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Cortical necrosis in a kidney transplant recipient due to leptospirosis

A 64-year-old woman suffered from end-stage renal failure due to unknown cause. She received kidney transplantation in 2003 and her maintenance immunosuppression comprised corticosteroids, cyclosporine A and azathioprine. She presented with fever, graft pain and reduced urine output in May 2013. Her serum creatinine level rose from 82 μmol/L to 279 μmol/L, and then rapidly deteriorated into oliguric renal failure. Complete blood picture revealed leukocytosis (13.3 × 10/L; neutrophil predominant) and concomitant liver derangement (aspartate aminotransferase, 724 U/L; alanine aminotransferase, 288 U/L; total bilirubin, 33 μmol/L; lactate dehydrogenase, 2183 U/L). The haemoglobin level, platelet counts, clotting profiles and urinalysis were unremarkable. Blood film showed no fragmented red cells and lupus anticoagulant was negative. Ultrasound did not demonstrate vascular thrombosis or obstruction and renal isotope scan only showed mildly impaired perfusion. Allograft biopsy revealed extensive cortical necrosis involving both glomeruli and tubules, with thrombi within the glomeruli (Fig. 1A) and fibrinoid necrosis of arterioles but no evidence of rejection (Fig. 1B). The Panbio Leptospira IgM ELISA (Standard Diagnostic, Gyeonggi-Do, Korea) was repeatedly positive. In retrospect, the patient volunteered that she had experienced occupational exposure to sewage water. Her urine output returned to normal after 2 weeks of temporary haemodialysis and i.v. meropenem. Her serum creatinine was 324 μmol/L 6 months after her initial presentation. Leptospirosis is a zoonotic disease caused by the spirochete Leptospira spp. Classical renal histological changes of leptospirosis include tubulointerstitial nephritis and acute tubular necrosis, while extensive cortical necrosis has not been reported previously. As the Doppler ultrasound and renal isotope scan did not reveal significant abnormalities, we postulate that the extensive renal necrosis in this case might have been related to thrombosis and fibrinoid necrosis of small intrarenal vasculatures triggered by severe Leptospira infection. Indeed, cerebral venous thrombosis due to severe vasculitis has previously been reported in leptospirosis. Data regarding leptospirosis in renal transplant recipients are limited but these immunocompromised subjects can develop fulminant leptospirosis and succumb to multi-organ failure. Another reason for the poor outcomes is due to the diagnostic difficulty of leptospirosis in renal transplant recipients as it may mimic more common conditions such as graft pyelonephritis or acute rejection, and serological confirmation is often delayed. Therefore, one should initiate empirical antibiotics with activity against leptospirosis given a compatible clinical context and history of exposure, as this will significantly improve patient outcomes.