Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Living renal transplantation (Tx) was carried out on a 41-year-old male undergoing hemodialysis for a six-month period because of end-stage renal failure due to chronic glomerulonephritis. Tacrolimus (FK 506) was used as one of immunosuppressants. The graft worked immediately after Tx. However, his blood sugar level rose extremely high and use of insulin (IS) was required. At the second postoperative day, 0.3 mg/kg/day of FK506 was administered and the trough level (TL) was as high as 65 ng/ml. The serum IS level decreased from the pre-Tx value of 22 microU/ml to 12 microU/ml. With decrease in the dose of FK506, the TL was normalized, and the dose of IS could be decreased. FK506 has been reported to inhibit IS secretion. Therefore, we must be careful to evaluate the blood glucose level in the use of FK506 for patients with poor glucose tolerance.
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PMID:[A case of tacrolimus-induced glucose intolerance following renal allografting]. 754 64

Three etiologies of renal disease account for more than 80% of Medicare-supported (U.S. Federal Government sponsored) end-stage renal disease (ESRD) cases: diabetes mellitus, hypertension and chronic glomerulonephritis. Surprisingly, despite improvements in medical care, their incidence is increasing rapidly in many parts of the world. With the exception of autosomal dominant adult polycystic kidney disease, the DNA polymorphisms causing progressive renal failure in individuals with common diseases have not yet been identified. Although hypertension and diabetes mellitus are associated with ESRD, the majority of patients with these disorders never develop nephropathy. There is abundant evidence that both inherited factors and the environment affect the development of ESRD. Predisposition to nephropathy may be inherited independently from the environmental and hereditary components that produce the associated systemic disease. This review examines the evidence that ESRD results, in part, from inherited factors. It discusses the racially variable risk of renal disease, the familial clustering of ESRD and molecular genetic data in animals and humans with renal failure.
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PMID:The role of genetic factors in the development of end-stage renal disease. 764 17

Endogenous nitric oxide (EDRF) plays an important role in the regulation of systemic and renal blood pressure by an alteration of vascular tone. To assess the effect of L-arginine (160 mumol/min i.v. for 3 hours), the precursor of EDRF, on blood pressure, protein-excretion and renal function (GFR = glomerular filtration rate, RPF = renal plasma flow) we performed a prospective, double blind, placebo controlled study. 18 patients with chronic glomerulonephritis (51.3 +/- 11.5 years), renal insufficiency (GFR < 65 ml/min) and hypertension were investigated for changes in GFR and RPF by continuous inulin- and PAH-clearances and for changes in permselectivity by determination of protein-excretion. L-arginine infusion results in a reduction of proteinuria (p < 0.05, t-test). There is no significant effect on renal hemodynamics and mean arterial pressure (MAP). Comparing the excretion of the endogenous proteins, only albuminuria is decreased significantly (p < 0.01), whereas IgG-excretion is reduced slightly (p < 0.05). This can be considered as an indicator of a special influence on the mesangial cells or the basement membrane of the glomerulum itself by EDRF. In conclusion L-arginine reduces protein-excretion without significant alterations in renal hemodynamics and so might prevent a decline in renal failure.
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PMID:Does L-arginine alter proteinuria and renal hemodynamics in patients with chronic glomerulonephritis and hypertension? 778 Dec 5

A strong familial clustering of ESRD has been reported among African Americans, suggesting that factors predisposing to renal failure, whether genetic, environmental, or both, may disproportionately affect certain families. A case-control study was undertaken to determine if a familial risk of ESRD was present among white Americans, if this risk differed among causes of ESRD, and if variability in age at onset was attributed to familial factors. Data were obtained from 103 white American patients (cases) with ESRD receiving dialysis treatments at the Bowman Gray School of Medicine's affiliated dialysis facility in Winston-Salem, NC. One hundred three age-, sex- and race-matched non-ESRD controls were consecutively selected from the Wake Forest University Physicians internal medicine clinic. Odds ratios (OR) and associated 95% confidence intervals (CI) were calculated to signify the prevalence of a relative with ESRD among cases versus controls. The presence of either a first- or second-degree relative increased a white American's risk for developing ESRD nearly threefold (OR = 2.7, 95% CI 1.1 to 7.2; P = 0.038), whereas the presence of either a first-, second- or third-degree relative with ESRD increased the risk nearly fourfold (OR = 3.5, 95% CI 1.5 to 8.4; P = 0.004). Cases with chronic glomerulonephritis and Type II diabetic nephropathy as the cause of ESRD had relatives with ESRD more often than cases with Type I diabetic nephropathy, interstitial nephritis, or renal artery stenosis. The average correlation (f) of ages at onset of ESRD among individuals in a single family (cases and their relatives) was 55%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Familial risk, age at onset, and cause of end-stage renal disease in white Americans. 778 48

A 5-year prospective study of 699 children with various renal disorders from around the Rivers State, which is in the eastern part of Nigeria, was carried out to investigate the prevalence and significance of renal disorders in a third world country with no facilities for paediatric dialysis and transplantation. Renal disorders accounted for 1.1% of the total outpatients and hospital admissions. The commonest renal disorders were urinary tract infection (UTI, 68.9%); nephrotic syndrome (NS 14.6%) and acute post streptococcal glomerulonephritis (11.4%). Patients with UTI had no vesico-ureteric reflux (VUR); 22.5% of NS patients were steroid sensitive. Wilms' tumour (1.6%) was the second commonest childhood malignant tumour; 8 of 17 cases of obstructive uropathy were secondary to meatal stenosis following circumcision. Fifteen children developed end-stage renal failure (ESRF), mainly due to chronic glomerulonephritis, giving a prevalence rate of 7.5 children per year per million childhood population. Hence, renal disorders are common in Nigeria and although VUR is rare, ESRF may approximate figures seen in the western world. This highlights the need to improve the country's socioeconomic conditions, make medical facilities more available to children and prevent renal diseases that may lead to ESRF.
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PMID:Renal disorders in children: a Nigerian study. 757 26

The authors present a case report of a 62-year old woman, with hypertension for many years. She suffered from weakness, anorexia and weight loss in the last 6 months. On admission, anemia, elevated ESR, haematuria, proteinuria and renal failure were present. Renal biopsy was compatible with chronic glomerulonephritis. The clinical picture and positivity for P-ANCA suggested systemic vasculitis. Later evidence of maxillary sinusitis and nasal mucosae ulcers as well as pneumonitis, although biopsy did not reveal granulomas, suggested the diagnosis of Wegener Vasculitis. Medicated with Cyclophosphamide and Prednisolone, for a year, with improvement. The authors make a brief discussion of the clinical criteria for classification of ANCA-associated systemic vasculitis.
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PMID:[Vasculitis associated with ANCA]. 794 37

IgA nephropathy (IgAN) is the most common chronic glomerulonephritis of unknown cause. Two factors are important in the pathogenesis of IgAN; one is IgA immune complex (IgA-IC) formation and the other is IgA-IC deposition to mesangium. For the formation of IgA-IC, antibody of IgA class, T-cells which help the generation of IgA antibody, and antigen are necessary. The serum IgA level in patients with IgAN is elevated probably due not only to the activation of B-cell but also to the hyperactivity of alpha beta chain positive T-cells. Analysis of the immunoglobulin gene of IgAN patients indicated that the genetic polymorphism could be correlated with the production of IgA antibody. The gamma delta chain positive T-cell may play some role for the formation of IgA-IC. Food, bacteria, viral proteins are reported to be the antigens of IgA-IC. Regarding to IgA-IC deposition, cytokines from T-cells and the molecular weight of IgA-IC are also indispensable factors. Clinically, long-term prognosis of IgAN are not unanimously the same. Approximately 15% patients progress to renal failure over a period of 10 years, and 25% to renal failure within 20 years. Roughly, patients can be classified into three groups in view of clinical course. First group maintains stable renal function for more than 20 years, second exhibits progressive course in more than 20 years and third progresses more rapidly than the second. Although the exact mechanism(s) governing the fate of renal function in IgAN is unclear, non-immunological factors, such as intraglomerular hypertension, are presumed to participate in its progression.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pathogenesis and therapy of IgA nephropathy]. 808 68

We present a 57-year-old man with end-stage renal failure due to chronic glomerulonephritis, who had been on hemodialysis for 13.5 years and had suffered from recurrent painful swelling of the left leg for 4.7 years. A diagnosis of deep venous thrombosis was made by the phlebography. Coagulation studies showed decreased protein C activity despite a normal protein C antigen level. None of his relatives had decreased protein C activity, and the levels of the other coagulation factors synthesized by the liver were all normal. Accordingly, the patient was diagnosed as having acquired type II protein C deficiency.
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PMID:Acquired type II protein C deficiency in a long-term hemodialysis patient. 819 Jan 90

Prednisone withdrawal was attempted in 121 of 915 renal transplants recipients between 1967 to 1992. There were 57 males, 64 females. Age range was 21 to 62 (mean 39.2 years). Etiology of renal failure was chronic glomerulonephritis (54), diabetic nephropathy (36), interstitial disease (17), hypertensive nephrosclerosis (6), and other (8). Kidney source was from HLA-identical living-related donors (LRD) in 54 (Group I), one haplotype-matched LRD in 23 (Group II), and cadaver in 44 (Group III). Prior to the introduction of cyclosporin A (CsA) in 1984, prednisone withdrawal was attempted only in Group I. After 1984, prednisone withdrawal was also attempted in patients in Groups II and III, selected on the basis of having had no rejection episodes during the six months after transplantation. Forty-five patients in Group I were treated with azathioprine (Aza) and prednisone, and the remaining patients in Groups I to III were treated with Aza, prednisone and CsA. Mean follow-up was 93 months (6 to 207). Prednisone was gradually tapered and withdrawn in 94 of 121 patients after a mean period of 22.5 months (9 to 60). In 27 other patients, the prednisone dosage has been tapered to 5 mg/day or less with the aim of discontinuing the drug. There were seven episodes of acute rejection (3 during taper, and 1 each at 6, 7, 24 and 114 months after prednisone withdrawal); all seven were successfully reversed. Four other patients developed chronic vascular rejection (2 during taper and 2 after withdrawal).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prednisone withdrawal in HLA identical and one haplotype-matched live-related donor and cadaver renal transplant recipients. 824 66

We report our experience with 3 uraemic patients who were found to have transitional cell carcinoma of the renal pelvis, ureter and urinary bladder after undergoing haemodialysis for an average of 18 months (range 11-28). The underlying causes of renal failure were chronic glomerulonephritis or pyelonephritis. Bloody urethral discharge was the cardinal symptom. Because of anuria, it was often discovered at a late stage. In spite of their poor general condition and advanced stage, palliative surgical intervention was still performed. After a mean follow-up of 9 months, progression of disease was noted in 1 patient. The importance of regular follow-up in patients with end-stage renal disease for early detection of concomitant cancer cannot be over-emphasised. Uraemic patients with urothelial cancer should be treated in the same way as non-uraemic patients, since aggressive surgical intervention may improve their quality of life and prolong their survival.
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PMID:Uraemia with concomitant urothelial cancer. 826 4


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