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)

The concentration of free amino acids in the plasma and lumbar CSF of 11 patients with steady-state chronic renal failure has been measured and the CSF: plasma concentration ratios calculated. The results have been compared with the corresponding data from 37 control subjects. In renal failure, elevation of the mean plasma concentration of total amino acids and a reduction in the ratio of essential to total amino acids have been found. Whereas some individual plasma amino acid concentrations in renal failure were higher than normal, others were lower. Striking abnormalities of the CSF amino acid concentration have been observed. Some amino acids have shown similar patterns of abnormality in both CSF and plasma, whereas in the case of others, the changes have been restricted to either CSF or plasma. Significant variations from normal of the CSF: plasma concentration ratios were observed for four amino acids.
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PMID:Studies of cerebrospinal fluid and plasma amino acids in patients with steady-state chronic renal failure. 42 49

In seven patients with chronic renal failure in an advanced stage 17 episodes of upper abdominal pain, hypertension, vomiting and (in some of them) coma occurred during peritoneal dialysis with sorbitol-containing dialysate. The signs recurred in some of the patients but did not when glucose-containing dialysate of otherwise identical composition was used. Very high levels of sorbitol in CSF and serum were measured in the comatose patients. The precipitating factor is probably a reduced metabolic breakdown of sorbitol in renal failure with preferential intracellular deposition of sorbitol and subsequent cellular oedema. To avoid this dangerous reaction it is necessary to use glucose instead of sorbitol in peritoneal dialysates, despite the technical problems of sterilisation. Where this is not possible, glucose should be added in order to reduce the sorbitol concentration in the dialysate to less than 15g/l.
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PMID:[Severe side-effects during peritoneal dialysis caused by sorbitol-containing dialysate (author's transl)]. 114 25

110 cases of viral fever patients receiving Qing Wen oral liquid were observed. The total effective rate was 94.5% in comparing to 86.5% in the control group, P < 0.01. The shortening of time concerning both the beginning on the declining of fever and normalization of body temperature were obvious in comparison with the control. The remedy was also effective in improving symptoms and signs, alleviating renal failure, improving microcirculation and providing bi-directional regulation to the immune system, thus the progression of the disease was controlled. Animal experiments showed that Qing Wen oral liquid could protect the rabbits with hemorrhagic fever, delay the incubation period and the peak of fever, lower the febrile index and PGE content, improve the hemorheology and enhance the cell-mediated immunity in CSF.
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PMID:[Clinical and experimental study of qing wen oral liquid in the treatment of viral infectious fever]. 136 99

rhG-CSF (recombinant human granulocyte colony stimulating factor) promotes production and release of neutrophil from bone marrow, and it enhances neutrophil function. In this study, the pharmacokinetics, effects on neutrophil and immune functions and efficacy and safety of rhG-CSF were studied in patients with end-stage renal failure (CRF). To 9 patients with CRF; 2 patients on conservative therapy and 7 patients under regular hemodialysis, 50 micrograms/m2 rhG-CSF were administered intravenously under the schedule of single or 2 week consecutive injection. In single injection study, serial changes in plasma rhG-CSF concentration and peripheral blood cell count were examined following the administration. In consecutive injection study, plasma rhG-CSF concentration, anti-rhG-CSF antibody, peripheral blood cell counts, blood chemistry and coagulation factors, and neutrophil and immune functions were examined. As the results, 1) Half life of rhG-CSF, 2.87 +/- 0.65 hr, was about 2 times longer than that in healthy subjects, and it was not affected by hemodialysis treatment. 2) Marked increase in leukocyte and neutrophil counts and mild increase in lymphocyte count were observed during single and consecutive administration of rhG-CSF. There was no significant change in other leukocyte differentiations, RBC, or platelet count. 3) Neutrophil alkaline phosphatase score increased significantly during single and consecutive administration, and other neutrophil function also improved in several patients with impaired neutrophil function. 4) Slight bone pain and increase in serum alkaline phosphatase were observed in about a half of patients during consecutive injection study. Neither antibody nor accumulation of rhG-CSF was noted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effects and pharmacokinetics of rhG-CSF on the treatment of neutropenia in patients with renal failure]. 172 29

We measured methylmalonic acid, which accumulates in the blood and tissues of patients with cobalamin deficiency, in the CSF of 65 patients using capillary-gas chromatography and mass spectrometry. In 58 control patients, methylmalonic acid concentrations were always higher in CSF than in serum (mean CSF: serum ratio, 2.65; range, 1.17 to 7.78). In contrast, in six patients with elevated serum methylmalonic acid levels due to renal failure, CSF concentrations were normal in five and the CSF: serum ratio was less than one in four. In three patients with neuropsychiatric syndromes due to cobalamin deficiency and one patient with a normal serum cobalamin level who was an abuser of nitrous oxide, CSF concentrations were markedly increased (mean level, 600 times that of controls), out of proportion to those in the serum (mean CSF: serum ratio, 8.38; range, 3.5 to 13.5). The potential usefulness of CSF metabolite levels in the diagnosis of cobalamin deficiency is undetermined.
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PMID:Cerebrospinal fluid methylmalonic acid levels in normal subjects and patients with cobalamin deficiency. 192 6

1. A 43-year-old male developed acute kidney failure due to ethylene glycol poisoning. He was treated with bicarbonate to combat metabolic acidosis, ethanol as an antimetabolite and haemodialysis to remove the glycol and its toxic metabolites. He was kept on a respirator and sedated with morphine. Peritoneal dialysis was given for 36 d. Following sedation with morphine for 11 d, the patient was given naloxone and then extubated. The antidote had to be continued for 14 d to prevent respiratory depression, until kidney function improved. 2. Only morphine-6-glucuronide (M-6-G) was found in the plasma and CSF at concentrations which might explain the opioid effects observed in the patient during the days after the cessation of morphine treatment. The ratio of the area under the concentration-time curve (AUC) of morphine-3-glucuronide (M-3-G) to M-6-G was 2:1. The elimination half-lives of M-3-G and M-6-G were 55 and 82 h, respectively. The clearance data indicate that most of the glucuronides were eliminated by peritoneal dialysis during renal failure. 3. The data suggest that M-6-G exerts opioid effects and is retained in acute kidney failure. Morphine should therefore not be used preferentially as a sedative/analgesic in pronounced kidney failure.
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PMID:Morphine-6-glucuronide might mediate the prolonged opioid effect of morphine in acute renal failure. 226 Dec 46

ANF is an exciting, newly discovered hormone that has significant potential for furthering our understanding of the complex interactions involved in fluid and electrolyte balance. In addition to effects on water and salt balance, it is a potent vasodilator, as well as inhibitor of renin, angiotensin II, aldosterone, and vasopressin. ANF is primarily produced in the atria, but production in the brain is suggestive of action as a neuropeptide and as a potential regulator of CSF production. Receptors are found throughout the heart, vascular tree, kidney, adrenal gland, and brain. The stimulus for release appears to be atrial stretch, which may be secondary to intravascular fluid changes. It causes hemoconcentration and may be an important regulator of interstitial fluid distribution as well as capillary permeability. Patients with CHF and renal failure have been found to have elevated levels that decrease in response to treatment. Potentially, it may be useful as a therapeutic agent in acute renal failure, CHF and other fluid disturbances. ANF is a testament to the incredible advances in peptide biology. Within 2 years of the discovery, ANF was sequenced and cloned. Since that time, literally thousands of papers describing its actions have been published. Our knowledge about this hormone grows at an exponential rate. It is clear that this hormone is intimately involved in the regulation of fluid and electrolyte balance, vascular tone, and the pathophysiology of CHF but many questions remain unanswered. Continued research will provide many of the missing pieces to this very complex, new hormone system.
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PMID:Atrial natriuretic factor. 252 98

There are many reports on the disequilibrium syndrome due to dialysis in patients with chronic renal failure. However, they do not mention the findings of CT cisternography and MRI. We intend to investigate the mechanism of CSF dynamics in a patient with disequilibrium syndrome by means of these radiological examinations. A 31 year-old woman who had suffered from renal failure for 18 years was found to have prominent increase of serum creatinine (18.1 mg/dl) and BUN (127 mg/dl) 3 years ago. At that time, digital marking of the skull was already present by X-ray examination without other destruction in bone survey of the whole body. She was hemodialysed by the hollow fiber kidney three times weekly (dialysis time 4.5 hours, dialysate osmotic pressure 270 mOsm/kg H2O). Three months ago, she began to complain of severe headache, nausea and vomiting 2 hours after the beginning of dialysis, so that she was referred to Kosei Hospital. On admission, she showed exophthalmus, concentric narrowing of the visual field, optic atrophy and hyperreflexia in jaw and four extremities. After admission, she received hemodialysis therapy thrice weekly (dialysis time 5 hours, dialysate osmotic pressure 290 mOsm/kg H2O). At the same time, 200 ml of glycerol (contents of glycerin 10, fructose 5, NaCl 0.9%) was administered intravenously during dialysis, which ameliorated the symptoms of intracranial hypertension. Laboratory studies revealed marked decrease of serum creatinine, BUN and uric acid levels and osmotic pressure, and increase of blood pH at the time of postdialysis compared with predialysis. Manometric CSF pressure increased up to 310 mmH2O at the day without dialysis before the glycerol administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of chronic renal hemodialysis and intracranial hypertension--a study on CSF dynamics]. 276 3

The neurotoxic potential of benzylpenicillin administered as a continuous intravenous infusion was studied in rabbits with intact blood-CNS barriers, experimentally established Enterobacter cloacae meningitis and experimental renal failure, secondary to cephaloridine-induced acute tubular necrosis after iv administration. The concentrations of benzylpenicillin in serum, CSF and brain tissue fluid were assayed at the onset of epileptogenic electroencephalographic activity. The brain tissue concentrations of benzylpenicillin were consistently higher than those in CSF in both infected and uninfected animals. The highest brain tissue fluid concentrations of benzylpenicillin were found in rabbits with renal failure after cephaloridine pretreatment. The brain tissue fluid concentrations of benzylpenicillin rather than the CSF concentrations were decisive for neurotoxicity. Cephaloridine-induced uraemia, but not the combination of uraemia and meningitis, resulted in a significantly increased tolerance of high intracerebral concentrations of benzylpenicillin before EEG-changes were precipitated.
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PMID:Neurotoxicity of benzylpenicillin in experimental renal failure and Enterobacter cloacae meningitis. 279 45

The neurotoxic potential of intravenous administered benzylpenicillin (BPC) was studied in rabbits with intact blood-CNS barriers and rabbits with experimental E. coli meningitis. At onset of epileptogenic EEG activity or seizures, serum, CSF and brain tissue were collected for assay of BPC. Based on the fact that, in tissues, BPC seems to remain extracellularly, brain concentrations of BPC were expressed as brain tissue fluid (BTF) levels, calculated as 10x the concentration in whole brain tissue. Neurotoxicity could be precipitated in all rabbits. In normal rabbits BTF levels of BPC were considerably higher than those in CSF indicating a better penetration across the blood-brain barrier (BBB). BPC penetrated better to CSF and BTF in meningitic rabbits than in normal controls, suggesting some degree of damage of the BBB concomitant with meningeal inflammation. E. coli meningitis did not increase the neurotoxicity of BPC. In control rabbits the intracisternal injection of saline resulted in some degree of pleocytosis. Unmanipulated animals are therefore preferable as controls. Epileptogenic EEG-changes was the most precise of the two variables used for demonstration of neurotoxicity. EEG-changes were therefore used as neurotoxicity criterion in the following rabbit experiments. To evaluate the effect of uraemia alone and uraemia plus meningitis on the neurotoxity of BPC in rabbits, cephaloridine was used to induce uraemia. Meningitis was induced by intracisternal inoculation of a cephalosporin resistant strain of E. cloacae. Untreated rabbits were used as controls. Uraemia resulted in increased BTF penetration of BPC, possibly explained by permeability changes in the BBB and/or decreased binding of BPC to albumin. Uraemia did not result in increased penetration of BPC into the CSF of non-meningitic rabbits. Uraemic non-meningitic rabbits had the highest BTF levels of BPC at the criterion, indicating that cephaloridine-induced renal failure increased the epileptogenic threshold in these rabbits. The combination of uraemia and meningitis increased the neurotoxicity of BPC since the criterion was reached at considerably lower BTF levels of BPC. Meningitis, either alone or together with uraemia, did not increase the neurotoxicity in comparison to control rabbits. Higher BTF levels of BPC were found in meningitic rabbits than in controls with intact blood-CNS barriers at onset of EEG-changes. In all groups of rabbits there was a pronounced variability of BPC levels in the CSF while the intra-group variations in BTF levels were much smaller. Thus, BTF and not CSF levels were decisive for the neurotoxicity of BPC.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurotoxicity of beta-lactam antibiotics. Experimental kinetic and neurophysiological studies. 324 57


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