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)

Since January, 1, 1976, epidemiologic study of renal diseases has been leading in a French rural area of 400,000 inhabitants located in north coast of Britanny. Annual incidence of end stage renal failure (ESRF) treated by dialysis increased of 25% when two consecutive periods of five years each were compared: A (1976-1980) 46 per 10(6) inhabitants, B (1981-1985) 62 per 10(6) inhabitants. In 1986, the progression was confirmed: 96 per 10(6). At the time of the beginning of dialysis treatment, mean age (+/- SD) was not different between two periods: 53 +/- 17 yrs (A) vs 51 +/- 17 yrs (B) but it increased in 1986: 61 +/- 14 yrs. Sex ratio (M/F) progressed from 1 (A) to 1.75 (B). The study of causes of ESRF showed a net increase of secondary renal diseases (diabetes, amyloidosis), interstitial nephropathies due to obstructive uropathy (lithiasis) and drugs. For the period B, 91% of primary glomerulonephritis reaching ESRF had had renal biopsy. Idiopathic IgA nephropathy was the first cause of ESRF (13.7%, 0.85 pts/100,000) before diabetes (12%, 0.75/100,000), Polycystic disease (11.3%, 0.70/100,000), reflux nephropathy (9.6%, 0.60/100,000), focal and segmental glomerulosclerosis (8.8%, 055/100,000). Prevalence of ESRF for primary glomerulonephritis was calculated to 20.6% and according to the histological type to 28.3% for idiopathic IgA nephropathy, 34.8% for local and segmental glomerulosclerosis, 40% for idiopathic crescentic glomerulonephritis and only 6.6% for membraneous nephropathy. In the studied area, 58% of patients were treated out of hospital (at home or in self-dialysis units) whose 46% by hemodialysis and 12% by CAPD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Epidemiology of terminal renal insufficiency treated by dialysis and therapeutic options in a population of 400,000 inhabitants (1975-1986)]. 333 May 78

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

An oral glucose tolerance test and an assay of insulin receptor activity were performed in patients with chronic glomerulonephritis (CGN) to elucidate the aberration of glucose metabolism in such patients. Ninety of 123 patients with CGN without renal failure showed abnormal glucose tolerance, including 72.6% with IgA nephropathy, 81% with benign recurrent hematuria, 87% with chronic proliferative glomerulonephritis, 100% with membranoproliferative glomerulonephritis, and 80.0% with membranous nephropathy. Insulin responses in CGN patients during oral glucose tolerance tests showed lower levels of basal insulin and significantly higher levels after 90, 120, and 180 min compared with those of normal controls. The binding of radiolabeled insulin to blood mononuclear cells in 22 CGN patients with abnormal glucose tolerance was significantly (P = 0.0023) decreased in comparison with 5 normal controls. However, plasma obtained from such patients showed no significant (P = 0.4761) inhibition of the binding of insulin to normal mononuclear cells. It was concluded that glucose tolerance capacity was impaired in 80.4% of patients with CGN without renal failure. Such impairment of glucose metabolism might be due to decreased activity of insulin receptors on cells in CGN patients.
Diabetes Care
PMID:Abnormal glucose tolerance in patients with chronic glomerulonephritis without renal failure. 635 11

A case of polymyositis associated with scleroderma, adult coeliac disease, diabetes mellitus and IgA nephropathy is reported in a 33-year-old male.
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PMID:Polymyositis associated with several immunological disorders. 652 90

Report on a diabetic patient with IgA nephropathy whose kidneys were examined by biopsy four times during a period of four years. Morphologically the typical findings were observed: Outstanding deposits of IgA, hypercellularity and increase of matrix within the mesangium. The findings persisted during the period of observation. The differential diagnosis between IgA nephropathy and a slight diffuse glomerulosclerosis in diabetes mellitus is discussed. IgA nephropathy is diagnosed with certainty only by the aid of immunohistology.
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PMID:[IgA nephropathy in diabetes mellitus (author's transl)]. 721 Sep 32

The intrarenal hemodynamics was examined in 101 patients with chronic glomerulonephritis (CGN) and 111 patients with type I diabetes mellitus. Intrarenal hypertension was diagnosed from renal functional reserve (RFR) depletion. In CGN intrarenal hypertension was revealed in all clinical and morphological variants of nephritis: in 40% of patients with a nephrotic variant, in 25% with a latent variant and in 83% of patients with nephritis concurrent with the severe urinary syndrome. In focal segmental glomerulonephritis and fibroplastic nephritis, the depleted RFR was encountered 4 times more frequently than the preserved one. There was a association between RFR and arterial hypertension, albuminemia, blood creatinine. In diabetes mellitus intraglomerular hypertension was diagnosed in 34% of patients without renal damage (those having normal albuminuria), in 79% at the preclinical stage of diabetic nephropathy (in microalbuminuria) and in 93% at its clinical stage. Intrarenal hemodynamic disorders in diabetes mellitus are primary and provoked by hormonal metabolic disorders. The morphological signs of renal hyperperfusion failure develop at the preclinical stage of diabetic nephropathy.
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PMID:[Disorders of intrarenal hemodynamics in glomerulopathies]. 762 86

We studied the relationships of renal lesions with clinical features and renal prognosis in 128 Japanese patients with noninsulin-dependent diabetes mellitus (NIDDM). Diabetic glomerulosclerosis (DMGS) was found in 108 cases (84.4%), and DM-associated glomerulonephritis (GN), IgA nephropathy and membranous nephropathy, was in 20 cases (15.6%). There was no significant difference in age at renal biopsy, age at DM onset, DM duration, glomerular filtration rate (GFR), urine protein and serum IgA level between patients with DMGS and DM-associated GN. With respect to histological parameters, the increase in mesangial matrix was more closely related to DM duration, GFR and urine protein than to the degree of glomerular sclerosis. The index of glomerular lesion (IGL), which was calculated by combining these two lesions, had a more significant correlation with the clinical features than the tubulo-interstitial lesions. We suggested that the mesangial change was an initiating reaction, and the interstitial one was secondary in NIDDM patients. The prognosis of renal function after renal biopsy of the patients whose serum creatinine level was less than 1.2 mg/dl, was poorer in cases with nodular lesion than in those with diffuse lesion. The grade of tubulo-interstitial lesion was also more severe in these patients with nodular lesion. However, the controls of blood glucose, blood pressure, serum total cholesterol were not different among the two groups. On the other hand, serum creatinine level of most patients with associated GN did not change for a long period, up to 10 years.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A light microscopic study of glomerulosclerosis in Japanese patients with noninsulin-dependent diabetes mellitus: the relationship between clinical and histological features. 799 33

Urinary levels of glycosaminoglycans (U-GAG) were measured in 72 patients with non-insulin-dependent diabetes mellitus, 12 patients with collagen diseases, 14 patients with IgA nephropathy and 35 healthy subjects as controls to investigate the clinical significance of urinary GAG. The mean urinary GAG levels in diabetics and patients with collagen diseases were 72.4 +/- 36.2 and 147.8 +/- 59.2 mg/g.cr, respectively. These were significantly higher than the level in healthy subjects (46.7 +/- 11.3 mg/g.cr, p < 0.01). The mean urinary GAG level in patients with IgA nephropathy was 56.4 +/- 21.0 mg/g.cr and did not differ from that in healthy subjects. The mean urinary GAG level in 35 normoalbuminuric diabetic patients (U-A1b < 30 mg/g.cr) was 64.4 +/- 25.6 mg/g.cr and was significantly higher than that in healthy subjects (p < 0.01). The mean urinary GAG levels in 24 microalbuminuric patients (30 < U-A1b < or = 300 mg/g.cr) and 13 patients with overt albuminuria (U-Alb > or = 300 mg/g.cr) were 71.4 +/- 30.1 and 95.8 +/- 58.4 mg/g.cr, respectively and were also higher than the level in healthy subjects (both p < 0.01). Urinary GAG levels correlated positively with urinary albumin levels (r = 0.251, p < 0.05) and urinary N-acetyl-beta-D-glucosaminidase activities in diabetics (r = 0.491, p < 0.01). The prevalence of diabetic macroangiopathies in diabetic patients with elevated levels of urinary GAG was significantly higher than that in those with normal levels of urinary GAG (p < 0.05).
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PMID:[Urinary glycosaminoglycans in patients with non-insulin-dependent diabetes mellitus, collagen diseases and IgA nephropathy]. 813 46

Extended HLA haplotypes frequencies were estimated from the HLA, C2, Bf and C4 phenotypes of 74 patients with non-insulin-dependent diabetes (NIDD), 92 with juvenile rheumatoid arthritis (JRA), 44 with Berger's disease (BD), 83 with insulin-dependent diabetes (IDD), and 140 healthy controls. The extended HLA haplotype B18 CF130 DR3 DQw2, which is common (around 10% phenotype frequency) in healthy Spaniards and in other populations of paleo-North African origin, was found to be significantly less frequent in NIDD, JRA and BD, whereas its frequency was normal in IDD (although DR3 DQw2 haplotypes were increased in the latter disease). These data support the existence of a common HLA-linked pathogeneic mechanism in NIDD, JRA and BD, and point to a genetic difference between IDD and NIDD at the HLA level. This effect is readily detectable in our population because the uncommon BfF1 allele marks that haplotype instead of the more common BfS, which marks B8 CS01 DR3 DQw2 in other Caucasians. Our results support the hypothesis of strong selective pressures operating at the HLA level to preserve extended HLA haplotypes with advantageous gene sets from dilution by crossing-over. Imbalanced incomplete haplotypes may give rise to inappropriate T-cell repertoire selection in the thymus and/or antigen handling in the periphery, and be partly responsible for the pathogenesis of certain HLA-linked diseases (i.e. NIDD, JRA, and BD).
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PMID:A decrease in the estimated frequency of the extended HLA haplotype B18 CF130 DR3 DQw2 is common to non-insulin-dependent diabetes, juvenile rheumatoid arthritis, and Berger's disease. 833 82

GM and KM immunoglobulin (Ig) allotypes and their interactions with HLA antigens have been analyzed in various autoimmune diseases: multiple sclerosis, rheumatoid arthritis, insulin-dependent diabetes mellitus (IDDM), systemic lupus erythematosus, coeliac disease, Crohn's 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. This review reports published results about associations or linkages, as well as the origins of the populations, the numbers of patients and controls tested. The possible role of Ig polymorphisms in the physiopathology of autoimmune diseases is discussed. Ig allotypes and statistical methods used to analyse the HLA and Ig data are also described.
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PMID:Immunoglobulin allotypes (GM and KM) and their interactions with HLA antigens in autoimmune diseases: a review. 878 16


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