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)

To evaluate the disease association with HLA-DR 3/4 heterozygotes, 1,074 subjects, who had been analyzed consecutively for HLA-DR antigens for organ transplantation or to study the disease association with HLA from June 1984 to June 1986, were enrolled in this study. Of these subjects, 278 had diabetes, 168 were healthy controls or donors, and 628 had other diseases. Of the 1,074 subjects, 35 subjects (3.2%) were DR 3/4 heterozygotes and 1,039 subjects (96.7%) were non-DR 3/4 heterozygotes. Among the 35 DR 3/4 positive subjects, 23 were diabetic (65.7%), two were healthy donors (5.7%), 10 had other diseases (28.5%) such as recurrent abortion (n = 3), hepatoma (n = 2), Graves' disease (n = 1), idiopathic hypoparathyroidism (n = 1), IgA nephropathy (n = 1), uveitis (n = 1) and gout (n = 1). Among the 23 DR 3/4 positive diabetics, 19 (82.6%) had insulin-dependent diabetes mellitus (IDDM), three (13.0%) had non-insulin-dependent diabetes mellitus (NIDDM), and one (4.3%) had maturity onset diabetes of the young (MODY). When these DR 3/4 positive diabetics were compared with the other disease and control/donor groups, significant increases in the relative risk were seen for IDDM patients (RR = 32.61, 43.80, respectively, p < 0.001). No significant association could be seen for NIDDM and MODY patients. In those non-diabetic patients positive for DR 3/4, there was no significant association with DR 3/4 heterozygotes. These findings suggest that: 1) DR 3/4 positive subjects are highly associated with IDDM; and 2) there is no significant association of DR 3/4 with NIDDM, MODY and other non-diabetic diseases.
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PMID:Assessment of the association of HLA-DR 3/4 heterozygotes with diabetes mellitus and non-diabetic diseases. 136 26

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 pathogenesis of diabetic nephropathy relative to the changes in the glomerular extracellular matrices was investigated. Renal tissues from 10 diabetic patients were immunostained with antibodies directed against heparan sulfate proteoglycans (HS-PGs), laminin, type IV collagen and fibronectin. Seven patients were nephrotic and had advanced glomerulosclerosis with nodular lesion, while the other 3 had no renal manifestations or minor glomerular tissue alterations. Controls included kidneys removed from patients with renal tumors and specimens obtained by renal biopsy from patients with IgA nephropathy. Relationships among proteinuria, intensity of fluorescence and glomerular changes were studied. In diabetes 3 patients with minor glomerular lesions were found to have no changes in various components of extracellular matrices. A marked reduction in the intensity of staining with anti-HS-PG antibodies was observed in renal specimens from patients with nodular glomerulosclerosis and proteinuria, while a mild decrease in the intensity of fluorescence was observed in tissues stained with antilaminin antibodies. An increase compared to normal control sample findings in type IV collagen and fibronectin was observed in the mesangium of sclerosing glomeruli. No loss of HS-PG was observed in patients with IgA nephropathy. These results indicate that glomerular extracellular matrix HS-PG is lost in association with diabetic nephropathy; this loss results in alteration of the charge-selective properties of glomerular capillaries. This alteration may, in part, be the cause of the proteinuria associated with diabetic nephropathy.
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PMID:Heparan sulfate proteoglycans are lost in patients with diabetic nephropathy. 150 38

The associations or linkages between the polymorphisms of the Gm and Km immunoglobulin allotypes and the susceptibility to autoimmune diseases, including diseases with immuno-pathological pathogenesis are reported in this review. These diseases include multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, insulin-dependent diabetes mellitus, Crohn's disease, coeliac disease, Graves' disease, atrophic thyroiditis, Hashimoto's thyroiditis, myasthenia gravis, chronic active hepatitis, alopecia areata, uveitis, vitiligo, Turner's syndrome, glomerular nephritis, Berger's disease and idiopathic dilated cardiomyopathy. Immunoglobulin allotypes are described as well as the statistical methods used to analyse the data.
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PMID:Gm and Km allotypes in autoimmune diseases. 162 73

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

1. Graft survival rates increased about 3-5 percentage points for patients with all primary diseases in 1989-1990. 2. Patients with different diseases had 1-year graft survival rates that varied from 73% for noninsulin-dependent diabetes (NIDDM) to 83% for IgA nephropathy (IgAN). Five-year graft survival varied from 40% for NIDDM to 66% for IgAN. 3. Our findings in Clinical Transplants 1990 that IgAN patients have a high graft survival was confirmed and 1-year graft survival improved by 5% in the last 2 years. 4. There was a 20 percentage point increase in full-time work status of patients after transplantation; 68% of patients with polycystic kidney disease (PKD) and chronic glomerulonephritis (CGN) had full-time work status after 3 years whereas patients with diabetes mellitus (DM) and atheronephrosclerosis (NS) had about 50%. 5. Good early graft function (urine output during the first 24 hours posttransplant, no dialysis within the first-week posttransplant, and no rejection episodes before discharge), predicted good 1-year graft survival for patients with different diseases but patients with NS and DM had a poorer graft survival beyond the first year posttransplant. Patients who had poor early function had 20% lower graft survival than those who had good function. However, in patients with IgAN, no urine at day 1 still resulted in graft survival comparable to those that produced urine. 6. More patients with DM were transplanted within 1 year after going into ESRD than those with other diseases. Conversely, 46% of those with NS did not get transplanted until more than 2 years after developing ESRD. 7. Only 77% of NS patients had functioning grafts at discharge compared to DM (84%), PKD (81%), IgAN (81%), and CGN (80%). 8. Black patients had a statistically significant higher incidence of anuria on the first day compared with Whites. They also had a higher incidence of dialysis and rejection during the first hospitalization. This was true for CGN, DM, PKD, and NS patients. Following excellent early function, Black CGN and DM patients had a higher incidence of rejection than White CGN and DM patients.
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PMID:Outcome of renal transplantation in different primary diseases. 182 Jan 24

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

Samples from 103 kidneys donated for transplant were studied under light microscopy (LM), electron microscopy (EM) and immunofluorescence (IM, with C3, C4, C1q, IgG, IgA, IGE, IgM and antifibrin) just before transplantation. Seven kidneys were obtained from a cadaver (CK). Glomerular damage attributed to perfusion (perfusion glomerulopathy) was present in 4 cases. Glomerular changes in apparently healthy donors were present in 33% of cases: minor glomerular lesions, such as type I collagen fibers in the mesangial matrix (3 cases); uniform widening of the basal membrane without prior evidence of diabetes (4); relative glomerular ischemia with basal membrane irregularities (9). Major lesions were found in 17.5% of kidneys: IgA mesangial deposits compatible with Berger's disease (9, including 2 pairs of siblings); dense mesangial deposits suggesting the same process (6); subacute bacterial endocarditis glomerulopathy with IgG++, C1q+ and IgM+ (1, a CK); a type I mesangio-capillary glomerulonephritis with C3++, IgG++, IgA+ and IgM+ (1); subpedicelar and transmembranous isolated glomerular deposits of the immune complex type (1, complicated with microhematuria after donation). None of these glomerulopathies was demonstrated by LM, hence the use of EM and IM is essential for diagnosis.
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PMID:[A morphologic study of 103 kidneys donated for renal transplantation]. 251 71

Among 1715 renal biopsies investigated by means of light microscopy, immunofluorescence, and/or electron microscopy, 20 cases of various glomerulopathies (GP) were found to be superimposed on diabetic glomerulosclerosis (DGS). The most frequently superimposed GPs were acute GN (nine cases) and cryoglobulinemic GN (six cases). Although the former association is known to occur, the latter has not so far been reported. In the other patients DGS was associated with crescentic GN (two cases), membranoproliferative GN, membranous GN, and IgA nephropathy (one case each). Morphologic clues allowing the identification of the superimposed GP and the diagnostic relevance of the available morphologic methods were stressed. In particular, light microscopy was sufficient to identify the superimposed crescentic GN, whereas immunofluorescence and/or electron microscopy were needed in the other cases in order to show the composition and the seat of the deposits, respectively. In addition, electron microscopy was useful in identifying some peculiar features such as humps, mesangial cell interposition, and organized deposits in cryoglobulinemic GN. The actual frequency of superimposed GPs is difficult to assess: either under or overestimation is possible. Pathologists must be aware that this miscalculation is not an episodic event and that the estimation must be carefully sought whenever clinical data are equivocal and not fully fitting with DGS alone. The duration of the diabetes seems to favor the superimposition of GN on DGS. In these patients the prognosis is poor, not only when it could be expected to be, as in the cases with superimposition of crescentic or membranoproliferative GN, but also when DGS is associated with acute GN, whose prognosis is generally favorable.
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PMID:Pattern of double glomerulopathies: a clinicopathologic study of superimposed glomerulonephritis on diabetic glomerulosclerosis. 276 90


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