Posters
Academic Level (Author 1)
Resident
Discipline/Specialty (Author 1)
Internal Medicine
Discipline Track
Patient Care
Abstract
Background: Acute Interstitial nephritis is a common and reversible cause of Acute Kidney Injury, accounting for 15-27% of renal biopsies performed because of this condition. Its incidence has been increasing worldwide. By and large, drug-induced AIN is currently the most common etiology, with antimicrobials and nonsteroidal anti-inflammatory drugs being the most frequent offending agents. The hallmark pathologic features are interstitial edema, interstitial inflammation, and tubulitis with a predominance of CD4+ T lymphocytes and mononuclear cells, with variable numbers of eosinophils. Patients with AIN typically present with nonspecific symptoms of acute renal failure, including oliguria, malaise, anorexia, nausea, and vomiting and a high-suspicious index is necessary. A case is described of a 29-year-old Hispanic obese and diabetic female, who developed AIN after an average period of 2 years of omeprazole. The symptoms were mostly fatigue and anorexia. She had non-nephrotic range proteinuria with pyuria with a mean serum creatinine of 4.72 mg/dl. Eosinophils in urine were normal. Patient also tested positive for ANA, and initially lupus nephritis was in the differentials along with Focal segemental glomerulo-sclerosis due to obestiry. Renal biopsy showed severe interstitial inflammation with lymphoid cells, scattered neutrophils, and very rate eosinophils, ruling out FSGS and lupus nephritis. Omeprazole was discontinued, and Prednisone 60 mg daily were started. Renal recovery was total in 6 weeks post-steroid therapy. Steroids were tapered as the kidney function improved.
Conclusion: Prompt recognition, elimination of the offending source of antigen and use of a limited course of steroid therapy are the mainstay of the treatment. This will result in complete resolution in ~ 65% of cases, partial resolution in up to 20%, and irreversible damage in the rest. Recent studies strongly suggest that early steroid administration (within 7 days after diagnosis) improves the recovery of renal function, decreasing the risk of chronic renal impairment.
Presentation Type
Poster
Recommended Citation
Bartl, Mery B. and Majzoub, Reham, "Proton-Pump inhibitors related acute interstitial nephritis. A case report" (2023). Research Colloquium. 35.
https://scholarworks.utrgv.edu/colloquium/2022/posters/35
Included in
Proton-Pump inhibitors related acute interstitial nephritis. A case report
Background: Acute Interstitial nephritis is a common and reversible cause of Acute Kidney Injury, accounting for 15-27% of renal biopsies performed because of this condition. Its incidence has been increasing worldwide. By and large, drug-induced AIN is currently the most common etiology, with antimicrobials and nonsteroidal anti-inflammatory drugs being the most frequent offending agents. The hallmark pathologic features are interstitial edema, interstitial inflammation, and tubulitis with a predominance of CD4+ T lymphocytes and mononuclear cells, with variable numbers of eosinophils. Patients with AIN typically present with nonspecific symptoms of acute renal failure, including oliguria, malaise, anorexia, nausea, and vomiting and a high-suspicious index is necessary. A case is described of a 29-year-old Hispanic obese and diabetic female, who developed AIN after an average period of 2 years of omeprazole. The symptoms were mostly fatigue and anorexia. She had non-nephrotic range proteinuria with pyuria with a mean serum creatinine of 4.72 mg/dl. Eosinophils in urine were normal. Patient also tested positive for ANA, and initially lupus nephritis was in the differentials along with Focal segemental glomerulo-sclerosis due to obestiry. Renal biopsy showed severe interstitial inflammation with lymphoid cells, scattered neutrophils, and very rate eosinophils, ruling out FSGS and lupus nephritis. Omeprazole was discontinued, and Prednisone 60 mg daily were started. Renal recovery was total in 6 weeks post-steroid therapy. Steroids were tapered as the kidney function improved.
Conclusion: Prompt recognition, elimination of the offending source of antigen and use of a limited course of steroid therapy are the mainstay of the treatment. This will result in complete resolution in ~ 65% of cases, partial resolution in up to 20%, and irreversible damage in the rest. Recent studies strongly suggest that early steroid administration (within 7 days after diagnosis) improves the recovery of renal function, decreasing the risk of chronic renal impairment.