SUN-267 - Secondary Arterial Hypertension Associated With Inadvertent Anabolic Steroid Use: a Case Report

A 28-year-old previously healthy man with recently diagnosed hypertension and a history of anabolic-androgenic steroid use was admitted with progressive dyspnea and dry cough, evolving to anasarca, hemoptysis, hypertensive emergency (BP 220×145 mmHg), and acute respiratory failure, requiring endotracheal intubation, intensive care unit admission, and urgent hemodialysis. On admission, laboratory tests showed urea of 272 mg/dL, creatinine of 11.2 mg/dL, massive nephrotic syndrome (24-hour proteinuria of 94.52 g/day, later 161.67 g/day; serum albumin 2.4 g/dL), and anemia (hemoglobin 8.4 g/dL, nadir 5.9 g/dL).

Chest computed tomography revealed ground-glass opacities and consolidations with central predominance, associated with mild septal thickening, small bilateral pleural effusions, and diffuse alveolar hemorrhage. Given the suspicion of a pulmonary-renal syndrome, pulse therapy with methylprednisolone was initiated while vasculitis was investigated. However, etiologic workup showed negative autoantibodies and normal complement levels, making this hypothesis unlikely.

Renal Doppler ultrasound demonstrated marked bilateral cortical thinning (0.6–0.8 cm), with patent renal arteries and preserved Doppler indices, consistent with advanced chronic parenchymal kidney disease. In this context, kidney biopsy was not performed due to lack of expected impact on management, and the patient was referred for kidney transplant evaluation. In parallel, echocardiography showed preserved ejection fraction (70%), left ventricular hypertrophy, left atrial enlargement, grade II diastolic dysfunction, and pulmonary hypertension, with NT-proBNP of 9000 pg/mL, suggesting heart failure with preserved ejection fraction as a major contributor to the congestive state.

This case highlights anabolic-androgenic steroid use as a possible contributing factor to severe, advanced chronic kidney disease in a young patient, along with cardiovascular findings consistent with possible secondary hypertension and myocardial dysfunction. An extensive etiologic investigation was performed and alternative diagnoses were excluded, with steroid use remaining the only identifiable risk factor. The relevance of this finding is supported by recent data demonstrating a 2.81-fold higher mortality risk among anabolic-androgenic steroid users compared with controls, including increased rates of both natural and unnatural deaths, underscoring the importance of investigating this exposure in atypical presentations of hypertension and advanced chronic kidney disease in young adults.

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