Oliguric renal failure in blackwater fever

Dukes, D.C.; Sealey, B. J.; Forbes, Jessica

doi:10.1016/0002-9343(68)90188-5

Cited by 29 publications

(3 citation statements)

References 20 publications

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“…We found 13 similar cases in the literature that occurred during the same period; 6 of the patients were Italian, 5 were Belgian, and 2 were French (table 3) [13,14,[16][17][18]. These 34 cases reported during a 10-year period indicate a resurgence of BWF in European expatriates, since a review of the literature from the 30 previous years revealed only 5 comparable cases [19,20]. Further evidence of a resurgence of BWF among European expatriates is that the current ratio of BWF cases over falciparum malaria cases (table 2) is comparable to that seen in similar populations during the first half of the 20th century [1].…”

Section: Discussionmentioning

confidence: 87%

Resurgence of Blackwater Fever in Long-Term European Expatriates in Africa: Report of 21 Cases and Review

Brunee

Gachot

Wolff

et al. 2001

Clinical Infectious Diseases

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Blackwater fever (BWF) is a severe clinical syndrome, characterized by intravascular hemolysis, hemoglobinuria, and acute renal failure that is classically seen in European expatriates chronically exposed to Plasmodium falciparum and irregularly taking quinine. BWF virtually disappeared after 1950, when chloroquine superseded quinine. We report 21 cases of BWF seen in France from 1990 through 1999 in European expatriates who lived in sub-Saharan Africa. All patients had macroscopic hemoglobinuria, jaundice, and anemia. Acute renal failure occurred in 15 patients (71%), 7 of whom required dialysis. The presumed triggers of BWF were halofantrine (38%), quinine (24%), mefloquine (24%), and halofantrine or quinine (14%). Glucose-6-phosphate dehydrogenase (G6PD) activity was normal in the 14 patients who underwent this test. Low-level P. falciparum parasitemia was found in 8 patients. All 21 patients survived. Our data and 13 cases reported in the literature suggest a resurgence of classic BWF among Europeans living in Africa and a need to discuss attendant therapeutic implications.

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Section: Discussionmentioning

confidence: 87%

Resurgence of Blackwater Fever in Long-Term European Expatriates in Africa: Report of 21 Cases and Review

Brunee

Gachot

Wolff

et al. 2001

Clinical Infectious Diseases

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“…The present study provides evidence for the requirement o f constant monitoring of renal function in such patients. In this way, the involvement of chloroquine in renal complications (Dukes et al 1968;Gerristen 8( van der Zwan 1992) can be detected at an early stage, to enable therapeutic intervention. The role of chloroquine as a precipitating factor of renal diseases has long been disputed (Molenaar 81 Voors 1963) with some studies suggesting the involvement of the drug in the aetiology of renal disease (Gerristen 81 van der Zwan ~9 9 2 ) .…”

Section: Discussionmentioning

confidence: 99%

Arginine vasopressin mediates the chloroquine induced increase in renal sodium excretion

Musabayane

Windle

Forsling³

et al. 1996

Tropical Med Int Health

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SummaryWe postulated that chloroquine increases plasma arginine vasopressin (AVP) concentrations thus altering renal Na' clearance. Therefore, we studied a relationship between plasma AVP concentrations and urinary Na' output in separate groups of Sprague-Dawley (SD) rats administered chloroquine (3 pg/min) for T h 20 min. We also monitored Na' excretion rates in Brattleboro AVP-deficient Di rats challenged with hypotonic saline load and administered chloroquine for I h 20 min. To establish whether chloroquine-induced changes in renal Na' excretion were mediated via AVP V, receptors, we studied Na' excretion rates in groups of SD rats administered chloroquine or AVP in the presence of AVP V, receptor antagonist 9.8 i 1.0 pmol/min to a peak of 14.1 f 0.9 pniol/rnin in SD rats ( n = 7 ) administered chloroquine. The Na' excretion rate remained unaltered around 8.5 pmol/min in rats simultaneously administered chloroquine and the AVP V, receptor antagonist. This compared with control rats ( 8 . 1 f 0.5 pmol/min, % = 7 ) and animals administered AVP V , receptor antagonist alone (8.7 f 0.6 p m o h i n , n=7). Chloroquine did not affect urine tlow, Na' or K' excretion rates in Brattleboro AVP-deficient Di rats. Administration of AVP alone was associated with significant increases in renal Na' excretion rate. Blockade of AVP V, receptors abolished the AVP-dependent increase in urinary Na' loss. We conclude that at least part of the chloroquine-induced increase in Na' excretion i s mediated by chloroquine stimulating an increase in plasma AVP concentration.The Na' excretion rate rose significantly (P

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“…A resurgence of this affliction, which occurred frequently during colonialism and had disappeared after chloroquine had replaced quinine, has lately been noticed [158][159][160][161][162]. In a prospective study from 1996-2000, 80% of BWF cases in the Ivory Coast were associated with irregular quinine ingestion or similar structural molecules such as halofantrine [158].…”

Section: Clinical Findingsmentioning

confidence: 99%

Malaria-induced renal damage: facts and myths

Ehrich

Eke

2007

Pediatr Nephrol

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Malaria infections repeatedly have been reported to induce nephrotic syndrome and acute renal failure. Questions have been raised whether the association of a nephrotic syndrome with quartan malaria was only coincidental, and whether the acute renal failure was a specific or unspecific consequence of Plasmodium falciparum infection. This review attempts to answer questions about "chronic quartan malaria nephropathy" and "acute falciparum malaria nephropathy". The literature review was performed on all publications on kidney involvement in human and experimental malarial infections accessible in PubMed or available at the library of the London School of Hygiene and Tropical Medicine. The association of a nephrotic syndrome with quartan malaria was mostly described before 1975 in children and rarely in adult patients living in areas endemic for Plasmodium malariae. The pooled data on malaria-induced acute renal failure included children and adults acquiring falciparum malaria in endemic areas either as natives or as travellers from non-tropical countries. Non-immunes (not living in endemic areas) had a higher risk of developing acute renal failure than semi-immunes (living in endemic areas). Children with cerebral malaria had a higher rate and more severe course of acute renal failure than children with mild malaria. Today, there is no evidence of a dominant role of steroid-resistant and chronic "malarial glomerulopathies" in children with a nephrotic syndrome in Africa. Acute renal failure was a frequent and serious complication of falciparum malaria in non-immune adults. However, recently it has been reported more often in semi-immune African children with associated morbidity and mortality.

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Oliguric renal failure in blackwater fever

Cited by 29 publications

References 20 publications

Resurgence of Blackwater Fever in Long-Term European Expatriates in Africa: Report of 21 Cases and Review

Resurgence of Blackwater Fever in Long-Term European Expatriates in Africa: Report of 21 Cases and Review

Arginine vasopressin mediates the chloroquine induced increase in renal sodium excretion

Malaria-induced renal damage: facts and myths

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