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Chronic kidney disease (CKD) causes secondary hyperparathyroidism (SHPT). The cardinal features of SHPT are persistence of normocalcemia as CKD progresses and dependence of the parathyroid hormone concentration ([PTH]) on phosphate influx (I P ). The tradeoff-in-the-nephron hypothesis integrates these features. It states that as the glomerular filtration rate (GFR) falls, the phosphate concentration ([P] CDN ) rises in the cortical distal nephron, the calcium concentration ([Ca] CDN ) in that segment falls, and [PTH] rises to maintain normal calcium reabsorption per volume of filtrate (TR Ca /GFR). In a clinical study, we set GFR equal to creatinine clearance (C cr ) and I P equal to the urinary excretion rate of phosphorus (E P ). We employed E P /C cr as a surrogate for [P] CDN . We showed that TR Ca /C cr was high in patients with primary hyperparathyroidism (PHPT) and normal in those with SHPT despite comparably increased [PTH] in each group. In subjects with SHPT, we examined regressions of [PTH] on E P /C cr before and after treatment with sevelamer carbonate or a placebo. All regressions were significant, and ∆[PTH] correlated with ∆E P /C cr in each treatment cohort. We concluded that [P] CDN determines [PTH] in CKD. This inference explains the cardinal features of SHPT, much of the evidence on which other pathogenic theories are based, and many ancillary observations.

Tradeoff-in-the-Nephron: A Theory to Explain the Primacy of Phosphate in the Pathogenesis of Secondary Hyperparathyroidism