The Case | Acute renal injury in a young Burmese immigrant

A 20-year-old Burmese refugee was admitted with weakness, vomiting, lower abdominal pain, and dark red urine. She was not pregnant. From the age of 15 years, she had a history of recurrent jaundice, anemia needing a total of 30 blood transfusions, and (allegedly) consequent hepatitis, but no history of known malaria. Physical examination showed a weak, pale, and jaundiced young woman, afebrile and normotensive but mildly fluid overloaded; she did not have hepatosplenomegaly, lymphadenopathy, or cutaneous or mucosal bleeding tendencies. Urinalysis showed 200 mg/dl of protein and large amount of blood with o10 RBCs/h.p.f. without eosinophiluria. The urinary protein to creatinine ratio was o1.8, serum creatinine was 4 mg/dl, and peripheral blood hemoglobin was 5.2 g/dl, with normal white blood cell and platelet counts. Serum ASO titer, 3rd and 4th components of the complement, hepatitis A IgM antibody, hepatitis B surface antigen, hepatitis C antibody, HIV test, serum protein electrophoresis, anti-nuclear and anti-neutrophil cytoplasmic antibodies, and cryoglobulins were all either negative or normal. Unadjusted reticulocyte count was 3.9%, with low serum haptoglobin (16 mg/dl, 435 normal) and elevated lactic dehydrogenase level of 1872 IU (o220 normal). Direct Coombs test was negative, and peripheral blood smear showed no schistocytes or malarial parasite with Giemsa staining. Hemoglobin electrophoresis and screening tests for pyruvate kinase and glucose-6 phosphate dehydrogenase deficiency were negative. She had normal-sized kidneys, and renal biopsy showed normal glomeruli, with acute tubular cell injury, hemosiderin crystals in the tubular epithelial cells, and focally in sloughed epithelium in the tubular lumen. Arteriolar thrombotic changes were absent (Figure 1).