Renal calcium transport is described as the result of two processes, a paracellular, gradient-dependent process that predominates in most segments of the nephron and a transcellular, energy-dependent step that characterizes calcium transport in the distal convoluted tubule (DCT). Transcellular calcium transport involves entry into the DCT cell, possibly via channels, intracellular movement which appears to be facilitated by the presence of the vitamin D-dependent, cytosolic calcium-binding protein (CaBPr, calbindin D28k, mol mass approximately 28 kDa), and extrusion via the Ca-ATPase. Although much is known about calcium channels, their presence in renal tissue has only been demonstrated by preliminary studies. Quantitative data on CaBPr content of rat DCT are also unavailable, but theoretical analysis and early experimental values of intracellular self-diffusion of calcium have confirmed the need for an intracellular calcium "ferry," i.e., a molecule like CaBPr to amplify intracellular calcium movement. Available data on the plasma membrane Ca-ATPase are consistent with the extrusion kinetics attributed to the renal Ca-ATPase, but it has not been isolated, nor has its gene been cloned. Regulation and disorders of renal calcium transport are likely to involve one of the three transcellular steps, but indirect regulation by modification of the cell walls and molecules constituting the paracellular pathway cannot be excluded.