Caucasoid controls and patients with insulin-dependent diabetes mellitus, celiac disease, dermatitis herpetiformis, and idiopathic membranous nephropathy and also in South Indian controls and diabetics. We found no significant differences between the controls and patients with any disease in either ethnic group, a result which contrasts with previous reports of associations with both insulin-dependent diabetes mellitus and idiopathic membranous nephropathy. However, the most striking finding was a marked disparity between the genotype distribution in our Caucasoid control population and that previously reported by other investigators.
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PMID:T-cell receptor beta-subunit gene polymorphism and autoimmune disease. 196

Following 689 percutaneous renal biopsies, membranous glomerulonephritis was proved in 68 patients. In 16 (23.5%) an underlying primary disease was verified, and thus the glomerulonephritis the secondary form. The primary disease was SLE in 5 cases, diabetes mellitus in 5 cases, rheumatoid arthritis in 3 cases, chronic active hepatitis in 2 cases, an ulcerative colitis and eosinophilic angiolymphoid hyperplasia in 1 patient. As initial sign, nephrotic syndrome emerged in 87.5% of the 16 cases. Microscopic haematuria was observed in half of the patients, as was hypertension, while acute renal failure presented in only 1 case. Histologically, in 13 cases the predominance of early glomerular alterations was characteristic, while in 9 cases the picture proved to be equivocal and accompanied by some degree of interstitial alterations. During combined treatment, remission was achieved in 75%. Two patients with SLE died, but not as a consequence of renal failure. Transient side-effects of the treatment were registered in 5 cases. The principal pathogenetic and clinical differences between the individual secondary nephritis forms, and the difficulty of their differentiation from the idiopathic cases, even on repeated examination, are emphasized. In 3 patients the possibility of secondary renal processes was suggested by the histological picture, and this was proved by the detailed clinical findings.
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PMID:[Secondary membranous glomerulonephritis]. 199 1

We evaluated the clinical course of 700 renal transplantations, including 1,305 transplant histologies performed in 611 patients between 1970 and 1988, to estimate the influence of cyclosporine A (CsA) after kidney transplantation on the incidence of recurrent or de novo renal disease. Primary renal disease recurred in 11 of 583 functioning transplants (1.9%) with transplant loss in seven patients (1.2%): focal segmental glomerulosclerosis (FSGS, three patients); membranous glomerulonephritis (GN, one patient); mesangiocapillary GN (one patient); rapidly progressive IgA nephropathy (one patient); hemolytic-uremic syndrome (HUS, three patients); and oxalosis in two transplants (one patient). De novo renal disease occurred in six patients (1.0%), including mesangiocapillary GN type I (three patients); nonpurulent focal GN in septicemia (one patient); HUS (one patient); and nodular glomerulosclerosis in steroid diabetes (one patient). De novo membranous GN was seen in 14 additional cases (2.4%). No statistically significant difference could be established between the treatment groups without (n = 225) and with (n = 358) CsA in recurrent and de novo renal disease (n = 7/225 v 10/358, NS); in recurrent and de novo GN (n = 4/225 v 6/358, NS); in recurrent FSGS (n = 1/7 v 2/8, NS); in recurrent and de novo HUS (n - 1/1 v 2/7, NS); and in de novo membranous GN (n = 7/225 v 7/358, NS). Transplant loss by recurrent and de novo GN was higher without than with CsA (n = 4/4 v 1/6, P = 0.004). On the basis of our investigation, we conclude that recurrent and de novo renal disease in the transplant occur rarely and are not prevented by CsA. However, even if the incidence of transplant GN is unchanged by CsA treatment, its clinical course seems to be mitigated. CsA treatment also does not increase the incidence of HUS.
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PMID:Recurrent and de novo renal disease after kidney transplantation with or without cyclosporine A. 202 53

Nonsteroidal anti-inflammatory drugs, especially indomethacin, have variable effects on proteinuria when used alone, but can dramatically reduce proteinuria if combined with diuretics and sodium restriction. Reduction of angiotensin II concentrations in plasma and kidney following angiotensin-converting enzyme inhibition also reduces proteinuria, not only in nephrotic conditions but also in diverse diseases, including diabetes mellitus, glomerulosclerosis following subtotal nephrectomy, and membranous nephropathy. The reduction of proteinuria appears independent of decrements in blood pressure since other hypotensive agents do not alter proteinuria in these conditions.
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PMID:Prostaglandins, angiotension II, and proteinuria. 211 84


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