Dengue haemorrhagic fever-induced acute kidney injury without hypotension, haemolysis or rhabdomyolysis

Abstract

Dengue fever (DF) is currently the most important human viral mosquito-borne infection of public health significance, with millions of infections each year. The main dengue vector is the female of the Aedes aegypti mosquito. There are four serotypes of the dengue virus (DEN-1–DEN-4), a RNA flavivirus. They are antigenically closely related, but whereas infection with one serotype produces lifelong immunity to that serotype, immunity to other serotypes lasts only a few months [1,2]. Approximately half the world’s population lives in areas potentially at risk for dengue and 50–100 million cases are estimated to occur annually [1,3]. Brazil is the leading American country in absolute number of cases and has the highest incidence rate of the disease in this geographic area [4]. The epidemiology of dengue in Brazil comprised two distinct periods. In the first (1986–1993), epidemic waves occurred in localized areas. In the second (1994–2002), there was a nationwide epidemic and endemic virus circulation. In this period, a total of 2 826 948 cases of dengue were reported, giving an incidence of 454/100 000 inhabitants. The number of infested municipalities increased from 44.5% in 1996 to 58.3% in 2002 [5]. Dengue virus infection may manifest clinically as undifferentiated fever, dengue fever (DF), dengue haemorrhagic fever (DHF) or dengue shock syndrome (DSS) [3]. Renal injury comprising creatinine increase, proteinuria, glomerulonephritis, acute kidney injury (AKI) and haemolytic uraemic syndrome has been reported in dengue patients [6–22]. To date, all DHF-induced AKI described cases have occurred in association with shock, haemolysis or rhabdomyolysis [11,12,14,15]. We describe, to the best of our knowledge for the first time, a case of DHF-induced AKI, where the renal injury occurred without haemodynamic instability, haemolysis, rhabdomyolysis or use of nephrotoxic drugs.