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)

There were 122 deaths among 803 children registered, randomized, and followed in the second National Wilms' Tumor Study; 17 occurred in children apparently free of disease and were attributable to causes other than tumor progression. Seven deaths were attributed to infection during periods of drug-induced leukopenia; four were due to liver failure; and one each was attributable to radiation pneumonopathy, intestinal obstruction, renal failure, myocardial disease, and encephalopathy. The cause of one death was unexplained. Of particular concern were four (of 47) infants under one year of age with group I or II disease who had toxic deaths. Subsequent to these experiences the doses of all chemotherapeutic agents were reduced by 50% for infants under one year of age. No deaths from toxicity were observed thereafter in infants. An analysis of the therapeutic effect of this dose reduction showed three of 47 relapsed on full dose and five of 54 on half dose. The difference is not statistically significant. This report is a further demonstration of the potentially serious vulnerability of infants to standard doses of anticancer drugs even when they are calculated on a per kilogram basis.
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PMID:Toxic deaths in the Second National Wilms' Tumor Study. 608 9

Twelve scleroderma patients with hypertension, seven of whom had malignant hypertension and renal failure of scleroderma renal crisis, were treated with captopril. The first dose lowered mean pressure in all patients by 21.3 mmHg; in 6 patients it relieved encephalopathy. Blood pressure was controlled in all patients. Two of 7 patients with scleroderma renal crisis had improvement in renal function; the 5 patients who did not have malignant hypertension improved or stabilized. Despite good pressure control, however, renal failure developed in 5 patients with scleroderma renal crisis. The data indicated that captopril is effective antihypertensive therapy in scleroderma and, when given early, may prevent renal failure and death.
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PMID:Variable response to oral angiotensin-converting-enzyme blockade in hypertensive scleroderma patients. 627 17

Antacid ingestion may lead to side-effects related to their chemical composition. Aluminum hydroxide may cause the phosphate depletion syndrome even during short-term administration of high doses in patients at high risk, such as alcoholics. Long-term intake may lead to bone demineralization and to osteomalacia. Fluoride complexing in the gut and prevention of fluoride absorption may be an additional factor. The clinical relevance of aluminum absorption in patients with normal renal function is not clear. In contrast, in patients with renal failure, aluminum hydroxide ingestion may contribute to an increasing hyperaluminemia. Hyperaluminemia and tissue deposition of aluminum in these patients may contribute to the dialysis-associated encephalopathy. Magnesium hydroxide causes an alkalinization of the urine due to magnesium absorption and urinary excretion. Thus, in renal insufficiency, a life-threatening hypermagnesemia may develop if magnesium-aluminum-containing antacids are prescribed. The milk-alkali syndrome, rarely observed nowadays, may be caused by calcium carbonate- and sodium bicarbonate-containing antacids. Hypercalciuria and alkaluria predispose to nephrolithiasis. The possibility that these disturbances in mineral metabolism will develop in patients with normal renal function is unlikely unless there is an abuse of these "over the counter" antacids.
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PMID:Antacid therapy--changes in mineral metabolism. 629 43

In 9 patients undergoing chronic hemodialysis for 2-10 years and suffering from encephalopathy (dialysis dementia) and peripheral neuropathy, 10 mg of biotin was given daily in three doses for 1-4 years. Within 3 months there was a marked improvement in all patients in respect to disorientation, speech disorders, memory failure, myoclonic jerks, flapping tremor, restless legs, paresthesia and difficulties in walking. It is recommended to start giving biotin regularly in any patient with advanced renal failure before severe neural or muscular lesions become manifest. The correlation of biotin with uremic neurologic disorders and the possible mechanism of its therapeutic action are discussed.
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PMID:Biotin in the management of uremic neurologic disorders. 632 32

Among patients with renal failure, there have been impressive modifications of both the duration and quality of life as a result of dialysis, renal transplantation, and improved medical management. However, patients who have renal failure continue to manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. Even after the institution of otherwise adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous system dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. The central nervous system disorders of both untreated renal failure and that persisting despite dialysis are referred to as uremic encephalopathy. The dialytic treatment of end stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system: Dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. This disease also appears to be a complication of the therapy for renal failure.
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PMID:Pathogenesis of dialysis encephalopathy. 636 3

To add information about sporadic Legionnaires' disease, 87 cases of L. pneumophila pneumonia were reviewed. Twenty cases were nosocomial infections and 67 cases were community-acquired. Most cases (64%) occurred between July and October. The mean age of patients was 51.4 years and males outnumbered females 2.5:1.0. Thirty-one percent of patients were receiving corticosteroid, immunosuppressive, or antineoplastic chemotherapy when illness began. Immunosuppression at onset of illness was more common in nosocomial infections (90%) than in community-acquired infections (14%). Seventy percent of patients had underlying diseases. Malignancies, renal failure, and transplantation were the most common conditions underlying nosocomial infections. Chronic lung disease and malignancies were the most common diseases underlying community-acquired infections. The case-fatality rate in nosocomial infection (70%) was greater than that in community-acquired disease (22%). Clinical, laboratory, and radiologic features of the cases were examined. Illness ranged from mild to severe. Extrapulmonary findings of encephalopathy and renal failure were more common in fatal than in non-fatal cases. Indirect immunofluorescent and microagglutination antibody responses plateaued by the fourth week of illness. Twenty-nine patients died. The case-fatality rate of patients receiving erythromycin (6%) was less than that of patients receiving penicillin (36%), ampicillin (28%), cephalosporin (32%), or aminoglycosides (41%). Despite erythromycin therapy, the case fatality rate for nosocomial L. pneumophilia pneumonia was unacceptably high (25%).
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PMID:Sporadic Legionnaires' disease: clinical observations on 87 nosocomial and community-acquired cases. 646 87

The consequences of renal functional impairment on aluminum (Al) excretion are not clear inasmuch as little is known about its glomerular filtration, tubular reabsorption, or secretion. The association of Al and the etiology of the dialysis encephalopathy syndrome and osteomalacia among patients with uremia suggests that renal functional impairment is a prerequisite for increased body Al stores. However, considerable evidence argues against the concept that tissue Al accumulation occurs as a simple consequence of renal failure. Many dialysis patients have high parathyroid hormone (PTH) concentrations that have been associated with neurologic abnormalities, bone disease, and anemia. The toxicity of PTH could be either direct or indirect by influencing the metabolism of potentially toxic substances such as Al. Our studies in normal rats suggest that gastrointestinal Al absorption and specific tissue burdens are enhanced by PTH, but not irreversibly, because the withdrawal of PTH resulted in Al egress. Dialysis patients are often treated with vitamin D analogs to prevent or control consequences of hyperparathyroidism and impaired 1,25-dihydroxycholecalciferol synthesis. Although some reports suggest that high bone Al in osteomalacia may be responsible for vitamin D resistance, our studies with normal rats suggest that its metabolites may also increase tissue Al burdens independent of PTH action. Thus, several factors operative in uremia other than impaired renal function may contribute to altered Al metabolism and, consequently, to its toxicity.
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PMID:Impaired renal function and aluminum metabolism. 661 95

Malignant hypertension still constitutes a medical emergency, particularly when complicated by renal failure, encephalopathy, or left ventricular failure. A shift to the right of the autoregulatory curve of cerebral blood flow (and probably of renal blood flow) is known to occur in patients with hypertension. Local cerebral edema, complicating the malignant phase, is likely to aggravate this trend. While inadequate or tardy treatment leads to encephalopathy, renal and cardiac failure, over aggressive treatment may also result in damage to brain, heart, and kidney. Recent reports of neurological damage, sometimes fatal, following aggressive hypotensive treatment suggests the need for a reappraisal of current practices. More investigation is needed to determine the effects of the various classes of antihypertensive drugs on organ perfusion, particularly of brain, heart, and kidney, in both normal and hypertensive humans. Other hypertensive crises include raised arterial pressure in association with acute dissection of the aorta and in the presence of stroke or subarachnoid hemorrhage. While there is agreement about the need for urgent hypotensive treatment in patients with aortic dissection, there is no information with which to base rational decisions in the management of high arterial pressure in the acute phase of stroke or subarachnoid hemorrhage.
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PMID:Management of hypertensive crises. 662 56

A case of reversible hepatic failure due to cardiogenic shock following acute myocardial infarction is described. The hepatic failure was characterized by portal systemic encephalopathy and markedly abnormal results of liver function tests. Concomitant renal failure required peritoneal dialysis. Long-term survival (nine years) and return of normal liver function were observed.
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PMID:Shock liver. Case report with long-term survival. 671 80

Patients with renal failure may manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. After the institution of adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. These central nervous system disorders are referred to as uremic encephalopathy. The dialytic treatment of end-stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system; dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation, and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. There are at least three different forms of dialysis encephalopathy: sporadic, epidemic; and that associated with renal disease in children. In addition to the foregoing neurologic diseases which are specifically related to uremia and/or dialysis, a number of other neurologic disorders occur with increased frequency in patients with end-stage renal disease on chronic hemodialysis. These include subdural hematoma, electrolyte disorders, vitamin deficiencies, drug intoxication, hypertensive encephalopathy, and acute trace element intoxication. Renal transplantation is associated with a variety of central nervous system infections, reticulum cell sarcoma, and central pontine myelinosis. The present manuscript will review the clinical, structural, and biochemical components of those neurologic disorders which are peculiar to the uremic state and its treatment with dialysis.
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PMID:Uremic encephalopathies: clinical, biochemical, and experimental features. 675 30


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