Abstract

Infections are responsible for about 50% of cases with acute kidney injury (AKI) in the tropics. Many tropical infections can cause AKI by direct invasion of the renal parenchyma, inducing a systemic inflammatory response, critically altering the renal hemodynamics and/or provoking a morbid immune response. Genetic, environmental, and socioeconomic factors interact in increasing morbidity from tropical infections, including AKI. Drug nephrotoxicity may confer additional damage. The clinical syndrome of tropical AKI is confounded by the associated primary disease, multiorgan affection, rhabdomyolysis, hemolysis, disseminated intravascular coagulation, preexisting morbidities, malnutrition, multiple infections, and late referral. The typical laboratory features reflect the catabolic state of infection, the associated humoral re­sponse, and the manifestations of tissue hypoxia. In most patients, AKI is reversible by adequate treatment of infection, hydration, and supportive treatment. Unfortunately the lack of equipment and experience with continuous renal replacement therapy limit its use in endemic areas. Intermittent dialysis is the only available alternative. Plasmaphere­sis or blood exchange may be useful in a few infections.

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