A Rare Presentation of Chronic Nonsteroidal Anti-inflammatory Drug-induced Acute-on-chronic Kidney Disease with Secondary Hyperaldosteronism and Hyperparathyroidism in a Young Male with Refractory Hypertension.

Refractory hypertension in young adults warrants evaluation for secondary causes. Chronic nonsteroidal anti-inflammatory drug (NSAID) use, though common, is an underrecognized cause of chronic kidney disease that may lead to biochemical abnormalities, including electrolyte disturbances and hormonal dysregulation. A 37-year-old male presented with headache, vomiting, and abdominal pain. Examination revealed severe hypertension (210/190 mmHg) with epigastric tenderness. Electrocardiography (ECG) showed a Wellens type A pattern with Q waves. Initial laboratories revealed hyponatremia, hypokalemia, and deranged renal function. Despite correction of hyponatremia by day 4, hypokalemia persisted. Investigations revealed elevated aldosterone (37.4 ng/dL) with normal renin (16.9 ng/mL), significant proteinuria (24-h urinary protein: 2.58 g/day), and low creatinine clearance (27 mL/min/1.73 m 2 ). Imaging showed bilaterally small kidneys with loss of corticomedullary differentiation, ruling out renal biopsy. Persistent hypokalemia was refractory to supplementation due to NSAID-induced gastritis. Elevated intact parathyroid hormone (193 pg/mL) and Vitamin D deficiency indicated secondary hyperparathyroidism. Upon detailed history, the patient admitted to chronic NSAID use. A diagnosis of NSAID-induced acute-on-chronic interstitial nephritis with secondary hyperaldosteronism and hyperparathyroidism was made. Management included antihypertensives (labetalol, nicardipine, and prazosin), potassium correction, and withdrawal of NSAIDs. This case highlights the importance of thorough history taking and evaluation of secondary causes in young-onset refractory hypertension. Chronic NSAID use can precipitate progressive renal dysfunction, leading to complex metabolic and endocrine complications, including secondary hyperaldosteronism and hyperparathyroidism.