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)

An Australian Aboriginal family, extending four generations, with a high incidence of renal disease was investigated. Twenty-eight of 114 members screened had hematuria. Of those tested, five had hypertension, four maturity onset diabetes, one a raised serum creatinine concentration, five elevated serum IgA levels and two cortical scarring on intravenous pyelogram. Of the eight members who underwent renal biopsy, five had IgA nephropathy and one had light and electron microscopy evidence of glomerulonephritis, but no IgA was seen on immunofluorescence. One had mild nonspecific changes by light microscopy but no immunofluorescence or electron microscopy was available and the remaining patient had mild changes consistent with hypertension and diabetes. HLA typing, carried out for 27 family members, showed an increased incidence of HLA-B22, B27, B39, and DR1 when compared to Yuendumu Aborigines (B27 and DR1), or Australian Caucasians (B22), or both (B39). This may be due to an association with IgA nephropathy, or a family clustering of antigens. Overall, this study suggests a genetic mechanism in the pathogenesis of IgA nephropathy in some patients and, as there was evidence of renal disease in 25% of those tested, may indicate an underlying high incidence of renal disease in the Aboriginal community.
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PMID:Familial IgA nephropathy: a study of renal disease in an Australian aboriginal family. 349 24

Utilizing a monoclonal antibody (Poly C9-MA) to a neoantigen of the C9 portion of the membrane attack complex of complement (MAC), immunoelectron (IEM) and immunofluorescent (IF) microscopy were performed on kidney tissue from normal humans and patients with insulin-dependent diabetes mellitus (IDDM) and type II membrano-proliferative glomerulonephritis (MPGN II). Comparative studies were conducted using polyclonal antibodies to human C3, C5, IgG, IgA, and IgM. In normal human tissue, there was a close correlation between increasing chronologic age and the quantity of MAC deposited in the mesangial stalk, along the interstitial aspect of and within tubular basement membranes (TBMs) and in arteriolar walls. IF of kidney tissues from 12 patients with IDDM with varying degrees of mesangial expansion and glomerulosclerosis demonstrated a direct relationship between the degree of tissue damage and the amount of MAC deposited in the mesangium. IEM of three normal and four diabetic specimens revealed reaction product of Poly C9-MA on linear and circular membranous structures within the mesangium, TBMs, and vessel walls, and within the glomerular basement membranes (GBMs) in diabetic subjects. Evidence is presented that these structures, which have been previously described by routine electron microscopy, represent cellular debris in these loci on which Poly C9-MA has been deposited. In MPGN II, Poly C9-MA and C3 were distributed within subepithelial deposits, along either side of the dense deposits (DDs) within the GBMs and TBMs, and around circular masses of DDs within the mesangium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ultrastructural localization of the membrane attack complex of complement in human renal tissues. 354 35

A patient with the classic form of Wegener's granulomatosis with severe dabetes mellitus and rapidly progressive glomerulonephritis is described. This 61-year-old male presented with epistaxis and nasal pain and obstruction. The nasal cavities were filled with crusts covering eroded mucosa. The diagnosis was made by biopsy of nasal and bronchial mucosa, and laboratory data. The epistaxis was stopped by 10 Gy irradiation over the nasal cavities. The patient had severe diabetes mellitus. His blood sugar was not controlled by diet and insulin injection. His general condition worsened rapidly as the growth of granuloma in the nose and lung. Accordingly, prednisolone therapy reinitiated to suppress the granuloma although it has a reverse effect on diabetes mellitus. Approximately one month after admission, he died of acute renal failure. Autopsy was carried out. Granulomatous lesions were noted in the nasal cavities, lungs and spleen. Many petechiae were found macroscopically over the cortex of the kidney. Hyalinization or sclerosis with crescent formation was found microscopically in estimated 85% of the glomeruli. Immunohistologic analysis of the renal tissue demonstrated an irregular linear pattern deposition of IgG, IgA and C3 and a granular pattern deposition of IgM and C1q.
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PMID:Wegener's granulomatosis: report of a case with rapidly progressive glomerulonephritis and diabetes mellitus. 359 30

The 24-h urine excretion and renal clearance of albumin, alpha I-acid glycoprotein, transferrin, IgG, IgA and haptoglobin were studied in 30 albustix-negative diabetics with no clinical data for diabetic nephropathy aiming at the precise characterization of proteinuria in patients with diabetes mellitus. The diabetic patients were divided into two groups - 15 patients with newly diagnosed diabetes and 15 - with a longer duration of diabetes. Thirteen healthy subjects, at the same mean age, served as a control group. The results reveal increase of the clearances and 24-h excretion of the proteins studied in the patients with diabetes mellitus, in those with a short duration of the disease including, with authentic difference for albumin, transferrin, IgG and haptoglobin among the patients with a longer duration of the disease and the healthy controls and authentic difference for albumin between those with the newly diagnosed diabetes and the healthy control. The possible prognostic significance of the indices studied is discussed as well as their importance for the early diagnosis of diabetic nephropathy.
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PMID:[Urinary excretion and renal clearance of several specific plasma proteins in diabetics]. 361 8

Sixty-five patients with histologically proven chronic active hepatitis of unknown cause but associated with the antiliver/kidney microsome antibody type 1, confirmed by immunofluorescence and immunoprecipitation, were selected as forming a special entity. This disease was found to be rare with a prevalence of 5/1,000,000. The female to male ratio was 8:1. The condition occurred at all ages but was most common between the ages of 2 and 14 years. In 22 of the 65 cases, the hepatitis was associated with an autoimmune disease, most commonly insulin-dependent diabetes, autoimmune thyroid disease and vitiligo. The same autoimmune diseases were present in first-degree relatives from seven families. In 36 cases, the onset of disease resembled acute viral hepatitis. Serum biochemical tests showed marked elevation in aminotransaminases and hypergammaglobulinemia. Paradoxically, serum and salivary IgA levels were often normal or low. Histologic findings were multifocal hepatic necrosis with bridging in the acute stage, and aggressive hepatitis with mononuclear cell infiltration or macronodular cirrhosis in the late stages. Serologically, apart from the presence of antiliver/kidney microsome antibody type 1, the disease was characterized by the absence of antiactin, antimitochondria and antinucleus antibodies; however, organ-specific autoantibodies were often present. The clinical course was usually severe: six patients in the acute stage presented with fulminant hepatitis, and all, except two, other patients progressed to cirrhosis. Prolonged treatment with corticosteroids and immunosuppressants was usually effective in rendering the cirrhosis inactive. The cumulative survival rate was 51% at 14 years. We propose to call this entity "anti-LKM1 chronic active hepatitis" or "autoimmune hepatitis type II" to differentiate it from classical "lupoid hepatitis" or autoimmune hepatitis type I.
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PMID:Chronic active hepatitis associated with antiliver/kidney microsome antibody type 1: a second type of "autoimmune" hepatitis. 367 93

Jejunal biopsy was performed without selection in 110 of 201 children with insulin-dependent diabetes mellitus; serum reticulin antibody, antigliadin antibody by enzyme-linked immunosorbent assay, and serum IgA were studied in all 201 children. Seven children had severe jejunal villous atrophy, giving a prevalence of celiac disease of at least 3.5%. Of the serum tests used, antigliadin antibody with ELISA was the most sensitive. Four patients adhered to a gluten-free diet, and their jejunal structure became normal; three had subsequent gluten provocation, and the jejunal mucosa relapsed in every one. Six had HLA-B8 and -DR3 antigens, and one had B15 and -DR4 phenotypes. In most patients, a gluten-free diet had little effect on insulin dosage, urinary excretion of glucose, or serum level of hemoglobin A1.
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PMID:Celiac disease in insulin-dependent diabetes mellitus. 370 14

Sixty-five insulin-dependent diabetes mellitus (IDDM) patients at the Steno-Memorial Hospital entered the present study. Of these, 43.1 percent had one or more late diabetic complication, 19.3 percent had circulating immune complexes (CIC)--there was a tendency for CIC to be related to late diabetic complications (P = 0.1) - and 16.9 percent had elevated total S-IgG. Elevated S-IgG values were related neither to CIC, to complications, nor to IgG deposits in the skin. Three patients had elevated total S-IgM, IgD and, IgE, respectively. No patients had elevated total S-IgA. Insulin antibodies were present in 41.9 percent. They were related to neither CIC nor clinical complications. No patients had rheumatoid factors (RF) or granulocyte-specific antinuclear antibodies (ANA). 12.3 percent had a low titre of organ non-specific ANA. No relationship could be established between ANA and complications or CIC. As regards skin deposits IgG was present at the dermo-epidermal junction zone (DEJ) and/or in the dermal vessels in 75.4 percent of the patients; IgA was present in 35.4 percent; and IgM in 32.3 percent. IgD and IgE were absent in all patients. Fibrinogen deposits were found in 80 percent and complement C3 in 32.3 percent. No correlation was found between skin deposits and CIC, on one hand, or clinical complications, on the other. From the present work, we conclude that humorally mediated immunological processes are active in IDDM. However, the exact role of this activity still remains to be defined.
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PMID:Circulating immune complexes, insulin antibodies, and deposits of immunoglobulins in the skin in diabetes. 372 Mar 67

Deposition of immunoglobulins or acute phase reactant (APR) proteins in the dermal and glomerular capillary walls from patients with diabetes mellitus was examined to determine whether development of microangiopathy in such patients was related to exudation and/or entrapment of these proteins. Skin and renal biopsy specimens were obtained from patients with diabetic nephropathy and diabetes mellitus without nephropathy. These biopsy samples were stained with FITC-labeled anti-human IgG, IgA, IgM, C3, APR proteins, and beta-lipoprotein antisera. Linear depositions of IgA, IgG, and/or APR proteins were observed in the dermal and/or glomerular capillary walls from some patients with diabetic nephropathy or diabetes mellitus without nephropathy. It is indicated that deposition of such immunoglobulins in the dermal and glomerular capillary walls might be due to exudation and/or entrapment of these substances in patients with diabetes mellitus.
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PMID:Detection of immunoglobulins and other serum proteins in the dermal and glomerular capillary walls from patients with diabetes mellitus. 377 32

Linear deposition of IgA immunoglobulin was found along the glomerular basement membrane in two patients with normal renal function and no pulmonary abnormalities. One patient had recurrent gross hematuria and a mild focal proliferative glomerulonephritis without deposits on electron microscopy; the second patient had a renal cell carcinoma. This observation of linear IgA antibody deposition in the absence of Goodpasture's syndrome or diabetes mellitus extends the spectrum of diseases associated with glomerular basement membrane-IgA deposition.
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PMID:Idiopathic linear glomerular IgA deposition. 377 52

An edematous rash developed on the abdominal skin of a 76-year-old woman who had had diabetes mellitus for ten years. Some months later, the affected skin became thickened and indurated. Histopathologic examination revealed marked dermal fibrosis with excessive deposition of collagen. The patient also had IgA (k-type) paraproteinemia. Fibroblast cultures from the affected and unaffected skin were studied for collagen metabolism. Procollagen synthesis was elevated about sixfold on fibroblasts derived from the affected skin. A similar increase was detected in messenger RNA (mRNA) levels using a complementary DNA clone specific for human pro alpha 1(l) collagen mRNA. The elevated mRNA level could be the result of increased transcriptional activity of collagen genes or decreased degradation of collagen mRNAs. Our findings suggest that increased collagen deposition may account for the marked dermal fibrosis that we observed in this patient.
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PMID:Scleredema and paraproteinemia. Enhanced collagen production and elevated type I procollagen messenger RNA level in fibroblasts grown from cultures from the fibrotic skin of a patient. 381 96


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