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

The effects of furosemide and furosemide with dopamine on renal function were studied in 23 patients with acute renal failure due to falciparum malaria whose serum creatinine ranged from 230 to 947 mumol/l. Furosemide given intravenously at the dosage of 200 mg 6 hourly for a period of 4 days did not alter the clinical course of renal failure. Intravenous administration of furosemide (200 mg 6 hourly) with dopamine (1 microgram/kg/min) for 4 days increased creatinine clearance and arrested the progress of renal failure when the serum creatinine was less than 400 mumol/l, but failed to alter the course of renal failure when the serum creatinine exceeded 600 mumol/l.
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PMID:Furosemide and dopamine in malarial acute renal failure. 265 49

Tests for renal function were performed in 75 smear positive children with acute malaria together with 10 control children. Plasmodium vivax and Plasmodium falciparum accounted for 52 and 46 per cent cases, respectively. Renal impairment in the form of decreased endogenous creatine clearance (less than 65 ml/min/m2) was noted in 36 of the 75 children with malaria. Plasmodium falciparum was responsible for 66 per cent and P. vivax accounted for 30 per cent cases of renal impairment. Plasmodium falciparum parasitaemia produced significantly greater reduction in endogenous creatine clearance (r = 0.198). Fourteen of 36 patients with decreased endogenous creatine clearance who attended for follow-up showed that their creatinine clearance had returned back to normal.
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PMID:Renal function in acute malaria in children. 269 10

Five weeks after re-induction treatment and nine days after discharge from hospital, remittent fever occurred in a 34-year-old woman with promyelocytic leukaemia in full remission. She also had haemolytic anaemia and thrombocytopenia, as well as a reduced creatinine clearance. Findings on physical examination were unremarkable, but Falciparum malaria was found in the blood smear. Infusion of erythrocyte or platelet concentrates, administered in treating the leukaemia, was the probable source of the infection. Ten days after starting the administration of chloroquine and sulfadoxine-pyrimethamine she was discharged from hospital, cured of the malaria.
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PMID:[Transfusion malaria in promyelocytic leukemia]. 305 88

Ninety-four per cent of 169 patients with cerebral malaria developed anaemia (haematocrit less than 35 per cent) and 30 per cent required blood transfusion to maintain the haematocrit at more than 21 per cent. Anaemia was at its worst on admission in 58 patients (34 per cent); in the rest the haematocrit fell further, reaching its nadir one to 17 days later (mean 2.3 days). The mean lowest haematocrit was 24.3 +/- 7.2 per cent (+/- 1 SD) and the mean maximum fall was 7.9 +/- 5.6 per cent. Anaemia was more severe in patients with bacterial infection, retinal haemorrhages, schizontaemia and in pregnancy. The lowest haematocrit correlated with admission parasitaemia (r = -0.33, p less than 0.001), total serum bilirubin (r = -0.25, p less than 0.01) and serum creatinine (r = -0.22, p less than 0.01). In 23 patients with uncomplicated falciparum malaria the mean serum iron on admission was 53 micrograms/dl (range 16-157) and the mean serum ferritin 1773 ng/ml (range 170-10 000). There was a significant (p less than 0.001) rise in serum iron 96 h after starting antimalarial treatment; the serum ferritin declined slowly over several weeks. Stainable iron was present in all marrows examined and in eight patients the characteristic pattern of the anaemia of chronic disorders was seen. Seventy-three per cent of patients had dyserythropoiesis which was moderate to gross in 36 per cent. Dyserythropoiesis and erythrophagocytosis were often present on admission but sometimes appeared after the parasitaemia had cleared and persisted for at least three weeks into convalescence. These disturbances in iron metabolism and haemopoiesis are not completely explicable by red blood cell parasitisation. They may contribute more to the anaemia than has previously been recognised.
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PMID:The importance of anaemia in cerebral and uncomplicated falciparum malaria: role of complications, dyserythropoiesis and iron sequestration. 352 85

The prevalence and pathogenesis of renal involvement was investigated in 74 patients with malarial infections. A rise in proteinuria of 150 to 5,000 mg per day was seen in 12 out of 27 patients with Plasmodium falciparum infections. SDS-polyacrylamide gel electrophoresis revealed either an increase in albumin and high molecular weight proteins alone or an increase in low and high molecular weight proteins. Serum creatinine and urea were increased in 5 patients. In P. vivax infections, 8 out of 46 patients developed a proteinuria level of up to 462 mg per day. Low and, to a lesser degree, high molecular weight proteins were increased. In one patient with quartan malaria infection, proteinuria rose as far as 432 mg per day. There was a correlation between the appearance of proteinuria and fever; however, there was no correlation between the amount of proteinuria and the height of fever. It is therefore unlikely that a rise in temperature is the only cause of proteinuria in malarial infections. The electrophoretic analyses of proteinuria indicate that in malarial infections, glomerular as well as tubular lesions may cause reversible proteinuria.
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PMID:Origin of proteinuria in human malaria. 389 Jan 20

Retinal hemorrhages were seen in 21 patients among a group of 144 with strictly-defined cerebral malaria. Hemorrhages were multiple in 17 cases and bilateral in 14. There was subhyaloid extension in two. Soft exudates were seen in two, the retinae were considered edematous in four and in one there was bilateral papilledema. Retinal hemorrhages were significantly associated with several indices of severity of Plasmodium falciparum infection: high parasitemia with schizontemia, anemia, elevated serum creatinine and reduced plasma antithrombin III. Only two patients with hemorrhages were both severely anemic and thrombocytopenic. It is suggested that retinal hemorrhages, a frequent finding in cerebral malaria, may be visible evidence of vascular lesions involved in the pathogenesis of this condition.
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PMID:Retinal hemorrhage, a common sign of prognostic significance in cerebral malaria. 635 55

The involvement of the brain, lungs and kidneys was studied in a lethal rat malaria. Lewis inbred rats were infected with Plasmodium berghei K173. The disease proved fatal within 10-14 days. Parasitaemia showed an increase of up to 43% parasitised red blood cells on Day 10 p.i. The haematocrit decreased from 50% to 12%. The systolic blood pressure dropped from 99 to 56 mmHg. The lactate dehydrogenase activity rose to 2,543 U/l. BUN and serum creatinine doubled during the course of the disease. The transaminases increased tenfold and the cholinesterase decreased from 943 U/l to 271 U/l. Morphologically the kidneys showed an immune complex glomerulo-nephritis with a normal tubulo-interstitial system. The brain, heart and lungs were normal by light microscopic examination. Marked anaemia and shock were the main causes of death in the above-mentioned specimen rat, showing that the course of the disease is significantly different from lethal infections in humans with Plasmodium falciparum who show severe pulmonary, renal and cerebral complications.
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PMID:Causes of death in lethal rat malaria. 661 21

The value profiles of 5 intracellular enzymes, 15 metabolites (with 2 associated ratios), and 3 electrolytes were monitored over time in 9 captive-reared African black-footed penguins (Spheniscus demersus) with different avian malaria clinical status: uninfected, subclinically infected, and clinically infected with fatal outcome. Fatal infections were caused by Plasmodium relictum. Numerous schizonts were visible in the lungs, liver, spleen, and interstitial tissue of the kidneys. The reference ranges of 23 serum clinical chemistry parameters and 2 ratios were established for S. demersus. The mean values obtained for 8 of 23 parameters of the infected penguins were significantly different from those recorded for the uninfected birds, indicating impaired renal function, hepatic dysfunction, and nonspecific tissue damage related to the infestation with exoerythrocytic schizonts. Analysis of sensitivity, specificity, and negative and positive predictive values (PPVs) showed that gamma-glutamyltranspeptidase (GGTP), alanine aminotransferase (ALT), and creatinine reached PPVs and a specificity over 57% for avian malaria infections in penguins. Creatinine, ALT, and GGTP values should be consulted in evaluation of the clinical malaria status of S. demersus.
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PMID:Evaluation of serum chemistry values associated with avian malaria infections in African black-footed penguins (Spheniscus demersus). 762 90

Disturbances in calcium metabolism in acute renal failure (ARF) remain incompletely understood. Most data are from patients with rhabdomyolysis. As renal impairment commonly accompanies severe malaria in the absence of rhabdomyolysis, falciparum malaria provides an alternative model of mineral homoeostasis in ARF. We studied 25 Vietnamese subjects, aged 18-63 yr, with severe malaria and 10 controls. Fourteen patients had a serum creatinine level of 250 mumol/L or less during treatment (group 1), five developed ARF but were not dialyzed (group 2a), and six required dialysis (group 2b). Group 1 patients presented with mild hypocalcemia (mean +/- SD serum ionized calcium, 1.18 +/- 0.05 vs. 1.23 +/- 0.02 mmol/L in controls; P = 0.01) that persisted until discharge in the presence of normal serum phosphate, PTH, and vitamin D metabolite levels. Group 2 patients were more hypocalcemic on admission (1.10 +/- 0.08 mmol/L; P < 0.0001 vs. controls), especially those in group 2b whose serum ionized calcium fell to 0.88 +/- 0.13 mmol/L when renal dysfunction was maximal. In group 2 patients, the admission serum PTH level was raised (5.4 +/- 3.8 vs. 2.7 +/- 0.9 pmol/L in controls; P < 0.02) and changed reciprocally with calcemia. Significant rises in serum phosphate occurred only in group 2b patients who had depressed serum free 1,25-dihydroxyvitamin D levels throughout. Hypercalcemia did not accompany the diuretic phase of ARF. These data suggest that parathyroid gland dysfunction is a cause of hypocalcemia in severe malaria without ARF, as seen in group 1 patients; in patients with ARF, the effect of the combination of phosphate retention and altered vitamin D metabolism on skeletal PTH sensitivity is of prime significance.
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PMID:Mineral homoeostasis in acute renal failure complicating severe falciparum malaria. 767 21

We report two patients who had cerebral malaria, heavy parasitemia, hyperbilirubinemia, hypercatabolism with rapid rises of blood urea and serum creatinine and acute renal failure. There was no evidence of intravascular hemolysis. Renal biopsy was consistent with acute tubular necrosis. Both patients responded to treatment with intravenous quinine and dialysis.
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PMID:Acute renal failure in falciparum malaria. 767 79


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