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Although our previous results showed HIV\u20101(+) children with acute <jats:italic>Plasmodium falciparum<\/jats:italic> malaria [<jats:italic>Pf<\/jats:italic>(+)] have more profound anemia, potential causes of severe anemia in coinfected children remain unknown. As such, children with <jats:italic>P. falciparum<\/jats:italic> malaria (aged 3\u201336 months, <jats:italic>n<\/jats:italic> = 542) from a holoendemic malaria transmission area of western Kenya were stratified into three groups: HIV\u20101 negative [HIV\u20101(\u2212)\/<jats:italic>Pf<\/jats:italic>(+)]; HIV\u20101 exposed [HIV\u20101(exp)\/<jats:italic>Pf<\/jats:italic>(+)]; and HIV\u20101 infected [HIV\u20101(+)\/<jats:italic>Pf<\/jats:italic>(+)]. Comprehensive clinical, parasitological, and hematological measures were determined upon enrollment. Univariate, correlational, and hierarchical regression analyses were used to determine differences among the groups and to define predictors of worsening anemia. HIV\u20101(+)\/<jats:italic>Pf<\/jats:italic>(+) children had significantly more malarial pigment\u2010containing neutrophils (PCN), monocytosis, increased severe anemia (Hb &lt; 6.0 g\/dL), and nearly 10\u2010fold greater mortality within 3 months of enrollment. Common causes of anemia in malaria\u2010infected children, such as increased parasitemia or reduced erythropoiesis, did not account for worsening anemia in the HIV\u20101(+)\/<jats:italic>Pf<\/jats:italic>(+) group nor did carriage of sickle cell trait or G6PD deficiency. Hierarchical multiple regression analysis revealed that more profound anemia was associated with elevated PCM, younger age, and increasing HIV\u20101 status ([HIV\u20101(\u2212) \u2192 HIV\u20101(exp) \u2192 HIV\u20101(+)]. Thus, malaria\/HIV\u20101 coinfection is characterized by more profound anemia and increased mortality, with acquisition of monocytic pigment having the most detrimental impact on Hb levels. Am. J. 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