Roger A.L. Sutton

Renal Handling of Calcium: Overview

There have been several comprehensive recent reviews of renal calcium handling, emphasising either clearance data, micropuncture data, or both (1–4). In this review we will be concerned particularly with the extent and possible mechanisms of calcium transport in successive segments of the nephron, from glomerulus to collecting system and with the sites of action of those factors — both physiological and pharmacological — which have specific effects upon tubular calcium transport.

Effects of Vitamin D and Parathyroid Hormone on Renal Tubular Calcium Reabsorption

Both parathyroid hormone (PTH) (Talmage and Kraintz, 1954) and 25 hydroxy Vitamin D3 (25(OH)D3) (Puschett, Moranz et al, 1972) have been shown to enhance the renal tubular reabsorption of calcium. In the present micropuncture studies we have shown that, in the thyroparathyroidectomised (TPTX) dog, both of these agents enhance calcium reabsorption relative to sodium at a site beyond the late proximal tubule.

Tubular Handling of Calcium

The renal tubular handling of calcium is essentially a filtered load-tubular reabsorption process. Micropuncture studies in the last few years have considerably expanded our knowledge of the reabsorptive system at different nephron segments available to free flow micropuncture of surface tubules (Sutton & Dirks, 1975). A considerable focus of these studies has been to relate Ca to Na reabsorption. More recent studies have been directed at assessing the effects of parathyroid hormone and Vitamin D metabolites, diuretics and physiological circumstances such as altered acidbase balance. The overall view that has developed is that the major bulk of filtered Ca is coupled proportionately with Na through direct or indirect mechanisms. However, the fine and independent control of Ca reabsorption takes place in the distal tubule and collecting ducts.

Effect of Metabolic Acidosis and Alkalosis on Renal Tubular Calcium Transport

Chronic metabolic acidosis is associated with a reduction in the renal tubular reabsorption of calcium (Lemann et al, 1967). The ingestion of sodium bicarbonate has been noted to decrease urinary calcium excretion in man (Parfitt et al, 1964).