Abstract: PUB147
When Painkillers Cause Pain: A Case of Dual Kidney Injury from Nonsteroidal Anti-Inflammatory Drugs
Session Information
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Sinha Ray, Abhisekh, Creighton University School of Medicine, Omaha, Nebraska, United States
- Mareedu, Neeharik, UPMC Western Maryland, Cumberland, Maryland, United States
- Lathiya, Maulik, Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Errabelli, Praveen K., Allina Health, Minneapolis, Minnesota, United States
Introduction
Non-steroidal anti-inflammatory drugs (NSAIDs) are widely utilized for their analgesic and anti-inflammatory effects, yet their potential to induce renal adverse events remains a significant clinical consideration. While various forms of kidney injury can occur, chronic interstitial nephritis (CIN) and proximal renal tubular acidosis (pRTA) are less common but important complications associated with long-term NSAID exposure. This report describes the case of a patient presenting with both chronic interstitial nephritis and proximal renal tubular acidosis secondary to chronic NSAID use, highlighting the diagnostic journey and management.
Case Description
A 70-year-old female with a history of chronic NSAID use presented with weakness and palpitations. She was found to have atrial fibrillation, severe hypokalemia (K 1.5 mmol/L), non-anion gap metabolic acidosis (HCO3 11 mmol/L), hypophosphatemia (1.2 mg/dL), acute kidney injury (creatinine 2 mg/dL), and rhabdomyolysis (CK 15,620 U/L).
Despite aggressive electrolyte repletion and NSAID cessation, her electrolyte imbalances and renal impairment persisted. Urinalysis showed proteinuria, hematuria, and sterile pyuria, with a positive urine anion gap suggestive of pRTA.
Her electrolytes improved with aggressive supplementation and addition of spironolactone. At a 4-week follow-up, she still required significant oral supplements, and her creatinine remained elevated.
A renal biopsy confirmed CIN with moderate interstitial fibrosis and tubular atrophy (IFTA). The patient was started on 4-week course of prednisone taper with improvement in creatinine to 1 mg/dL, and normalization of electrolytes without the need for further supplementation. These improvements were sustained at a 3-month follow-up.
Discussion
This case illustrates severe chronic NSAID-induced kidney injury, confirmed as CIN by biopsy, with associated (pRTA. Atypically, her electrolyte issues and need for supplementation persisted despite stopping NSAIDs, only resolving after corticosteroid treatment. However, her creatinine did not fully normalize, likely due to underlying moderate IFTA from chronic NSAID use. This highlights that NSAID nephrotoxicity can be variable and prolonged, underscoring the need for high suspicion, the value of renal biopsy, and the critical role of steroids in achieving significant renal recovery in severe or persistent cases.