Subclinical urolithiasis in patients with asymptomatic primary hyperparathyroidism

Primary hyperparathyroidism (PHPT) is slowly becoming an ‘asymptomatic’ disorder. The diagnostic incidence has increased considerably due to the introduction of modern multichannel biochemical analysis, including routine assay of serum calcium.1 The elevated parathyroid hormone (PTH) levels in PHPT are related to a shift in the set point of calcium-regulated PTH secretion such that despite the normal inverse sigmoid relationship, higher plasma calcium levels are needed to suppress PTH.2,3 Such high levels of PTH lead to increased renal resorption of calcium, increased osteoclastic bone resorption, phosphaturia and increased renal synthesis of 1,25(OH)2D (calcitriol), which in turn increases intestinal calcium absorption.2,4,5

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