The kidney is a principal target-organ for parathyroid honnone (PTH). Be sides the stimulation of gluconeogenesis and synthesis of 1, 25 (OHh-vitarnin D3, the major physiological effect of PTH is on the regulation of tubular transport processes (39). PTH reduces proximal tubule reabsorption of phos phate and bicarbonate and in more distal nephron segments, enhances the reabsorption of magnesium (thick ascending limb of Henle's loop) and of calcium (distal tubule). PTH-related peptide (PTHrP), associated with humor al hypercalcemia of malignancy, exerts effects comparable to PTH on renal function and is thought to interact with renal PTH receptors (31). The proximal tubule effects of PTH and PTHrP include inhibition of brush border transport systems (NalPi-cotransport, NalH-exchange) transmitted through PTH receptor-mediated production of intracellular messengers (inositoltris phosphate (IP3), diacylglycerol (DAG), cytosolic free calcium ([Ca2+] i and cAMP), and activation of specific intracellular regulatory pathways (protein kinase C, protein kinase A).