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Kidney Week

Abstract: SA-PO0313

A Wasteful Case Series: Tubulointerstitial Nephritis Secondary to Inflammatory Bowel Disease

Session Information

Category: Acute Kidney Injury

  • 101 AKI: Epidemiology, Risk Factors, and Prevention

Authors

  • Mathias, Jay, The Ohio State University Wexner Medical Center; Division of Nephrology, Columbus, Ohio, United States
  • Satoskar, Anjali A., The Ohio State University Wexner Medical Center; Division of Nephrology, Columbus, Ohio, United States
  • Brodsky, Sergey V., The Ohio State University Wexner Medical Center; Division of Nephrology, Columbus, Ohio, United States
  • Nadasdy, Tibor, The Ohio State University Wexner Medical Center; Division of Nephrology, Columbus, Ohio, United States
  • Parikh, Samir V., The Ohio State University Wexner Medical Center; Division of Nephrology, Columbus, Ohio, United States
Introduction

Tubulointerstitial Nephritis (TIN) is characterized by inflammatory infiltration of the renal tubules and surrounding interstitium. It is caused by a variety of etiologies and will lead to irreversible damage if left unchecked. Renal manifestations such as nephrolithiasis, IgA nephropathy and TIN have been associated with inflammatory bowel disease (IBD). To reinforce IBD as a potential trigger for TIN, we present three TIN cases later found to have IBD on colon biopsy.

Case Description

Case 1: A 41-year-old Indian male with a creatinine of 2.8 mg/dL is referred and found to have sterile pyuria and otherwise unrevealing workup. Renal biopsy revealed acute interstitial nephritis. Creatinine improved to 1.7 mg/dL with steroids, but worsened upon discontinuation. Repeat biopsy showed chronic active interstitial nephritis. Patient started on Mycophenolate (MMF) and steroid taper and maintained on MMF with stable creatinine. Patient underwent screening colonoscopy with biopsies revealing colitis and later diagnosed with IBD after persistent colitis despite stopping MMF which was thought to be cause of his TIN. Treatment for IBD started and MMF was changed to azathioprine with no relapses.

Case 2: A 46-year-old male referred to nephrology with a creatinine of 2.6mg/dL with an associated bland urinalysis and unrevealing workup. Renal biopsy revealed active tubulointerstitial nephritis of uncertain etiology. He later reported chronic abdominal discomfort. Underwent endoscopy and biopsy due to diarrhea which showed colitis suggestive of IBD which was believed to be etiology of his TIN.

Case 3: A 22-year-old female referred to nephrology with a creatinine level of 1.8 mg/dL with pyuria and otherwise unrevealing workup. Renal biopsy showed chronic and focally active tubulointerstitial nephritis with non-necrotizing granulomas to which patient started on steroids. IgG4 was negative. Patient underwent diagnostic colonoscopy with biopsies for bowel changes which revealed colitis suggestive of inflammatory bowel disease which was believed to be etiology of her TIN.

Discussion

TIN treatment primarily addresses the underlying etiology. TIN is often a delayed diagnosis which can lead to irreversible damage. IBD is known to have renal manifestations, but IBD should also be considered as part of the differential when TIN is the presenting manifestation.