Pathogenesis of secondary hyperparathyroidism in chronic renal insufficiency

Hyperparathyroidism is recognized to be an invariable complication of chronic renal insufficiency. Biochemical and/or histological evidence of hyperparathyroidism occurs in many patients with mild renal insufficiency (glomerular filtration rate of 50-75 ml/min) and predictably so when the glomerular filtration rate is less than 40-50 ml/min. A reduction in the serum concentration of 1,25-dihydroxyvitamin D, the biologically active metabolite of vitamin D, can contribute to the pathogenesis of the hyperparathyroidism, at least in part, by decreasing gut absorption of calcium and by increasing the set point for calcium suppression of parathyroid hormone release. In patients with mild and moderate renal insufficiency, both the serum concentration of 1,25-dihydroxyvitamin D and that of immunoreactive parathyroid hormone are importantly determined by the dietary intake of phosphorus. The pathogenesis of secondary hyperparathyroidism in patients with severe renal insufficiency is complex and multifactorial.