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)

1. To assess the risk of end-stage renal disease (ESRD) associated with the regular use of three classes of non-narcotic analgesics, we performed a case-control study of 340 patients with ESRD on a haemodialysis maintenance program and 673 hospital controls. 2. The overall odds ratio estimate for non-narcotic analgesics taken at least every other day for 30 days or longer before the first symptom of renal disease was 2.89 (95% CI, 1.78 to 4.68). 3. The risk increased in relation to the use duration. 4. The previous regular consumption of combinations containing phenacetin was strongly associated with ESRD (odds ratio, 19.05; 95% CI, 2.31 to 157.4). The odds ratio for previous regular consumption of salicylates was 2.54 (95% CI, 1.24 to 5.20) and for pyrazolones 2.16 (95% CI, 0.87 to 5.32). 5. An analysis for possible confounding by a history of repeated headaches, arthritis, kidney stones, hypertension, and diabetes did not alter the results. 6. The odds ratio estimates for different pathological subgroups of ESRD patients in relation to previous use of any non-narcotic analgesic were glomerulonephritis. 10.57 (95% CI, 1.25 to 89.0), interstitial nephritis, 3.33 (95% CI, 1.21 to 9.17), cystic kidney disease, 0.71 (95% CI, 0.25 to 1.97), and unknown, 5.15 (95% CI, 2.29-11.57). 7. The results of this study suggest that the regular consumption of analgesics should be routinely considered as a risk factor for any non-congenital cause of chronic renal failure. They also suggest that the risk of ESRD associated with the regular consumption of phenacetin is much higher than the risk associated with other non-narcotic analgesics.
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PMID:End-stage renal disease and non-narcotic analgesics: a case-control study. 227 70

Between January 1976 and December 1987, 278 patients (172 men, 106 women) aged over 15 and living in a region of some 400,000 inhabitants were treated with dialysis for end-stage chronic renal failure (CRF). The annual incidence of new cases treated was evaluated separately for 3 consecutive 4-year periods: 1976-79 (period A), 1980-83 (period B) and 1984-87 (period C). The incidence rose from 4.6-4.9 in periods A and B to 7.8/100,000 in period C, i.e. a 38 per cent progression. At the start of dialysis the mean age of women did not significantly vary throughout the 3 periods, whereas it increased significantly in men during period C. There was a significant increase of primary glomerulonephritis (GN) throughout the 3 periods: 1.25, 1.70 and 2.35/100,000 respectively; this disease accounted for 27.3, 34.6 and 30.6 per cent of all causes of CRF. Similarly, the incidence of secondary nephropathy (diabetes, amyloidosis) treated with dialysis increased from 0.6 (A) to 1.0 (B) and 1.9/100,000 (C) (P less than 0.05 with period A). The same happened with polycystic kidney: 0.25, 0.65 and 0.93/100,000. During period C, when 95 per cent of primary GN were diagnosed histologically, igAGN (13 per cent), diabetes (13 per cent) and polycystic kidney (12 per cent) were the main causes of CRF. During the whole 12-year period under study, when 80 per cent of primary GN were diagnosed, the prevalence of causes of CRF varied according to the patients' age. In patients under 65 at the start of dialysis primary GN were the principal causes of CRF (36.8 per cent, including 15.5 per cent of IgAGN), followed by secondary nephropathies (20.3 per cent, including 10.7 per cent of diabetes), chronic interstitial nephropathies (18.7 per cent, including 9.6 per cent of reflux nephropathy), hereditary nephropathies (14.4 per cent, including 10.7 per cent of cystic kidney) and vascular nephropathies (7 per cent). Above the age of 65, the principal causes of CRF were chronic interstitial nephropathies (27.7 per cent, including 8.9 per cent of drug-induced nephropathy), followed by secondary nephropathies (20 per cent, including 6.7 per cent of amyloidosis and 11.1 per cent of diabetes), vascular nephropathies (20 per cent), primary GN (12.2 per cent), and hereditary nephropathies (12.2 per cent) including 11.1 per cent of polycystic kidney).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Epidemiology of chronic renal insufficiency treated by dialysis in a region in France. Changes in a 12-year period]. 297 86

This 1993 report of the Lombardy Regional Dialysis and Transplant Registry refers to all the data collected between January 1, 1983, and December, 31, 1992, by means of individual patient questionnaires sent to all of Lombardy's 44 renal units (100% replies). The number of patients recorded by the Registry as being alive progressively increased; by the end of 1992, the number was 6,014 (655 patients per million population): 4,770 patients were on dialysis treatment (515 patients per million population, 79.3%) and 1,244 patients (140 patients per million population, 20.7%) had received a kidney graft. The acceptance rate for dialysis increased from 64 per million population in 1983 to 102 per million population in 1992; the increase in the transplant rate was much lower (from 18.7 to 21.3 per million population). The percentage of primary nephropathies in the new patients accepted for dialysis treatment were 22.0% glomerulonephritis, 13.8% interstitial nephritis, 15.2% vascular diseases, 10.1% cystic kidney, and 10.6% diabetes. The use of acetate hemodialysis declined over the 10-year period from 72.4% to 17.5%; that of bicarbonate hemodialysis increased from 8.8% to 50.1% and that of hemodiafiltration increased from 0.2% to 11.1%. The prevalence of hospital hemodialysis was stable, ranging from 55.4% to 52.2%; home hemodialysis decreased from 15.7% to 5.3%, continuous ambulatory peritoneal dialysis increased from 13.3% to 19.6%, and limited care increased from 13.7% to 22.4%. The crude death rate increased from 7.5% in 1983 to 10.5% in 1992. The survival rate (Kaplan-Meier) of all patients on dialysis was 78.8% at 2 years, 62.2% at 4 years, and 40% at 8 years; for transplanted patients, the survival and graft survival rate at 2 years was, respectively, 95% and 86%. The relative death risk of the patients on peritoneal dialysis with respect to those on hemodialysis was 1.419, as estimated by the Cox proportional hazard regression model. The main causes of deaths of patients on dialysis treatment during the year 1992 were cardiovascular diseases (47.0%) and cachexia (19.5%); in transplanted patients, they were cardiovascular diseases (36.6%) and infections (34%). Registries are not only important for planning health care but are also very useful instruments for clinical research.
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PMID:1983 to 1992: report on regular dialysis and transplantation in Lombardy. 781 May 25

We report a case of an infected renal cystic mass associated with bacterial meningitis in a 70-year-old woman who had had poorly-controlled diabetes mellitus for approximately 30 years. She suffered from bacterial meningitis due to Klebsiella pneumoniae, which was successfully treated with antimicrobial chemotherapy for 1 month. Approximately 2 weeks later she developed left flank pain and a high fever. A CT scan and an ultrasonogram revealed a left renal cystic mass, which was considered to be an infected renal cyst. Turbid and thick fluid was obtained by percutaneous aspiration which contained numerous white blood cells. Culture of this fluid yielded K. pneumoniae. The bacterial meningitis was considered to be a secondary infection of the septicemia which resulted from the infected renal cystic mass.
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PMID:Infected renal cystic mass associated with bacterial meningitis: a case report. 884 88

In acquired cystic kidney disease cysts develop in kidneys with impaired excretory function. Bleeding, cyst infection and a possible relation to kidney cell carcinoma resulted in an interdisciplinary concern about this disease. Kidney tissue slides from 125 autopsies of dialysis patients were studied. Of totally 967 cysts, 52% were lined by a cuboidal epithelium, with either clear or eosinophilic cytoplasm; 34% showed a flat epithelium. Multilayered epithelium was present in 8.3% and bleeding stigmata in 5.3%. Cyst counts rose with duration of dialysis, with a higher average cyst count in men. There was no correlation between cysts and (1) age, at the time of death of at the beginning of dialysis, (2) type of renal disease, (3) blood group, (4) body weight, (5) coronary heart disease, and (6) diabetes mellitus. More studies on the development of cysts, parameters of cyst formation and complications are necessary, as they are the basis for the interpretation of new imaging techniques, as well as, for a clinical risk assessment.
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PMID:[Acquired, cystic kidney disease in chronic dialysis patients: a retrospective study of 125 autopsies. 1: Cysts]. 974 14

After renal transplantation for congenital cystic kidney disease of unknown origin, a 14-year-old boy, who was previously normoglycemic, had "steroid-induced" diabetes mellitus, which was treated with insulin. Transplant failure from chronic rejection and subsequent transplant nephrectomy allowed discontinuation of corticosteroids, the gradual withdrawal of insulin and normoglycemia. The recent description of renal cysts and diabetes (RCAD) syndrome and a strong paternal family history of early-onset diabetes mellitus prompted genetic screening of the hepatocyte nuclear factor-1beta gene. A novel heterozygous frameshift mutation in exon 1 was identified, adding to the 12 kindreds thus far described. This case highlights the unmasking of the hyperglycemic component of the RCAD syndrome in the immediate postoperative period after renal transplantation and emphasizes the pleiotropic manifestations of this important genetic kidney disease.
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PMID:Severe hyperglycemia after renal transplantation in a pediatric patient with a mutation of the hepatocyte nuclear factor-1beta gene. 1246 54

Mutation of HNF-1beta gene has been reported in early onset diabetes or MODY families and this gene has been defined as MODY5 gene. The aim of our study was to examine whether HNF-1beta mutation contribute to early onset or multiple affected diabetes pedigrees in Chinese. Molecular scanning of HNF-1beta gene promoter region, nine exons and flanking introns was performed in 154 unrelated probands from early onset and multiple affected diabetes Chinese pedigrees. The family members of probands with mutations or variants and 58 nondiabetics were also examined. Clinical examinations of renal morphology, renal function and beta-cell function were performed in the HNF-1beta gene mutation carriers and family members. Mutation of HNF-1beta gene causing the substitution S36F was found in two subjects of an early onset diabetic family. One carrier has early onset diabetes, renal function impairment and renal cyst, while the other has impaired glucose tolerance only. This is the first case of MODY5 gene mutation diabetes found in the Chinese. Three HNF-1beta variants were identified and no significant differences in allele frequencies for these variants were detected between the nondiabetic and diabetic groups. Nucleotide 66 of intron 8 of HNF-1beta gene was G in the Chinese population rather than A as noted in the GenBank sequence. These results suggest that HNF-1beta gene mutations may be associated with nondiabetic renal dysfunction and diabetes in Chinese, but they are responsible for only a small percentage of early onset or multiple affected diabetes pedigrees including MODY.
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PMID:Scanning for MODY5 gene mutations in Chinese early onset or multiple affected diabetes pedigrees. 1566 Jan 95

Hepatocyte nuclear factor-1beta (HNF-1beta) is a Pit-1/Oct-1/Unc-86 (POU)/homeodomain-containing transcription factor that regulates tissue-specific gene expression in the kidney, liver, pancreas, and other epithelial organs. Mutations of HNF-1beta produce maturity-onset diabetes of the young type 5 (MODY5) and are associated with congenital cystic abnormalities of the kidney. Transgenic mice expressing mutant HNF-1beta under the control of a kidney-specific promoter develop kidney cysts and renal failure, which is similar to the phenotype of humans with MODY5. Similarly, kidney-specific deletion of HNF-1beta using Cre/loxP recombination results in renal cyst formation. HNF-1beta directly regulates the Pkhd1 promoter. HNF-1beta mutant mice show decreased expression of Pkhd1, the gene that is mutated in humans with autosomal-recessive polycystic kidney disease (ARPKD). These studies demonstrate that HNF-1beta is required for the development of the mammalian kidney. They establish a previously unrecognized link between two renal cystic diseases, MODY5 and ARPKD, and suggest that the mechanism of cyst formation in humans with mutations of HNF-1beta involves down-regulation of PKHD1 gene transcription.
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PMID:Roles of HNF-1beta in kidney development and congenital cystic diseases. 1622 Nov 71

A total of 684 patients who had not been diagnosed with renal cyst but had undergone abdominal ultrasonography for various reasons were evaluated. Patients with and without renal cyst were classified into two groups and were compared in terms of hypertension (HT), hyperlipidemia (HL), diabetes mellitus (DM) and obesity (body mass index: > or = 30 kg/m2) prevalence. Although 94 patients (13.7%) were established with a renal cyst, 590 patients (86.3%) did not have a renal cyst. The mean age of the patients established with a simple renal cyst was 67.3 +/- 12.1 years (range: 28-82 years); 54 (57.4%) of them were women and 40 (42.6%) were men. Of the patients established with a simple renal cyst, 64 (68.1%) had HT, 40 (42.6%) had DM, 20 (21.3%) had HL, 42 (44.7%) were obese, 18 (19.1%) had nephrolithiasis, and 6 (6.4%) had urinary tract infection. Of the patients without a cyst, 272 (46.1%) had DM, 212 (35.9%) had HT, 122 (20.7%) had HL, and 96 (16.3%) were obese. HT and obesity were significantly higher in patients with a renal cyst when compared with those without a cyst. However, although HL incidence was higher in patients with a cyst, the difference was not significant statistically. HT, HL, and obesity are more prevalent in patients with a renal cyst when compared with patients without. Consequently, patients with a simple renal cyst should be evaluated and followed up in terms of atherosclerotic risk factors.
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PMID:Simple renal cyst prevalence in internal medicine department and concomitant diseases. 1653 73

Collectrin is a type I membrane protein and shares significant homology with C-terminal domain of angiotensin-converting enzyme-2 (ACE2). However, collectrin lacks catalytic domain and it suggests the presence of uncharacterized physiological functions of collectrin. Collectrin is transcriptionally regulated by hepatocyte nuclear factor-alpha and -beta and is highly expressed on renal proximal tubules and collecting ducts as well as pancreatic beta-cells. Recent in vitro and in vivo studies demonstrated interesting physiological roles of collectrin related to insulin secretion, formation of primary cilia, renal cyst formation and amino acid transport. The common underlying molecular mechanism may be suggested by the evidence that collectrin binds to SNARE complex by interacting with snapin. Collectrin is involved in the process of vesicle transport and membrane fusion and thus it delivers insulin for exocytosis or various membrane proteins to apical plasmalemma and primary cilia. Collectrin may be the new therapeutic target for various pathological processes such as diabetes, polycystic kidney disease, hypertension and aminoaciduria.
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PMID:Collectrin, a homologue of ACE2, its transcriptional control and functional perspectives. 1782 89


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