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

Abstract

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

A 70-year-old woman with a history of chronic NSAID use presented with weakness and palpitations. She had atrial fibrillation, severe hypokalemia (K 1.5 mmol/L), non-anion gap metabolic acidosis (HCO₃ 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.

Keywords: Interstitial nephritis; Non-steroidal anti-inflammatory drugs; Renal tubular acidosis; Hypokalemia; Steroids; Tubular dysfunction; Case report

Core Tip: This article underscores the importance of maintaining a high level of clinical suspicion for interstitial nephritis (IN) in case of non-steroidal anti-inflammatory drugs (NSAID)-induced persistent renal injury and dyselectrolytemia suggestive of renal tubular acidosis, and the critical role of biopsy in NSAID-induced IN. Role of steroids in drug-induced IN is debated; some study suggests their role only in early cases before fibrosis ensues. Our article emphasizes the potential role of steroids in persistent renal impairment and metabolic disturbances, even after discontinuation of NSAIDs, provided there is evidence of active interstitial inflammation and tubulitis on renal biopsy.