Primary hyperaldosteronism, secondary hyperparathyroidism, low bone mass and kidney stones - an underappreciated relationship

Document Type

Conference Proceeding

Publication Date

9-27-2024

Publication Title

J Bone Miner Res

Abstract

Primary hyperaldosteronism (PHA) is increasingly recognized as a cause of hypertension. Given that sodium excretion is linked with calcium excretion, PHA can lead to kidney stones, secondary hyperparathyroidism (SHPT), and reduced bone density (BMD). Here, we present a case of PHA, renal stones, and low bone mass in a patient who additionally experiences muscle weakness associated with episodes of hypokalemia and hypophosphatemia. A 38-year-old male with history of hypertension and renal stones status post lithotripsy sought consultations with a neurologist and nephrologist due to proximal muscle weakness. Key findings from his biochemical assessments were mild hypokalemia, hypophosphatemia (with normal serum calcium) and mild metabolic alkalosis. Vitamin D was normal and parathyroid hormone was elevated. His renin was 2.6 (ref. range 3.1 - 57.1 pg/mL), aldosterone of 35.8 (ref. range <=39.ng/dL), and cortisol levels of 8.8 (ref. range 2.9-19.4 ug/dL). He had two episodes of severe hypokalemia (2.8 mmol/L) and hypophosphatemia (0.7 mg/dL) after surgical procedures. A 24-hour urine aldosterone test showed levels of 29 (ref. range 2.0-20 mcg/24 hours). Abdominal CT scan showed normal adrenals and left-sided hydronephrosis. An isotope renal scan indicated 17.3% function in the left kidney and 82.7% in the right kidney. EMG nerve conduction velocity tests were normal, as was serum carnitine. BMD showed osteopenia. Genetic testing did not identify any mutations related to channelopathies. He was diagnosed with PHA and SHPT by endocrinologists and began treatment with 100mg of eplerenone. Genetic testing for mutations related to PHA and periodic paralysis will be pursued further. Low BMD and kidney stones have been linked with PHA. In PHA, excessive sodium intake can lead to increased calcium excretion. When coupled with low calcium intake, it can trigger SHPT, which subsequently promotes phosphaturia. Sodium restriction is crucial in managing PHA as it not only reduces the renin-aldosterone ratio but also helps conserve calcium. It has been shown that sodium restriction can decrease phosphaturia and enhance bone alkaline phosphatase levels, suggesting potential osteo-anabolic effects. Furthermore, there is a hypothesized bidirectional relationship between aldosterone and parathyroid hormone, where aldosterone may stimulate parathyroid hormone secretion and vice versa. Given that both hyperaldosteronism and secondary hyperparathyroidism are common conditions, it is essential to recognize and manage kidney stones and low bone mass in patients with primary hyperaldosteronism.

Volume

39

First Page

344

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