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Kidney International Reports ; 7(9):S527, 2022.
Article in English | EMBASE | ID: covidwho-2041723

ABSTRACT

Introduction: Acute Interstitial Nephritis (AIN) is an important cause of Acute Kidney Injury (AKI), and infections are the second most common etiology, after the drugs. However, AIN following fungal infections is rare. We describe two cases of AIN, which on the investigation turn out to be candidemia following fungal infective endocarditis. Methods: CASE 1: A 65-year-old man with hypertension and diabetes without diabetic or hypertensive retinopathy and prior normal renal function, presented to us with vague abdominal pain with steadily creeping creatinine to 2mg/dl within 2 weeks, and urine showed no albuminuria and sediments. There was no history of any specific drug intake. His hematological and other parameters were normal. Blood and urine cultures were sterile. He underwent a renal biopsy which revealed acute interstitial nephritis (Figure 1). He was started on prednisolone at 1mg/kg/day for 1-week following which he had a rapidly worsening azotemia requiring hemodialysis. Steroids were stopped. Repeat blood cultures were sent which grew candida albicans resistant to flucytosine. Re-evaluation of the fundus revealed macular infarct in the right eye with vitreoretinitis in the left eye suggestive of endophthalmitis. PET CT showed increased FDG uptake in both kidneys suggestive of pyelonephritis. Trans-esophageal echocardiography (TEE) showed aortic valve vegetations. He was treated with antifungals for 3 months. He was dialysis-dependent for 2 weeks. He gradually regained normal renal function 3 weeks after starting anti-fungal agents. CASE 2: A 57-years-old man with diabetic, hypertensive, and no diabetic retinopathy had severe covid pneumonia in June 2021 requiring oxygen and tocilizumab 80 mg for 4 days, recovered with normal renal function. He presented to us 1 month later with unexplained non-oliguric severe AKI requiring dialysis, with bland urine sediments. Renal biopsy showed lymphocytic infiltrates in the interstitium suggestive of AIN (Figure 2). Blood cultures were sterile, but serum beta-D-glucan was elevated at 333 pg/ml. He was Initiated on 1mg/kg of prednisolone, on the presumption of drug-induced AIN. Simultaneously workup for systemic infection revealed mitral anterior leaflet endocarditis. He was initiated on anti-fungal therapy on the advice of an infectious disease specialist and the steroid was stopped. He continued to be dialysis-dependent after 6 weeks, despite anti-fungal agents. Results: [Formula presented] Conclusions: AIN contributes a significant proportion of cases in unexplained AKI. Prompt evaluation with a renal biopsy is warranted. Acute interstitial nephritis particularly due to candidemia can be oligosymptomatic as seen in our two cases. Since steroids have a significant role in treating early AIN, a dedicated search for underlying silent endocarditis and candidemia is advisable before initiating steroid therapy. Ophthalmic fundus evaluation, TEE, and repeat blood culture may be necessary to identify hidden candidemia. We recommend an evaluation to exclude fungal endocarditis in patients with AIN who present with minimal or no symptoms and no definitive cause for AIN is present. No conflict of interest

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