Renal tubular acidosis complication of non-steroidal anti-inflammatory drugs induced interstitial nephritis and its complete resolution with steroids: A case report

BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) are extensively utilized for their analgesic and anti-inflammatory properties; however, their potential to induce renal adverse events remains a significant clinical concern. NSAID-induced interstitial nephritis (IN) and renal tubular acidosis (RTA) are rare but important complications of prolonged NSAID consumption. NSAID-induced RTA has been documented in limited case reports and usually resolves after stopping NSAIDs. However, our case shows a persistent, severe hypokalemia and hypophosphatemia linked to RTA from NSAID-induced IN, which resolved with steroid therapy. CASE SUMMARY: 11 mmol/L, anion gap 11), hypophosphatemia (1.2 mg/dL), acute kidney injury (creatinine 2 mg/dL from 0.6), and rhabdomyolysis (creatine kinase 15620 U/L). Urinalysis showed pH 6.5, proteinuria, sterile pyuria, and a positive urine anion gap, indicating RTA. Electrolytes improved with supplementation and spironolactone, but didn't normalize. At 4 weeks post-hospitalization, she still required supplementation; creatinine remained high. Renal biopsy revealed interstitial inflammation with active tubulitis, moderate interstitial fibrosis, and tubular atrophy. She was treated with 4 weeks of prednisone, leading to normalized electrolytes and improved creatinine (1 mg/dL), and the improvements were sustained 6 months post-treatment. CONCLUSION: Our patient exhibited persistent metabolic disturbances even after the cessation of NSAID therapy. Despite moderate chronicity, active interstitial inflammation responded favorably to corticosteroid treatment, resulting in improved renal function and restoration of tubular function, with normalization of acid-base and electrolyte parameters.