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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The plasma concentrations of quinine and its main metabolite, 3-hydroxyquinine (3OHQn), were measured in 5 adult Thai patients with severe Plasmodium falciparum malaria and acute renal failure. Two patients required peritoneal dialysis but all survived. During acute renal failure plasma concentrations of 3OHQn rose to reach up to 45% of the levels of the parent compound. The estimated median (range) quinine clearance was 0.83 mL/kg/min (0.58-1.16), and 3OHQn clearance/fraction of quinine converted was 3.40 mL/kg/min (2.58-4.47). The estimated 3OHQn terminal elimination half-life was 21 h (16.5-32.5). These data suggest that 3OHQn contributes about 12% of the antimalarial activity of the parent compound in patients with falciparum malaria and acute renal failure. It is also likely that 3OHQn contributes to adverse effects, although this metabolite is not quantitated routinely by current high-performance liquid chromatography quinine assays.
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PMID:Pharmacokinetics of quinine and 3-hydroxyquinine in severe falciparum malaria with acute renal failure. 1049 95

The use of dopamine for the prevention and treatment of acute renal failure is widespread. Its use is based on physiology suggesting selective renal vasodilation when it is infused at low dose. This article reviews the available data on the clinical use of dopamine. When used to prevent acute renal failure in high-risk treatments there is no evidence of benefit of dopamine but, given the low incidence of significant renal failure, the studies are underpowered. In treatment of acute renal failure, the quality of the data is poor. Only in one small randomised trial of moderate acute renal failure in patients with malaria was a clinically significant benefit of dopamine shown. The rest of the data, in the form of case series, showed either no benefit of dopamine or small benefits of little clinical significance. Again, these studies are of insufficient power for conclusions to be drawn as to the overall benefits and risks. We conclude that benefits of dopamine use cannot be ruled out by currently available data but its use cannot be advised until trials examining clinically important endpoints in large numbers of patients have been performed.
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PMID:Can the use of low-dose dopamine for treatment of acute renal failure be justified? 1053 29

Falciparum malaria is a disease of tropical climates which affects 270 million people annually and has an overall mortality of 1%. While the incidence of acute renal failure in malaria is less than 1%, mortality is reported to be as high as 45% in those with renal failure. We report the clinical course and outcome in 5 patients with falciparum malaria-induced acute renal failure treated at the Singapore General Hospital between June and July 1997. All 5 males, with mean age of 35.2 +/- 13.1 years, were admitted with history of fever and reported travel to a known malarious zone. Mean laboratory parameters upon admission included serum creatinine 725 +/- 515 mumol/L and serum urea 47 +/- 31 mmol/L. Three patients with hypotension on admission were started on haemodiafiltration, of whom 2 were subsequently converted to haemodialysis as their haemodynamics improved. Two remaining patients were started on intermittent bicarbonate haemodialysis. The overall mortality in our series was 20%, with 1 patient having died of complications of adult respiratory distress syndrome, disseminated intravascular coagulation and multiorgan failure. The remaining 4 survived and recovered their renal function. The single patient mortality occurred in the patient with admission serum creatinine of 1632 mumol/L, a value significantly higher than that of the 4 patients who survived (mean serum creatinine, 499 +/- 106 mumol/L, P < 0.002). These results suggest that falciparum malaria associated with acute renal failure is associated with a high morbidity, but early presentation and intervention with appropriate antimalarial and renal replacement therapy is associated with improved survival and recovery of renal function.
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PMID:A case series of falciparum malaria-induced acute renal failure. 1056 76

Malaria coma induced by P.falciparum was diagnosed in 51 of 390 adult African patients who had been admitted to the therapeutical unit of the Donk Central Hospital and were receiving parenteral quinine at day 1 of the onset of coma. Examining some clinical and laboratory manifestations of malaria coma indicated that fatal outcome was significantly recorded among the patients with severe concomitant anemia and among the patients who had not or had received inadequate liquid parenterally on the first day of coma. The occurrence of acute renal failure in 4 patients with malaria coma resulted in 3 deaths. No great impact on the prognosis of malaria "hyperparasitemia", the severity of fever, the values of blood pressure was found. Whether it is advisable to use the parameters characterizing the opportuneness and scope of health care delivered to patients with severe malaria is discussed.
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PMID:[The importance of fluid perfusion for the outcome of the disease in malarial coma due to Plasmodium falciparum in adult Africans]. 1070 9

We report a case of traveller to Kenya who contracted severe plasmodium falciparum malaria complicated by disseminated intravascular coagulation and acute renal failure. She had taken no antimalarial prophylaxis in view of concerns in the media regarding the adverse effects of mefloquine. There was a protracted delay before the diagnosis of malaria was made. Clinical recovery occurred following treatment with intravenous quinine, haemofiltration and manual/automated red-cell exchange transfusions. Automated red-cell exchange transfusion resulted in a marked decrease in the parasitaemia, before a response to quinine therapy would have been anticipated, leading to a successful outcome thereafter. In conjunction with other groups we therefore feel that exchange transfusions should be considered in seriously ill patients with falciparum malaria, multiorgan complications and parasitaemias greater than 10%.
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PMID:Automated exchange transfusion for life-threatening plasmodium falciparum malaria--lessons relating to prophylaxis and treatment. 1071 92

Of 51 consecutive children with cerebral malaria, fever, convulsions, and drowsiness were the commonest presenting symptoms. Decerebrate and decorticate postures and absent cornea reflex were the commonest brain stem signs. Opening lumbar cerebrospinal (CSF) pressure was raised in all but one of 24 children in whom it was reliably measured [mean 15.2 +/- 5.7 mmHg, range 6-24]. Hyponatraemia occurred in 17 (33%). Acute renal failure was not uncommon; the combination of hypercreatininaemia (plasma creatinine > 100 mumol/L) and hyperkalaemia (plasma potassium > 6.0 mumol/L) was fatal in 5 out of 7 patients in whom it occurred. Disturbances of acid-base status were present in all 40 children in whom it was assessed on admission. Mortality rate was 16% (8 patients). Neurological deficits occurred in 7 (14%) of the survivors and included cortical blindness [3], aphasia [3], hypertonia [3], hearing loss [2], and dystonia [1]. In addition to the present measures aimed at reducing morbidity and morality in children with cerebral malaria, efforts should be directed at rapid assessment of renal function and prompt correction of such dysfunction if found.
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PMID:Clinical study of cerebral malaria in African children. 1089 20

Renal disease is a common complication in malaria infection. In acute falciparum malaria renal involvement is usually mild, but in severe disease acute renal failure is a major problem. Acute renal failure has been attributed to ischaemic tubular necrosis from hypovolaemia resulting from vasodilatation due to endothelial injury. Though myositis is recorded as a common manifestation in falciparum malaria, only 1 case with myositis and myoglobinuria with acute renal failure has been documented; but no renal biopsy was performed in the patient. In the present study we examined the case of a 17-year-old man with severe falciparum malaria with myositis and myoglobinuria who developed acute renal failure requiring dialysis. Muscle biopsy revealed severe myositis with macrophages and T lymphocytes including CD4+ cells. The kidney biopsy showed scanty T cells and macrophages in the glomeruli which were only mildly hypercellular. The renal tubules showed myoglobin casts in the lumen and foci of interstitial inflammatory cells, including macrophages and T lymphocytes but no CD4+ cells. Rhabdomyolysis induced by macrophages and T cells with myoglobinuria and acute renal failure is a problem in severe falciparum malaria infection.
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PMID:Acute renal failure from myoglobinuria secondary to myositis from severe falciparum malaria. 1097 Sep 90

Acute renal failure (ARF) associated with liver disease is a commonly encountered clinical problem of varied etiology and high mortality. We have prospectively analyzed patients with liver disease and ARF to determine the etiology, clinical spectrum, prognosis and factors affecting the outcome. Other than hepatorenal syndrome patients, out of 221 cases, 66 developed ARF secondary to various liver disease like cirrhosis (n = 29, mortality 8, risk factors-older age p < 0.01, grade III/IV encephalopathy p < 0.05), fulminant hepatic failure (n = 25, mortality 15, risk factor-prolonged prothrombin time p < 0.01), and obstructive jaundice (n = 12, mortality 7, risk factor-sepsis p < 0.01). In these three groups the factors leading to ARF were volume depletion (24), gastrointestinal bleed (28), sepsis (34), drugs (27) [aminoglycosides (9) and NSAID (18)] along with hyperbilirubinemia. Various types of ARF with contemporaneous liver injury were malaria (n = 37, mortality 15, risk factors-higher bilirubin p < 0.001, higher creatinine p < 0.05, anuria p < 0.05 and dialysis dependency p < 0.05), sepsis (n = 36, mortality 22, risk factors-age p < 0.001, higher bilirubin p < 0.01, oliguria p < 0.05), hypovolemia with ischemic hepatic injury (n = 14, mortality 5, risk factors-higher creatinine p < 0.05 and SGPT p < 0.01), acute pancreatitis (n = 12, mortality 4, risk factors-higher bilirubin p < 0.001, higher SGPT p < 0.01, dialysis dependency p < 0.05), rifampicin toxicity (n = 10, no mortality), paroxysmal nocturnal hemoglobinuria (n = 3, no mortality), CuSO4 poisoning (n = 3 mortality 2), post abortal (n = 11, mortality 6, risk factors higher creatinine p < 0.05 and SGPT p < 0.01), ARF following delivery including HELLP syndrome (n = 12, mortality 4, risk factors-higher bilirubin p < 0.01 and SGPT p < 0.01), and of uncertain etiology (n= 14 mortality 4). 133 patients (60.2%), required hemodialysis hemodialfiltration or peritoneal dialysis. ARF associated with liver disease is having high mortality (42.5%). Avoidance of dehydration, hypotension, nephrotoxic drugs and sepsis, with promote dialytic support are necessary to reduce mortality and morbidity.
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PMID:Acute renal failure associated with liver disease in India: etiology and outcome. 1104 Dec 94

Since 1991, quinidine gluconate, a class 1a anti-arrhythmic agent, has been the only parenteral antimalarial available for use in the United States (1). It is indicated for the treatment of patients with life-threatening Plasmodium falciparum malaria (2), including those who cannot tolerate oral therapy, have high-grade parasitemia, or have complications (e.g., cerebral malaria or acute renal failure).
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PMID:Availability and use of parenteral quinidine gluconate for severe or complicated malaria. 1119 Jan 19

Renal failure secondary to acute tubular necrosis is a common complication of severe Plasmodium falciparum malaria. The purpose of this report is to describe two cases of severe malaria featuring acute renal failure observed in young patients who had failed to comply with chemoprophylaxis. Occurrence of renal failure was delayed four to seven days in relation to the beginning of the malaria attack. Hemodialysis was required in one case. Both patients were successfully treated by quinine perfusion. The main pathophysiology mechanisms underlying acute tubular necrosis are obstruction of capillaries and post-capillary venules by infected red blood cells and activation of monocytes that release cytokines such as tumor necrosis factor. Other nonspecific mechanisms may come into play including hypovolemia, release of catecholamines and subsequent activation of the rennin-angiotensin system, complement activation, and rhabdomyolysis. Acute tubular necrosis is the main renal complication of Plasmodium falciparum malaria but latent forms of acute glomerulonephritis have also been documented. Prognosis is usually favorable depending mainly on early diagnosis and prompt treatment.
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PMID:[Acute renal failure during severe malaria: physiopathology and therapeutic management. Apropos of 2 cases]. 1125 60


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