Kidney Week

Abstract: FR-PO1236

Ectopic ACTH from Small Cell Lung Cancer Presenting as Refractory Hypertension and Hypokalemia with Concomitant Phosphate Wasting

Session Information

• Onconephrology: Diagnostic Dilemmas, Therapy-Related Toxicities, and Clinical Cases
  October 23, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Onconephrology

• 1600 Onconephrology

Authors

• Santos, James Urbano, Stony Brook University Hospital, Stony Brook, New York, United States

James Urbano Santos, MD

• Mariuma, David, Stony Brook University Hospital, Stony Brook, New York, United States

David Mariuma, MD

Introduction

Renal physiology principles can aid in identifying rare paraneoplastic syndromes as a cause of secondary hypertension and phosphate wasting.

Case Description

A 66-year-old female with no prior medical history presented with headache and shortness of breath. She was hypertensive (200/104 mmHg), afebrile, and mildly hypoxemic. Labs showed creatinine 0.5 mg/dL, eGFRCr 102 ml/min/1.73m², potassium 3.1 mmol/L, phosphorus 0.9 mg/dL, and calcium 8.5 mg/dL. She was treated with amlodipine, losartan, labetalol, hydralazine, and escalating KCl supplementation reaching 180 mEq total in the day; with no improvement in potassium or blood pressure. Nephrology was consulted; work-up for hypertension, hypophosphatemia, and hypokalemia showed PTH 126.1 pg/mL, vitamin D 5 ng/mL, FePO4 75%, TmP/GFR 0.36 mg/dL, aldosterone <3.0 ng/dL, and renin activity 0.2 ng/mL/hr. Spironolactone and vitamin D supplementation were added, resulting in improvement of blood pressure and potassium. Further workup revealed an 8 AM cortisol of 39.0 µg/dL. This prompted measurement of ACTH, which was 236.0 pg/mL, concerning for ectopic ACTH production. CT chest show right hilar soft-tissue fullness, and fine needle aspiration biopsy confirmed small cell carcinoma. Chemotherapy with carboplatin and etoposide was initiated. Due to the chemotherapy protocol requiring high-dose dexamethasone, further evaluation for ectopic Cushing’s syndrome was postponed.

Discussion

The patient’s hypertension, hypokalemia, elevated ACTH, and markedly elevated morning cortisol with suppressed renin and aldosterone was consistent with apparent mineralocorticoid excess via cortisol saturation of 11B-HSD2, a recognized paraneoplastic manifestation of small cell carcinoma.^1,2 Elevated FePO4 and low TmP/GFR suggest concurrent oncogenic osteomalacia; while vitamin D deficiency may have contributed to secondary hyperparathyroidism, the degree of renal phosphate wasting exceeded what this alone would explain.^3,4 This case illustrates a wider principle: suppressed renin with suppressed aldosterone in refractory hypertension should prompt evaluation for cortisol-mediated mineralocorticoid receptor activation, including ectopic ACTH from occult malignancy. Coexisting renal phosphate wasting should raise concern for tumor-induced osteomalacia. Identifying one paraneoplastic syndrome should prompt a systematic search for others.