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Abstract: SA-PO868

Granulomatous Interstitial Nephritis due to Histoplasma spp. in a Kidney Transplant

Session Information

Category: Transplantation

  • 2002 Transplantation: Clinical

Authors

  • Davis, Alyssa Leigh, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Kapp, Meghan, University Hospitals, Cleveland, Ohio, United States
  • Concepcion, Beatrice P., Vanderbilt University Medical Center, Nashville, Tennessee, United States
Introduction

There are numerous causes of acute kidney injury (AKI) in an acutely infected kidney transplant recipient. Here we present an unusual cause of AKI secondary to granulomatous interstitial nephritis.

Case Description

A 51/M with a kidney transplant in 2010 (maintained on FK/MMF/Pred), afib and HTN presented in early fall with fever and AKI. He described 1 month of fevers, myalgias, night sweats, shortness of breath and abdominal pain. On presentation, temp was 101.9*F, BP 111/76, HR 130, RR 24, O2 sat 97% RA . Physical exam revealed an ill-appearing man in no acute distress, clear lungs bilaterally and mild epigastric tenderness to palpation. Initial laboratory exam was notable for Na129 mmol/L, K 6.9 mmol/L, bicarbonate 12 mmol/L, BUN 48 mg/dL and SCr 3.7 mg/dL (baseline 1.6 mg/dL). Urinalysis had no protein, 24 WBC and 19 RBC. Transplant ultrasound was normal. CXR revealed a new 1cm dense nodule in the right lower lobe. CMV, EBV, and BK virus were not detected. Urine bacterial culture had no growth. Urine histoplasma antigen returned strongly positive. His epigastric pain was evaluated with endoscopy and colonoscopy, and he was found to have erosions and friable tissue in the duodenum, colon, and cecum. Due to persistent kidney dysfunction, a kidney biopsy was performed. This revealed two foci of granulomatous inflammation comprised of histiocytes and small lymphocytes. A GMS stain highlighted fungal organisms in these areas consistent with Histoplasma spp. There was global granular mesangial staining for C3 (1+) and segmental granular mesangial staining for IgM (trace) suggestive of sequelae of infection. He was treated for disseminated histoplasmosis with liposomal amphotericin B (8 days) with good clinical improvement and was transitioned to maintenance isavuconazole (due to drug interaction of itraconazole with patient's amiodarone). On follow-up eight months later, SCr improved to 2 mg/dL, and the patient remains on isavuconazole.

Discussion

Granulomatous interstitial nephritis may occur in the setting of direct infection of the kidney by Histoplasma spp. as demonstrated in this patient’s kidney biopsy. In this case, prompt and appropriate treatment of the infection led to clinical improvement. Providers should be aware of unusual causes of AKI in an acutely infected kidney transplant recipient which may require a biopsy for diagnosis.