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Kidney Week

Abstract: TH-PO127

Acute Interstitial Nephritis Presenting with Isolated Glycosuria

Session Information

Category: Trainee Case Report

  • 102 AKI: Clinical, Outcomes, and Trials


  • Schwartz, Benjamin, Virginia Commonwealth University, Richmond, Virginia, United States
  • Kidd, Jason M., VCU Medical Center, Richmond, Virginia, United States

Acute Interstitial Nephritis (AIN) is often induced by drugs and is a common cause of acute kidney injury. The classical triad of AIN consists of eosinophilia, rash, and fever. However, clinically diagnosing AIN can often be challenging as these signs and symptoms rarely present in concert. The inflammatory pathology of AIN leads to renal tubule dysregulation which can be clinically observed as glycosuria, eosinophilia, leukocytes or white blood cell casts and proteinuria. We present a case of AIN presenting with acute kidney injury and isolated glycosuria without pyuria.

Case Description

A 34-year-old female presented to our institution with nausea, vomiting and abdominal pain. She had been treated for tonsillitis with amoxicillin a month prior to presentation. She had a blood pressure of 169/104 mmHg without antecedent history of hypertension. She was afebrile. Her physical exam was significant for trace lower extremity edema. She had no rashes. On admission, her serum creatinine was 7.7 mg/dL with a potassium of 3.1 mmol/L, and hemoglobin of 11.7 g/dL. Her white blood cell count was 10.2 without eosinophilia. Urinalysis was significant only for glycosuria of over 500 mg/dL with a serum glucose of 119 mg/dL. Urine sediment examination was unremarkable. Hepatitis and HIV serologies were negative, complement levels were normal, and urine immunofixation was negative. Ultrasound of kidneys was normal. Throughout admission she sustained glycosuria with normoglycemia. She underwent renal biopsy which demonstrated acute interstitial nephritis. She was started on high dose prednisone that was tapered over the course of three months. Two months following presentation her glycosuria resolved, and four months following presentation her serum creatinine was 1.2 mg/dL.


This patient had an atypical presentation of AIN that lacked classical diagnostic lab features and has been rarely reported. She had profound glycosuria in setting of normoglycemia, which resolved following a course of corticosteroids. Glycosuria was most likely due to proximal tubule damage from AIN. This case supports previous hypotheses that drug-induced AIN can cause SGLT dysfunction resulting in glycosuria in the absence of other identifiable proximal tubule dysregulations. We propose that resolution of AIN involves the repair and restoration of SGLT function.