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

Renal function was assessed in 40 children during the acute illness and after recovery from falciparum malaria. Creatinine clearance was significantly lower during the acute illness than after recovery. Six of 18 children with impaired creatinine clearance (< 50 ml/min/1.73 m2) had evidence of acute tubular dysfunction. Hyponatraemia occurred in 12.5% during the acute phase. Fractional sodium excretion was raised in 27% during the acute illness and continuing sodium wastage occurred in 17% after recovery. Plasma potassium was significantly higher and fractional potassium excretion (FeK) significantly lower during the acute illness than after recovery. There was a positive correlation between FeNa and FeK both during and after recovery from the illness but they did not exactly mirror each other in every individual. Urine sodium:potassium ratios were similar during and after recovery from the illness and was related to FeNa. Fractional glucose excretion was zero. Mild proteinuria occurred in 40% during the acute illness but were not related to creatinine clearance, body temperature at presentation, or peripheral parasite density. Proteinuria was absent after recovery. Acute intrinsic renal impairment occurs during apparently 'uncomplicated' falciparum malaria in children.
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PMID:Renal function in acute falciparum malaria. 866 27

The prevalence and likely cause of hyponatraemia in severe childhood malaria were investigated. One hundred and thirty two children, 47 of whom had cerebral malaria, were prospectively recruited and serial simple indices of fluid and electrolyte balance and renal function monitored during admission. In 55%, hyponatraemia (sodium < 135 mmol/l) was present on admission. Hyponatraemia was pronounced (sodium < or = 130 mmol/l) in 21%, and these children gained less weight during admission (mean weight gain 2.4% v 4.3%) than children with a normal sodium (135-145 mmol/l). Overall, 31% of survivors were at least moderately dehydrated on admission (5% weight gain by discharge). These children had higher plasma urea concentrations on admission (6.1 v 4.5 mmol/l) and were more acidotic (mean base excess -12.1 v -8.0) than children who were not dehydrated. There were changes in simple indices of renal function between admission and discharge in children who survived (creatinine 65.7 v 37.9 mumol/l and urea 5.5 v 1.9 mmol/l). The results suggest that dehydration is common in severe childhood malaria, that it may contribute to mild impairment in renal function, and that hyponatraemic children are less water depleted, showing appropriate rather than inappropriate secretion of antidiuretic hormone.
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PMID:Hyponatraemia and dehydration in severe malaria. 878 22

We studied 38 patients with acute renal failure (ARF) due to malaria over a 5-year period between 1990 and 1994 at the Institute of Urology and Transplantation. There were 30 males and 8 females who ranged in age from 13 to 75 years. Most were critically ill on presentation with blood urea levels between 116 and 587 mg% and serum creatinine concentrations between 3 and 30 mg%. Anemia accompanied by hyperbilirubinemia was a result of severe hemolysis. Antimalarial therapy consisted of quinine sulfate, chloroquine, or both. Of the 38 patients, 32 required hemodialysis and eventually recovered normal (n = 29) or near normal (n = 3) function. Six patients died.
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PMID:Predictors of outcome in malarial renal failure. 887 97

We have prospectively collected information during resuscitation in 24 children with life-threatening malaria. All had clinical respiratory distress and 16 were severely anemic (hemoglobin < or = 5 g/dL) on admission. Central venous pressure (CVP) measurements were normal (< or = 5 cm of water) prior to treatment but all had a metabolic acidosis. The geometric mean lactate level was significantly higher in children admitted with severe anemia than in those without severe anemia (11.2 mmol/l versus 4.2 mmol/l; P = 0.009). Hypovolemia (a CVP on admission < 0 cm of water) was associated, although not significantly, with a higher admission plasma creatinine concentration (94 mumol/l versus 64 mumol/l; P = 0.06) and probably contributed to the severely reduced creatinine clearances (0-39 ml/min/1.73 ml2) found in 12 of the 13 children in whom this was assessed in the first 24 hr. Treatment resulted in a rapid decrease in blood lactate in 16 of the 13 children in whom this was assessed in the first 24 hr. Treatment resulted in a rapid decrease in blood lactate in 16 of the 20 children transfused, which was most dramatic in severely anemic children, who were rapidly resuscitated. In nonanemic children, early and rapid administration of normal saline usually resulted in both metabolic and clinical improvement. However, in three children, two of whom died, acidosis persisted despite resuscitation. Metabolic acidosis often accounts for respiratory distress in life-threatening childhood malaria. Severe anemia and hypovolemia appear to play major roles in its pathogenesis, are readily treatable, and there appears to be little risk of congestive cardiac failure even with an aggressive approach to fluid replacement.
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PMID:Transfusion for respiratory distress in life-threatening childhood malaria. 894 Sep 85

The clinical features of severe falciparum malaria and risk factors for mortality were studied in 489 children admitted with malaria to Madang Hospital, Papua New Guinea. The most common severe manifestations of malaria were severe anaemia (22%) and coma (16%). Children with severe anaemia were younger than those with coma (median age 2.2 vs. 3.7 years) and had been ill for longer before admission (median 7 vs. 4 days, respectively). Although the clinical features of coma in Madang children with malaria resembled closely those reported in African children, mortality was lower (8% vs. 17-25%, respectively). Overall, 17 (3.5%) children died, most within 12 h of admission. A high level of plasma lactate (> or = 5 mmol/l) was common (20%) and was the major predictor of death in multiple regression analysis. Raised plasma creatinine and decreased plasma bicarbonate were also independent predictors of mortality. Coma was not predictive of death, although a high proportion of children with profound coma died. Investigation of the causes of acidosis in children with malaria is a high research priority. In view of the short time interval between admission and death in many children, emphasis must be placed on the prevention or early recognition and treatment of acidosis in the district health clinic as well as the central hospital.
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PMID:Severe malaria in children in Papua New Guinea. 894 34

We prospectively studied 50 Vietnamese patients with blackwater fever (BWF). All patients had fever and hemoglobinuria, 40 (80%) were jaundiced, 25 (50%) had hepatomegaly, 15 (34%) had splenomegaly, and 9 (18%) had hepatosplenomegaly. Twenty-one patients (42%) had impaired renal function, with creatinine clearances of < 50 mL/min/m2; however, only four (8%) developed oliguric renal failure, three (6%) of whom required dialysis. Forty-four patients (88%) developed anemia, which was severe (hematocrit, < 20% in 32 (64%). One patient died, representing a death rate for this once-feared disease that is considerably lower than that reported by earlier investigators. BWF was associated with quinine ingestion in 28 patients (56%), glucose-6-phosphate dehydrogenase (G6PD) deficiency in 27 (54%), and concurrent malaria infection in 16 (32%). There was no statistically significant difference in the severity of BWF associated with each of these three factors, as assessed by creatinine clearance and the hematocrit value on admission and by the number of units of blood transfused. There was considerable overlap in the occurrence of G6PD deficiency, quinine ingestion, and malaria, suggesting that these factors may interact and that it may not be justifiable to regard hemoglobinuria caused by G6PD deficiency as a separate syndrome.
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PMID:Blackwater fever in southern Vietnam: a prospective descriptive study of 50 cases. 940 15

Renal and systemic hemodynamics, plasma arginine vasopressin, plasma renin activity, plasma norepinephrine, blood volume and water loading test were studied in 10 patients with falciparum malaria without renal failure. Six patients responded to water load normally, while 4 patients had a decreased response to water load. The patients with a normal water load response had normal renal and systemic hemodynamics and a normal hormonal profile. The patients with a decreased response to water load had hyponatremia, hypervolemia, high cardiac index, low systemic vascular resistance, high plasma arginine vasopressin, high plasma renin activity, high plasma norepinephrine, low creatinine and p-aminohippurate clearances, low urine sodium and high urine osmolality. They had a lower mean arterial pressure during the acute phase of the disease than during the recovery phase. The findings suggest that a decreased response to water load is due to peripheral vasodilatation which results in a decreased effective blood volume leading to the release of vasopressin and norepinephrine, increased renin activity and decreased renal hemodynamics.
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PMID:Renal and systemic hemodynamics, in falciparum malaria. 895 63

Serum from 41 of 92 children admitted to Madang Hospital, Papua New Guinea, with cerebral malaria, previously assessed for serum levels of reactive nitrogen intermediates (RNI: nitrate plus nitrite), were re-assessed for creatinine levels on the day of admission. Further analysis of RNI levels on day 21 compared to day 0 was carried out. Children with the highest RNI levels on admission, and with the longest duration of coma, did not have elevated creatinine levels. The highest levels of creatinine occurred among those with the lightest coma and creatinine levels were similar in those with short (< 48 h) and long (> 48 h) duration of coma. Between days 0 and 21, RNI decreased in 30 of 57 children, increased in 23, and did not change in 4. There was a significant relationship between the decrease in RNI relative to the level of RNI on admission and the duration of coma. For children with a coma duration < 48 h (48/57), there was no difference between the numbers showing an increase or a decrease in RNI level, but 6 of the 9 children with coma duration > 48 h showed a decrease in RNI greater than 50% of the RNI levels on admission. None of these 9 children had elevated creatinine levels. Elevated RNI levels in severe cases were thus not associated with renal function in these children in Papua New Guinea.
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PMID:Serum creatinine levels and reactive nitrogen intermediates in children with cerebral malaria in Papua New Guinea. 923 Dec 2

Data were prospectively collected on 306 Kenyan children, including blood gases in 258 (75%). Severe malaria caused a predominantly high-anion-gap metabolic acidosis in at least 43% of children. Children with coma and respiratory distress (CM + RD) had greater evidence of renal dysfunction, lower mean pH and higher mean plasma osmolality than those with respiratory distress (RD) or coma (CM) as isolated findings (mean urea 10.7 vs. 6.0 vs. 4.3 mmol/l; mean creatinine 97 vs. 74 vs. 58 mumol/l; mean osmolality 301 vs. 288 vs. 283 mosmol/l; and mean pH 7.16 vs. 7.29 vs. 7.39, respectively, p < 0.001 for each comparison of CM + RD vs. RD or CM). In addition, children with CM + RD had a higher mean blood lactate (6.7 vs. 3.3 mmol/l, p < 0.001), a lower mean haemoglobin (5.5 vs. 7.0 g/dl, p = 0.002) and a lower mean age (26.4 vs. 41.9 months, p < 0.001) than children with CM and accounted for 15/24 (63%) of all deaths. These and previous data implicate hypovolaemia and renal impairment in the pathogenesis of metabolic acidosis in severe childhood malaria. In children who are acidotic, anaemia is strongly associated with lactic acidaemia and may therefore contribute to its pathogenesis. These data also imply that coma in acidotic children (CM + RD) and those with an isolated encephalopathy (CM) may result from quite different pathophysiological mechanisms.
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PMID:Acidosis in severe childhood malaria. 934 54

We investigated the pathophysiology of hypoglycaemia in severe malaria in African children, especially the potential importance of glycerol as a substrate for gluconeogenesis, and whether substrate limitation contributes to hypoglycaemia in severe disease. Of 171 children with moderate or severe malaria, 16% were hypoglycaemic on admission, while at least 9% of children with severe malaria treated with quinine and a concurrent 4% dextrose infusion had a definite episode of hypoglycaemia after admission. Blood levels of gluconeogenic precursors are as high (alanine and lactate) or higher (glycerol) in those with either hypoglycaemia on or after admission as they are in children never having an episode of hypoglycaemia. Among children with severe malaria, however, those having a definite episode of hypoglycaemia at some stage are more acidotic and have greater evidence of renal impairment than those who are never hypoglycaemic (mean base excess -14.4 vs. -7.2, p < 0.001, mean creatinine 97 vs. 64, p < 0.001 and mean urea 8.1 vs. 5.8, p = 0.03, respectively). These data do not support a role for reduced gluconeogenic substrate supply in the pathogenesis of hypoglycaemia in severe childhood malaria, but do support the hypothesis that gluconeogenesis is impaired. Commonly-used bedside blood glucose monitoring devices may overestimate blood glucose measurements in the normal range, and paradoxically may also seriously overestimate the frequency of hypoglycaemia.
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PMID:Hypoglycaemia on and after admission in Kenyan children with severe malaria. 960 71


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