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)

A new genetic variant of the red cell enzyme glucose-6-phosphate dehydrogenase is described. It was observed in a patient presenting with severe haemolytic anaemia and renal failure following ingestion of an overdose of Beserol (paracetamol and chlormezanone). The enzyme in the red cell had 12% of the activity of a normal B+ control, but only slightly lower activity in the kidney compared with a normal control. The red cell enzyme showed normal electrophoretic mobility and thermostability, a biphasic pH optimum curve, higher than normal utilization of the substrate analogues 2-deoxy-glucose-6-phosphate and deamino-NADP, and lower than normal Michaelis constants for both substrates, glucose-6-phosphate and NADP. The enzyme was strongly inhibited in vitro by high concentrations of paracetamol and chlormezanone. The extent of inhibition was similar to that for the enzyme from a normal B+ individual.
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PMID:G6PD hillbrow: a new variant of glucose-6-phosphate dehydrogenase associated with drug-induced haemolytic anaemia. 120 Dec 17

The morphofunctional status of red blood cells was studied in patients with terminal renal failure associated with pyo-inflammatory complications treated by means of ultraviolet radiation of autologous blood. The authors have established that ultraviolet radiation of autologous blood results in the increase of the discocyte count and red blood cell activation, evidenced by the rise of the young red blood cell count, of the red blood cell population with marked activity of glucose 6-phosphate dehydrogenase, of the content of sulfhydryl groups, and by the increase of erythrocytic adhesion.
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PMID:[The effect of ultraviolet irradiation of patients' blood on the morphofunctional status of erythrocytes]. 259 70

Three patients with typhoid fever, initially misdiagnosed, developed intravascular haemolysis, disseminated intravascular coagulation, haemoglobinuria and acute renal failure. 2 of the patients were deficient in erythrocyte glucose-6-phosphate dehydrogenase; Plasmodium falciparum was present in the blood of the third. Among the indigenous population of endemic areas, typhoid fever is the likely diagnosis in any pyrexial illness associated with haemoglobinuric renal failure.
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PMID:Haemoglobinuric renal failure and typhoid fever. 323 92

The effects of sodium chlorate and of sodium nitrite on human erythrocytes were studied in vitro. Nitrite rapidly oxidised haemoglobin and glutathione; reduction of methaemoglobin (Hbi) by methylene blue was complete during 3 h of incubation with nitrite. With chlorate, a concentration-dependent lag phase was seen before Hbi was formed. After prolonged incubation, Hbi could no longer be reduced with methylene blue. Several other effects were observed that explain the clinical picture of chlorate poisoning which involves haemolysis followed by disseminated intravascular coagulation and renal failure: increased permeability to cations, increased resistance to hypotonic haemolysis and prolonged filtration time through polycarbonate membranes with cylindrical pores of 5 micron diameter. This suggests an increased membrane rigidity due to membrane protein polymerisation, as demonstrated by SDS polyacrylamide gel electrophoresis. Simultaneously, erythrocyte enzymes were inactivated, primarily glucose-6-phosphate dehydrogenase which is necessary for the therapeutic effect of methylene blue. This explains the inefficacy of methylene blue in the treatment of a case of chlorate poisoning that we observed (Arch. Toxicol., 48 (1981) 281).
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PMID:Erythrocyte membrane alterations as the basis of chlorate toxicity. 671 May 38

The presence of creatine, guanidinopropionic acid (GPA) and guanidinobutyric acid (GBA) was demonstrated in red blood cells from uremic patients; they were found only in trace amounts in red blood cells of normal controls. The levels of creatine, GPA and GBA in the red cell did not change during dialysis in contrast to the simultaneous decrease in plasma level. Both creatine and GPA inhibited glucose-6-phosphate dehydrogenase (G6PD) in vitro in physiological concentration, while creatine also activated erythrocyte transketolase (ETK). These effects are consistent with the low red cell G6PD level and high ETK activity that were observed in our uremic patients. The unchanging levels of creatine and GPA in the red cell despite hemodialysis may explain the continuing autohemolysis in otherwise adequately hemodialyzed end-stage renal failure patients.
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PMID:The toxicity of guanidino compounds in the red blood cell in uremia and the effects of hemodialysis. 711 Apr 71

We prospectively studied 50 Vietnamese patients with blackwater fever (BWF). All patients had fever and hemoglobinuria, 40 (80%) were jaundiced, 25 (50%) had hepatomegaly, 15 (34%) had splenomegaly, and 9 (18%) had hepatosplenomegaly. Twenty-one patients (42%) had impaired renal function, with creatinine clearances of < 50 mL/min/m2; however, only four (8%) developed oliguric renal failure, three (6%) of whom required dialysis. Forty-four patients (88%) developed anemia, which was severe (hematocrit, < 20% in 32 (64%). One patient died, representing a death rate for this once-feared disease that is considerably lower than that reported by earlier investigators. BWF was associated with quinine ingestion in 28 patients (56%), glucose-6-phosphate dehydrogenase (G6PD) deficiency in 27 (54%), and concurrent malaria infection in 16 (32%). There was no statistically significant difference in the severity of BWF associated with each of these three factors, as assessed by creatinine clearance and the hematocrit value on admission and by the number of units of blood transfused. There was considerable overlap in the occurrence of G6PD deficiency, quinine ingestion, and malaria, suggesting that these factors may interact and that it may not be justifiable to regard hemoglobinuria caused by G6PD deficiency as a separate syndrome.
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PMID:Blackwater fever in southern Vietnam: a prospective descriptive study of 50 cases. 940 15

Haemolytic anaemia as a complication of acute hepatitis has been reported in up to 23% of patients. However, the incidence may rise up to 70-87% in patients who have glucose-6-phosphate dehydrogenase (G6PD) deficiency. Massive intravascular haemolysis with renal failure, hepatic encephalopathy and even death have been reported. In our retrospective study of patients with acute viral hepatitis, the overall incidence of acute haemolysis was 4% (17/434). Only 53% (9/17) of them had G6PD deficiency. Patients with acute haemolysis had a significantly higher peak bilirubin level and required more prolonged hospitalization. Since hepatitis A virus vaccination, unlike hepatitis B virus vaccination, is not yet recommended for routine immunization, we suggest subjects who are G6PD-deficient should be vaccinated against hepatitis A. In endemic areas of hepatitis A virus infection, universal immunization remains the definitive answer.
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PMID:Haemolysis complicating acute viral hepatitis in patients with normal or deficient glucose-6-phosphate dehydrogenase activity. 957 32

Hypercholesterolemia plays an important role in the lipid abnormalities in chronic renal failure (CRF). It is thought to contribute to both a progression of renal failure and atherosclerosis. Despite intensive research, the etiopathogenesis of hypercholesterolemia in CRF patients is still obscure. The present study was designed to evaluate the possible role of cholesterol overproduction in the development of hypercholesterolemia associated with experimental CRF. We found that plasma total cholesterol and cholesterol distributed in VLDL, LDL and HDL concentrations were significantly enhanced in CRF rats. Simultaneously, the rate of liver cholesterol biosynthesis in vivo (measured by determining the incorporation of tritium from tritiated water intraperitoneally injected into cholesterol ), liver microsomal 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activity and liver HMG-CoA reductase mRNA presence were elevated. Significant increases in activity of liver malic enzyme, glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase, NADPH-producing enzyme (required for cholesterol synthesis) have also been observed in CRF rats. In conclusion, the increased rate of liver cholesterol biosynthesis due to increase of HMG-CoA reductase and NADPH-producing enzyme gene expression could be one of the possible causes of hypercholesterolemia in CRF animals.
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PMID:Increased rate of cholesterologenesis--a possible cause of hypercholesterolemia in experimental chronic renal failure in rats. 1206 35

Eighty nine males aged 1-13 years diagnosed with dengue haemorrhagic fever (DHF) and admitted to the Department of Pediatrics Siriraj Hospital from March 1998 to April 2000 were included in this study. 17 cases (19.1%) had red blood cell glucose-6-phosphate dehydrogenase (G-6-PD) deficiency and 72 cases (80.9%) had normal G-6-PD enzyme activities. Most of the patients were classified as DHF grade II in severity. 3 of 17 G-6-PD deficient cases had serious complications and all of them had acute intravascular hemolysis requiring blood transfusions. One of these also had hematemesis, one had azothemia and the other one had renal failure and severe liver failure with hepatic encephalopathy. In the cases without obvious hemolytic or hepatic complications, G-6-PD deficient cases had mildly but significantly higher total birirubin and indirect bilirubin, as well as a lower hematocrit than those who had normal G-6-PD. Reticulocyte count was low during the acute phase, however, during recovery, the levels were significantly increased in both groups. In the non G-6-PD deficient group, G-6-PD enzyme levels were significantly decreased during the acute phase compared to the normal controls but rose significantly to normal levels during the recovery phase. There were no statistically significant differences in other laboratory data. All patients recovered fully from DHF. The prevalence of G-6-PD deficiency in male patients who had DHF in this study was 19.1 per cent which was higher than the prevalence in a previous study of 12 per cent in Bangkok. This may imply that G-6-PD deficient males suffer more from DHF compared to normal G-6-PD subjects.
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PMID:Effect of red blood cell glucose-6-phosphate dehydrogenase deficiency on patients with dengue hemorrhagic fever. 1240 28

Lipid disorders are one of the known metabolic changes associated with chronic renal failure (CRF) [1, 2]. They are present as: hypertriglyceridemia--existed in 60% of CRF patients and hypercholesterolemia observed in 20-30% of people with this syndrome. These disorders, what was shown also in our own studies, are existing in different intensity in patients treated with maintenance haemodialysis [3], peritoneal dialysis [4] and after renal transplantation as well [5]. Mechanism of hypertriglyceridemia, despite over thirty years of studies, is still not finally elucidated. The opinion that it is a result of impaired triglyceride removal (due to decreased activities of both lipoprotein and hepatic lipases) is well documented, however the role of lipogenesis in its development is obscure [6, 7]. The reports concerning this problem contain contradictory data. In our studies performed several years ago we have shown that lipogenesis rate in white adipose tissue of uremic rats is significantly augmented [8, 9, 10] due to activation of free fatty acid synthase. Therefore, recently we paid once again our attention on the activity of this lipogenesis rate limiting enzyme responsible for the long term regulation. We measured its activity, protein abundance and mRNA level in liver and epididymal white adipose tissue of rats with surgically induced renal failure (two-stage subtotal nephrectomy). The results support the thesis that lipogenesis takes a part in a hypertriglyceridemia found in renal failure. There have been observed a significant increase in plasma triglyceride and VLDL concentrations in uremic animals and it was associated with the increase of FAS activity, FAS protein abundance and FAS mRNA. The results were similar in both studied tissues. Moreover, there have been also observed the increased activities of malic enzyme, glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase. All these enzymes participate in NADPH production, which is a necessary substrate for fatty acid biosynthesis [11, 12, 13]. Concluding, it appears that the rise in plasma triglyceride and VLDL concentrations observed in CRF rats is not only the result of increased liver and white adipose tissue lipogenesis rate. One has to remember, that these date are strictly original and enabling to elucidation further pathogenesis of hyperlipidemia in CRF. In the second set of experiments performed also in rats with experimentally induced CRF we have found that hypercholesterolemia observed in those animals is dependent on the significant activation of cholesterol synthase, induced by increased production of this enzyme (increment of protein abundance and synthase mRNA [14, 15]. Simultaneously, we have performed original studies on the diurnal rhythm of cholesterologenesis, showing that activity of this process is significantly augmented during whole twenty four hours [15]. Summarizing, one have to underline that our observations have important impact to the elucidation of lipid disturbances pathomechanism. Nevertheless further studies are necessary to establish how experimental data are corresponding with human pathology.
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PMID:[Pathomechanism of hyperlipoproteinemia in chronic renal failure]. 1497 58


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