CHANGES IN RENAL HEMODYNAMICS AND TUBULAR FUNCTION OF SURGICALLY CURED PRIMARY HYPERPARATHYROID PATIENTS ARE PROBABLY DUE TO CHRONIC HYPERCALCEMIC NEPHROPATHY

To understand the mechanisms responsible for the persistent hypercalci uria and reduced glomerular filtration rate (GFR) previously found in 6 of 10 patients surgically cured of primary hyperparathyroidism (PHPx ), the tubular handling of lithium, sodium, calcium, and phosphate as well as the renal hemodynamics were evaluated in these 10 PHPx patient s, in 10 control subjects, and in 5 patients with renal hypercalciuria (RH), during fasting and after an oral calcium load. A positive corre lation between the fractional excretions of calcium and sodium was fou nd in all groups, but the PHPx patients excreted more calcium for the same amount of sodium than control subjects. The fractional proximal s odium reabsorption (FPRNa), distal delivery, and functional phosphate reabsorption were similar in all groups; a significant positive correl ation was found between the fractional calcium reabsorption and the FP RNa, indicating that proximal tubular function was preserved and that the urinary calcium losses in RH and in the hypercalciuric PHPx patien ts (h-PHPx) occurred in the distal nephron, However, only h-PHPx patie nts had reduced renal plasma now, renal blood now, and GFR, as well as a high renal vascular resistance, which was even more evident after t he calcium challenge. These findings lead us to conclude that RH and h -PHPx patients are very different, as far as kidney dysfunction is con cerned, and that a hypercalcemic nephropathy is the most probable caus e of the alterations in distal calcium reabsorption and renal hemodyna mics found in the h-PKPx patients.