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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension and diabetes mellitus are strongly associated conditions from epidemiologic, genetic, and pathophysiologic points of view. The prevalence of hypertension is high in patients with diabetes, and, conversely, many patients with essential hypertension are glucose intolerant. Proteinuria appears in 40-50% of patients with insulin-dependent diabetes mellitus and 20-30% of patients with non-insulin-dependent diabetes mellitus. Progressive renal failure occurs in 30-40 and 3-8% of patients, respectively, hypertension being a leading factor in its rate of progression. In various animal experiments, ACE inhibitors are able to prevent proteinuria and glomerular sclerosis, presumably by lowering transglomerular capillary pressure. In the diabetic human, ACE inhibitors are powerful antihypertensive drugs, devoid of metabolic side effects. Clinical studies indicate that ACE inhibitors reduce proteinuria and possibly slow the rate of decline in renal function. Such an effect is not observed with beta-blockers. Large-scale studies are needed to confirm this very important hypothesis.
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PMID:Angiotensin-converting enzyme inhibition and diabetic nephropathy. 138 63

In 1992, transplantation of the endocrine pancreas is placed at the interface between laboratory research and clinical medicine. Unlike other forms of transplantation, it is not life saving, and yet its potential to treat all patients with insulin dependent diabetes is limited only by the availability of donated organs. Arguably, the long term glucose homoeostasis provided by vascularised pancreas transplantation is the standard by which other forms of endocrine pancreas transplantation (islet cell, fetal islet, and xenogeneic transplantation) must be judged. For the small number of type I diabetic Australians who develop end-stage renal failure and would otherwise require a renal transplant, the combined transplant procedure is a technically viable treatment option and, with some justification, the treatment of choice.
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PMID:Transplantation of the endocrine pancreas in 1992. 140 13

The acute effect of amino acid based dialysis solution on peritoneal kinetics of amino acids and plasma proteins in comparison to conventional glucose-based dialysate was studied in 9 patients with end-stage renal failure on continuous ambulatory peritoneal dialysis. Instillation of 2.6% amino acid solution resulted in raised plasma concentrations of all essential amino acids included in the dialysis fluid (p less than 0.005). The amino acid solution induced an augmented leakage of plasma proteins into the dialysate at all dwell times investigated (1-8 h). After a dwell time at 8 h, the dialysate total protein increased from 2.62 +/- 0.45 g with glucose dialysate to 3.85 +/- 0.42 g with amino acid solution (p less than 0.05). Corresponding results were obtained for beta 2-microglobulin, albumin, transferrin, IgG, and for the non-essential amino acids alanine, citrulline, and glutamine (p less than 0.025) not included in the initial amino acid composition of the dialysis fluid. During the use of amino acid based dialysis fluid, the effluent prostaglandin E2 concentration increased by more than 80% in comparison to glucose dialysate (p less than 0.025). The augmented loss of proteins induced by the amino acid solution was positively correlated with increased dialysate prostaglandin E2 (r = 0.8894; p less than 0.001). Peritoneal ultrafiltration was not affected by the use of amino acid based dialysate fluid. The present results indicate that amino acid based dialysis fluid enhances the peritoneal permeability for plasma proteins and amino acids, probably mediated by locally generated prostanoids.
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PMID:Effect of amino acid based dialysis solution on peritoneal permeability and prostanoid generation in patients undergoing continuous ambulatory peritoneal dialysis. 141 67

Our studies aimed at determining a loss of active heparin from the peritoneal cavity after its intraperitoneal administration (250 JU/l of dialysis fluid) in 16 patients treated because of the end-stage renal failure with intermittent peritoneal dialysis and at comparing heparin influx clearance with that of glucose. It has been shown that heparin used in this dose loses 60-70% of its activity after 20-minute equilibration of dialysis fluid in the peritoneal cavity. Heparin influx clearance is higher than that of glucose but it depends on utilization of heparin in peritoneal cavity rather than on its penetration to the blood circulation.
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PMID:[Evaluation of loss of active heparin in the peritoneal cavity during intermittent peritoneal dialysis]. 143 98

Uremic hyperlipidemia was recently suggested to contribute to progression of chronic renal failure (CRF). To investigate the relationship between lipoprotein abnormalities and decline of renal function, plasma lipids with apoproteins A1, B, E, CII, CIII, CII/CIII and E/CIII ratios, parathyroid hormone (PTH), insulin and glucose levels were examined in 72 patients with different degrees of CRF and compared to 28 patients of a reference group. A significant decrease of CII/CIII ratio was already evident below a Ccr of 60 ml/min, while increased apo-CIII and triglycerides (TG) with reduced HDL-cholesterol (HDL-C) levels occurred below a Ccr of 30 ml/min. Both TG and apo-CIII showed a positive correlation with creatinine levels. On the contrary, apo-CII/apo-CIII and HDL-C inversely correlated with the progression of renal failure. PTH and insulin showed a positive correlation with TG, the former being also inversely related to apo-CII/apo-CIII ratio. Our results point to early apolipoprotein changes in the course of CRF. Elevated apo-CIII and reduced apo-CII/apo-CIII ratio may be considered the most typical features of uremic hyperlipidemia and likely account for the impaired TG removal and the hypertriglyceridemia (HTG). Secondary hyperparathyroidism may contribute to reduce peripheral lipolytic activity and cause HTG. A contributory role of hyperlipidemia in the progression of renal disease is also supported.
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PMID:Lipids and apolipoproteins change during the progression of chronic renal failure. 145 39

The authors give an account of views regarding the use of non-glucose energy sources in parenteral nutrition during the immediate post-load period/serious operations, severe injuries). Attention is devoted to the metabolic pathway of fructose and its disorders. In hereditary fructose intolerance an infusion of D-fructose or D-glucitol (= sorbitol) can induce life threatening hypoglycaemia (unless glucose is administered concurrently). According to some views, in subjects with this intolerance the organism is threatened also by hepatic and renal failure; their development may be independent on hypoglycaemia. Fructose and D-glucitol (sorbitol) therefore should not be administered by the parenteral route. This view is supported by cases where hereditary fructose intolerance could not be revealed from the case-history and clinical manifestations. Some countries have already eliminated fructose and D-glucitol (sorbitol) from their pharmacopoeias.
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PMID:[Fructose metabolism disorders and infusions]. 145 66

The renin-aldosterone system and plasma insulin were studied in 19 patients with familial Mediterranean fever (FMF). Their relationships to serum potassium level at rest and before and after oral glucose loading are described. An interesting finding is the occurrence of hyperkalemia in the absence of oliguria, in the advanced stages of renal failure. No differences were found in the activity of the renin-angiotensin-aldosterone system to explain these variations in serum potassium found in some of the patients. The response of the renin-aldosterone system to glucose loading showed no abnormality, and the regular relationship between serum potassium, plasma renin activity (PRA), aldosterone, insulin, and plasma pH is maintained. Levels of insulin, potassium, and bicarbonate in serum or plasma pH were found similar in FMF patients with normal renal function with and without proteinuria. Further decrease in renal function due to the progression of the underlying disease is manifested by an increase in FENa+ and FEK+ and a hyperchloremic metabolic acidosis, as is the case in other patients with chronic renal failure.
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PMID:Normal renin-aldosterone-insulin and potassium interrelationship in FMF patients and amyloid nephropathy. 146 7

We analyzed the overall results of 24 simultaneous pancreas and kidney transplantations (SPK), performed in our hospital between April 1986 and June 1990. All patients had type I diabetes mellitus and end-stage renal failure. We used bladder drainage of the pancreatic exocrine secretions through a duodenocystostomy. The blood vessels of both grafts were anastomosed to the iliac vessels. The immunosuppressive management was triple-therapy with cyclosporin, azathioprine and prednisone. All organs were transplanted without matching donors and recipients for HLA. At the time of transplantation, mean recipient age was 37 yr; the average duration of diabetes was 22 yr. After disappointing results in the first 4 patients, the pancreas was placed intraperitoneally instead of extraperitoneally and the antibiotic drug regimen was altered. In the second group (n = 20), patient survival was 100%; 1-yr pancreas and kidney graft survival were 65 and 62%, respectively. Duration of hospitalization and pancreas and kidney graft loss were positively correlated with the number of rejection episodes. After 1 yr of follow-up, the mean creatinine clearance was 62 ml/min and the mean HbA1c was 5.5%. Blood glucose levels and oral glucose tolerance tests were also normal. We conclude that patient and graft survival after SPK are satisfactory, although rejection-related morbidity is still a major problem.
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PMID:Simultaneous pancreas and kidney transplantation: a feasible procedure in selected patients. 149 98

Glomerular hyperfiltration and hypertension induced by extensive loss of renal parenchyma are suspected to accelerate progression of renal failure. Amino acid infusion or protein ingestion also modify renal hemodynamics and increase glomerular filtration rate (GFR). This phenomenon was used to study the influence of two commonly used antihypertensive agents, captopril and nifedipine, on renal hemodynamics at rest and during glomerular hyperfiltration. Thirteen healthy volunteers were studied on three separate days (days A, B, and C) in random sequence: inulin and p-amino hippurate (PAH) clearance were measured first under glucose infusion and afterwards under stimulation by amino acid infusion (0.35 mmol/kg/min; 4 mg/kg/min). Day A served as a control, where no medication was given. On day B, 10 mg nifedipine, and on day C, 25 mg captopril, were administered orally before study. Without premedication (= day A, control) GFR increased from 108.0 +/- 6.9 mL/min (SEM) to 131.7 +/- 7.0 mL/min (P less than 0.05). On day B (nifedipine), GFR before stimulation by amino acids was already elevated to 121.8 +/- 4.2 mL/min (P less than 0.05 compared with day A) and increased to 132.6 +/- 6.3 mL/min with infusion of amino acids, thus to the same range as on day A without medication. On day C, after captopril, GFR did not increase with infusion of amino acids (from 112.5 +/- 7.2 to 117.3 +/- 6.3 mL/min). Our results indicate the calcium channel antagonist nifedipine and the angiotensin-converting enzyme (ACE) inhibitor captopril differ in their effect on intrarenal hemodynamic parameters. Nifedipine induces hyperfiltration at rest and allows maximal hyperfiltration to develop under amino acid infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of nifedipine and captopril on glomerular hyperfiltration in normotensive man. 149 65

Patients with renal failure are highly susceptible to infection, in part because uremia decreases the killing capacity of phagocytic leucocytes. Phagocytosis-associated respiratory burst activity was investigated at different stages of renal impairment by measuring the 14CO2 production during metabolism of labeled glucose by phagocytic cells. Non-dialyzed end-stage renal failure and haemodialysis patients showed a decrease in phagocytosis to about 50% of normal (p less than 0.05). In a second phase of the study, six haemodialysis patients received 2 g cefodizime (CDZ) i.v. after dialysis for ten days (five doses). Phagocytosis was determined at baseline and was followed until day 29. A clear, long-lasting stimulatory effect of CDZ on phagocytosis after both latex and zymosan challenge was found. It is concluded that a usual CDZ dosage regimen stimulates depressed phagocytosis in haemodialysis patients, and that this stimulatory effect persists for at least two weeks after the end of treatment. Uremic patients with infection may benefit from this additional property of CDZ.
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PMID:Cefodizime: enhancement of depressed phagocytosis-associated respiratory burst activity in chronic uremic patients. 152 84


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