Severe Hemolysis and Acute Kidney Injury Due to Primaquine in a Patient With G6pd Deficiency: A Case Report

Plasmodium vivax malaria is endemic in the Brazilian Amazon, where glucose-6-phosphate dehydrogenase (G6PD) deficiency affects up to 5% of the male population. The use of 8-aminoquinolines, such as primaquine, in these patients can trigger severe intravascular hemolysis, with risk of acute kidney injury (AKI). This severe case report after accidental primaquine use highlights the importance of safe protocols in areas with endemic malaria and enzymatic deficiency. A 48-year-old Black male, with a history of three previous malaria episodes and G6PD deficiency confirmed by enzymatic assay, sought care at a tropical diseases referral service after a recent diagnosis of P. vivax by thick blood smear. He reported having received a prescription for chloroquine plus primaquine, despite the known contraindication. On the fourth day of treatment, he developed high fever (39.8°C), generalized jaundice, dark urine (choluria), anasarca, crampy abdominal pain, and dyspnea with minimal exertion. Admission laboratory tests revealed severe anemia (Hb 6.1 g/dL), AKI (creatinine 9.4 mg/dL; urea 194 mg/dL), metabolic acidosis (pH 7.28; HCO3 14 mEq/L), hyperkalemia (5.8 mEq/L), marked LDH elevation (6,996 U/L), and predominantly direct hyperbilirubinemia (5.6 mg/dL). Methemoglobinemia was 19%, and peripheral blood smear confirmed hemolysis (schistocytes +2/4 fields). The patient was admitted to the ICU, where he received urgent hemodialysis, transfusion of 4 units of packed red blood cells, high-flow oxygen therapy (FiO2 50%), and correction of fluid and electrolyte disorders. After immediate discontinuation of primaquine and intensive supportive care, progressive recovery was observed: spontaneous diuresis on day 5 (1.2 L/day), creatinine 1.2 mg/dL at discharge, and stable hemoglobin (10.5 g/dL). Serologies for HIV, hepatitis B/C, and Chagas disease were negative. Abdominal ultrasound ruled out renal obstruction, showing only bilateral hyperechogenic parenchyma. This case demonstrates the severe consequences of failing to screen for G6PD deficiency before prescribing primaquine in endemic areas, with preventable hemolysis resulting in AKI and high treatment costs. G6PD testing at the primary care level is recommended, along with professional training to identify at-risk groups and adoption of safe protocols for deficient patients, prioritizing therapeutic safety in malaria settings with genetic vulnerability.