#1291 Rosuvastatin induced acute kidney injury—a case report

Abstract Background and Aims Drug-induced acute interstitial nephritis (AIN) is a significant cause of acute kidney injury. According to the literature, AIN is most commonly induced by antibiotics or anti-inflammatory drugs. Secondary minimal change disease (MCD) can also have iatrogenic trigger, although very rare. In this case report, we present a 67-year-old female patient with biopsy-proven combined AIN and MCD induced by rosuvastatin. Case report This patient, with previously normal renal function and no significant comorbidities or chronic therapy, presented to the emergency department with acute onset of eyelid and extremities edema lasting for 10 days, along with decreased urination. She had no skin changes such as rash or pruritus but had a persistent cough and pain in the calves and heels. The workup revealed acute kidney injury (Urea: 26.3 mmol/L; Creatinine: 465 µmol/L; eGFR: 8 ml/min/1.73 m²) accompanied by hyperkalemia (5.5 mmol/L), hypocalcemia (2.05 mmol/L), hyperphosphatemia (2.23 mmol/L), hypoalbuminemia (27 g/L), and an elevated sedimentation rate (68 mm/3.6 s). The blood count, coagulogram, hepatogram, and ferrogram were unremarkable, and inflammatory parameters were stable. On examination, the patient was hypertensive (175/105 mmHg), oliguric and had anasarca. Urinalysis showed proteinuria (3+) and erythrocyturia (3+). The patient was admitted to the department for further treatment, and non-selective proteinuria of nephrotic range was confirmed in 24-hour urine collection (protein: 10,200 mg/dU; albumin: 5,500 mg/dU). Additional history revealed that she had been taking rosuvastatin, prescribed for mixed hyperlipidemia, for the past two months. Conservative supportive therapy was initiated to manage proteinuria, control blood pressure, and reduce peripheral edema. An ACE inhibitor was introduced at the maximum dose, and diuresis was stimulated with parenteral human albumin combined with diuretics. An ultrasound examination revealed bilateral kidneys of normal size (100 mm) with normal parenchyma. On the fifth day after admission a kidney biopsy was performed and sent for analysis by immunofluorescence, light, and electron microscopy. The findings from light and immunofluorescence microscopy were consistent with acute tubulointerstitial nephritis with eosinophilia and minimal change disease with extensive loss of podocyte foot processes on 85% of the examined surface. The histopathological and clinical findings were indicative of combined acute kidney injury caused by presumably rosuvastatin. Upon admission rosuvastatin was discontinued and renal function recovery was already underway, with a decrease in creatinine levels. Oral prednisone therapy (1 mg/kg of body weight daily for 14 days) was initiated, followed by tapering over four weeks. The patient was discharged with additional therapy consisting of perindopril, indapamide, amlodipine, and moxonidine. At the four-week follow-up after initiating corticosteroid therapy, the patient achieved complete recovery of renal function (Urea: 6.9 mmol/L; Creatinine: 86 µmol/L; eGFR: 61 ml/min/1.73 m²), correction of electrolyte imbalances (K: 4.0 mmol/L; Na: 140 mmol/L; Ca: 2.14 mmol/L; P: 1.7 mmol/L), and regular diuresis with proteinuria <60 mg/dU and albuminuria <10 mg/dU. Prednisone therapy was successfully tapered, with the recommendation to avoid statins. Conclusion To our knowledge and based on a review of the literature, this is so far the only case of combined AIN and secondary MCD induced by rosuvastatin use. In our patient, who had no other potential cause of acute kidney failure, eight weeks of rosuvastatin therapy led to acute renal injury with nephrotic syndrome. Kidney biopsy findings showed interstitial infiltrates predominantly composed of eosinophils and extensive podocyte foot processes effacement. Withdrawal of the culprit drug, combined with prednisone treatment (1 mg/kg/day), resulted in complete recovery of renal function.