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 examination of five pediatric patients with encephalopathy secondary to chronic renal failure has indicated a stereotyped sequence of neurologic signs and symptoms including ataxia, loss of motor abilities, myoclonus, seizures, dementia, and bulbar dysfunction. Both the patients with CNS dysfunction and a control group selected for a similar degree of renal failure had increased levels of serum phosphate, alkaline phosphatase, and parathyroid hormone. Serial EEGs in the affected group revealed progressive slowing and an increase in paroxysmal features. No specific neuropathologic findings were noted in one patient.
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PMID:Encephalopathy in infants and children with chronic renal disease. 729 12

In the Plymouth area, 95 patients with end-stage renal failure have undergone haemodialysis for 6 months or longer. Of the 47 patients beginning dialysis between 1967 and 1973, when water deionisers were not used routinely, a bone disease with multiple fractures, 'fracturing osteodystrophy', occurred in 18 patients and dialysis encephalopathy in 10. Of the 48 patients first dialysing between 1974 and 1979, when water deionisers used commonly, fracturing osteodystrophy occurred in only one and dialysis encephalopathy also in only one. Duration of dialysis without a water deioniser appeared to be the most important factor in the development of these two conditions. The use of water deionisers usually led to healing of fractures in patients with fracturing osteodystrophy and also led to improvement in 4 of the 11 patients with dialysis encephalopathy. Neither condition has occurred in any patient using a water deioniser from the first dialysis. Water deionisers, therefore, appeared to be effective in both the treatment and prevention of fracturing osteodystrophy and dialysis encephalopathy.
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PMID:Effect of water deionisers on 'fracturing osteodystrophy' and dialysis encephalopathy in Plymouth. 732 79

Three out of 140 patients with non-hodgkin's lymphoma treated in a Department of Internal Medicine showed hypercalcemia during their clinical course. Hypercalcemia was symptomatic in two patients causing renal failure in one of them and a metabolic encephalopathy in the other. In the third case hypercalcemia was a casual finding. Serum calcium levels varied between 14.8 and 16.6 mg/100 ml; serum phosphate and tubular reabsorption of phosphate were normal. Alkaline phosphatase were high in the three cases. Bone disease was present in two cases. Transient responses were obtained with the administration of prednisone and calcitonin associated to forced diuresis. Indomethacin was ineffective. Pathogenesis of hypercalcemia could be related to the release of an osteoclastic activator factor. The role of prostaglandins and the presence of PTH-like mechanisms were discarded in our cases by indirect methods. The poor prognosis of patients with non-hogkin's lymphoma and hypercalcemia in stressed.
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PMID:[Hipercalcemia and non-Hodgkin's lymphomas. Report of three patients (author's transl)]. 738 26

Some of the toxic and nutritional aspects of trace elements in patients with renal failure are reviewed. Data are presented that tend to disprove the hypothesis that aluminum poisoning alone is responsible for dialysis encephalopathy. Possible dietary restrictions imposed in uremic patients may impair iron, zinc, copper, manganese, or chromium nutritive.
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PMID:Trace elements in uremia and hemodialysis. 739 73

Aluminum levels were measured in a variety of tissues obtained from 36 control subjects, 30 nondialyzed uremic patients, 57 dialyzed uremic patients dying of a variety of different causes, and 38 dialyzed uremic patients dying of dialysis encephalopathy. The low aluminum levels consistently found in the control tissues support the fact that in health aluminum is largely excluded from the body. However, this ability to prevent aluminum accumulation is overcome with renal failure. Bone and liver aluminum levels were found to be significantly increased in 82% and 56% respectively in nondialyzed uremic patients and in 100% of the tissues examined from dialyzed uremic patients. In patients dying of dialysis encephalopathy, tissue aluminum levels were not only the highest but also affected in a different manner than that found in other dialyzed patients. It is suggested that dialysis encephalopathy occurs as a result of such rapid aluminum loading during dialysis that bone's ability to sequester this element is overcome, and it is shunted to liver and brain with resulting toxicity.
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PMID:Metabolism and toxicity of aluminum in renal failure. 739 74

Amoxapine is a second-generation tricyclic antidepressant structurally related to the neuroleptic loxapine. It was previously marketed as an alternative to traditional tricyclic antidepressants because of alleged shorter onset of action and fewer cardiotoxic effects. However, various adverse reactions, including cardiac dysrhythmias, renal failure, coma, seizures, and neuroleptic malignant syndrome, were reported during therapy or after acute overdose. A 14-year-old boy ingested 1900 mg of amoxapine and developed seizures, hypertension, hyperpyrexia, altered mental status, myoglobinuria, renal failure, and transient magnetic resonance imaging (MRI) changes suggestive of hypertensive encephalopathy and neuroleptic malignant syndrome. Since mitochondrial disorders can cause multisystem failure, including encephalopathy, renal tubular dysfunction, and myopathy, a transient, toxic disorder of mitochondrial function was considered as the basis for the patient's clinical and MRI changes.
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PMID:Amoxapine overdose in a young man: a transient mitochondrial abnormality? 747 9

Toxic Shock Syndrome (TSS) is a potentially fatal illness caused by a particular strain of Staphylococcus aureus. The clinical presentation is similar to that of septic shock. The incidence of TSS peaked in the late 1970s and early 1980s, probably as a result of availability of super absorbent tampons. Although most commonly associated with menstruation, the overall incidence of menstrual and nonmenstrual TSS in men and women ranges from 1 to 3 per 100,000. There are almost equal numbers of menstrual and nonmenstrual cases of TSS identified annually. S aureus, the causative microorganism in cases of TSS, has been isolated from many body tissues. Toxic shock syndrome presents as a flu-like illness with high fever, vomiting, diarrhea, general malaise, and muscle weakness. Nursing and medical management focus on controlling or preventing potentially serious complications, such as adult respiratory distress syndrome, renal failure, electrolyte imbalances, disseminated intravascular coagulation, encephalopathy, and cardiomyopathy. Judicious use of tampons and barrier contraceptive devices may decrease the risk of developing TSS.
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PMID:Toxic shock syndrome: an opportunity for nursing intervention. 865

Iatrogenic aluminium toxicity is reported in a patient who underwent an orthotopic liver transplant and who had concomitant renal failure requiring hemodialysis. Following transplantation the patient developed a metabolic encephalopathy with only mildly elevated blood ammonia concentrations. During the period following transplantation the patient received massive infusions of albumin and was on oral feeding (vivonexten), both of which contained aluminium, as did the dialysis fluid. Hyperaluminemia and profoundly elevated liver tissue aluminium concentrations were observed. Treatment with desferrioxamine, a trivalent ion chelator, decreased the plasma aluminium concentrations with an improvement in the patient's mental status.
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PMID:Hyperaluminemia associated with liver transplantation and acute renal failure. 757 38

The prognosis of acute renal failure in patients with preexisting liver decompensation is poor, and hemodialysis is considered futile, especially for hepatorenal syndrome (HRS). Since we observed a more favorable outcome in some patients, we retrospectively evaluated 107 patients with decompensated liver disease and acute renal failure (serum creatinine > 200 mumol/L) treated at the medical department of a university hospital in a 10-year period (1980-1990). HRS in the strict sense (urine-Na < 20 mmol/L while on furosemide) was diagnosed in 26 of 107 patients (24%). Renal function remained compensated in 25 patients, while 82 patients fulfilled the criteria for dialysis treatment (creatinine > 500 mumol/L and/or diuresis < 500 mL/day). In contrast to the current doctrine, 38 of the 82 patients were given hemodialysis (46%). Using the Cox proportional hazard model, the relative risk (presence vs. absence of a risk factor) of dying was increased 8.2-fold (3.9-17.2) in patients with thrombocytopenia < 100/nL, 3.9-fold (1.4-11.3) in those with hepatic encephalopathy and prothrombin time < 30%, 2.8-fold (1.6-4.8) in patients with malignoma, and 2.7-fold (1.5-4.8) in patients not submitted to dialysis despite its indication. In the CART statistics (classification and regression trees), the 33 patients with the poorest outcome were characterized exclusively by thrombocytopenia < 100/nL. HRS in the strict sense was not an independent risk factor. The CART group of 43 patients with favorable prognosis (compensated renal failure or treatment by hemodialysis, absent malignancy) had a 1-year survival rate of 38%. We conclude that thrombocytopenia, encephalopathy, and malignoma, but not HRS per se, are fatal signs that make hemodialysis futile in patients with acute renal failure and decompensated liver disease.
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PMID:Risk factors and outcome of 107 patients with decompensated liver disease and acute renal failure (including 26 patients with hepatorenal syndrome): the role of hemodialysis. 764 64

Racemic D,L-lactate has long been used in burn therapy as Ringer's lactate and in peritoneal dialysis fluid for treatment of renal failure. The D-lactate component of this racemic mixture is known to cause two forms of neurological toxicity in patients: encephalopathy and, in a subset of the population, panic reaction. Here we demonstrate that coma, similar in degree to that produced by blood levels of 75 mM ethanol was induced in rats by the intraperitoneal infusion of sodium D-lactate sufficient to raise serum D-lactate concentration to 25 mM, whereas infusion of equal quantities of sodium L-lactate produced no observable neurological effect. We further demonstrate that the intravenous infusion of racemic D,L-lactic acid into 48-hour fasted rats produced serious disturbances of cardiac rate and rhythm leading to death. When serum D-lactate concentration had reached 1-2 mM there was bradycardia, at 2-3 mM prolongation of QT interval, at 6-7 mM AV block with ectopic escape rhythms, and at 11 mM death in ventricular standstill or fibrillation. In contrast, intravenous infusion of L-lactic acid to blood levels of 25 mM failed to produce any change in cardiac rhythm. On the other hand, the isolated working heart, free of influence from the central nervous system, displayed no change of cardiac rhythm or physiological function when perfused with 25 mM sodium D,L-lactate.
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PMID:Neurocardiac toxicity of racemic D,L-lactate fluids. 769 35


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