SP202ACUTE KIDNEY INJURY IN PATIENTS WITH PLASMODIUM VIVAX MALARIA: CLINICOHISTOPATHOLOGIC PROFILE

Abstract

Introduction and Aims: Plasmodium vivax malaria has long been considered a benign parasite compared to plasmodium falciparum. However, recently an increased number of cases with multiorgan dysfunction including acute kidney injury have been attributed to P.Vivax monoinfection. The underlying mechanism is not yet completely understood. Only a few case reports in the literature have published the renal biopsy findings in these patients. This prompted us to conduct this study to evaluate the clinical and histopathologic profile of patients with P.vivax malaria monoinfection and acute kidney injury. Methods: The study included 128 patients diagnosed with P.vivax monoinfection on peripheral smear blood films and rapid diagnostic test ( positive for P.vivax specific lactate dehydrogenase). Detailed clinical and biochemical parameters were noted. Acute kidney injury (AKI) was defined based on WHO criteria for complicated malaria i.e. serum creatinine > 265 μmol/l or 3mg/dl. Patients were initiated on hemodialysis for persistent hyperkalemia, fluid overload, severe metabolic acidosis or uremic symptoms. Renal biopsy was performed in presence of active urinary sediments (proteinuria, hematuria) or persistence of renal failure> 21days. Results: Out of a total of 128 patients, 29 (22.6%) fulfilled AKI criteria. Patients with acute kidney injury were older (mean age 42.1±10.9 years), male, with a longer duration of illness (mean 12.3±10 days) and associated with multisystem dysfunction. The mean serum creatinine was 5.3±2.6 mg/dl, blood urea 132.3±43 mg/dl and total bilirubin 4.6±3.2mg/dl. Thrombocytopenia was seen in 69%, 21% had severe anemia requiring blood. Three of these patients developed acute respiratory distress syndrome, while two had hypotension unresponsive to intravenous fluid therapy. 12 patients were initiated on hemodialysis with a mean of 3.6±2.6 sessions. Renal biopsy was performed in 11 patients for various indications. Most common pattern was Acute tubular necrosis (5 patients), followed by acute cortical necrosis (3 patients), Membrano‐proliferative Glomerulonephritis (2 patients) and thrombotic microangiopathy (1 patient). Complete renal recovery was seen in 24 (82.7%), partial recovery in 3 (10.3%) and 2 patients were dialysis dependent. Conclusions: Acute kidney injury associated with p.vivax monoinfection is not rare as previously thought. Therefore, it should be considered in the differential diagnosis of any patient presenting with multi‐organ dysfunction.