c T3

Reabsorption and Excretion of Phosphate, Ca2+ and Mg2+

Phosphate metabolism. The plasma phosphate conc. normally ranges from 0.8-1.4 mmol/L, and a corresponding amount of ca. 150-250 mmol/day of inorganic phosphate Pi (HPO42- H2PO4) is filtered each day, a large part of which is reabsorbed. The fractional excretion (^ A1), which ranges between 5 and 20%, functions to balance Pi, H+, and Ca2+. Pi excretion rises in the presence of a Pi excess (elevated Pi levels in plasma) and falls during a Pi deficit. Acidosis also results in phosphaturia and increased H+ excretion (ti-tratable acidity, ^ p. 174ff.). This also occurs in phosphaturia of other causes. Hypocalcemia and parathyrin also induce a rise in Pi excretion (^ A3 and p. 290f.).

Pi is reabsorbed at the proximal tubule (^ A2,3). Its luminal membrane contains the type 3 Na+-Pi symport carrier (NaPi-3). The carrier accepts H2PO4- and HPO42- and cotrans-ports it with Na+ by secondary active transport (^ p. 26ff.).

Regulation of Pi reabsorption. Pi deficits, alkalosis, hypercalcemia, and low PTH levels result in the increased incorporation of NaPi-3 transporters into the luminal membrane, whereas Pi excesses, acidosis, hypocalcemia and increased PTH secretion results in internalization (down-regulation) and subsequent lysosomal degradation of NaPi-3 (^ A3).

Calcium metabolism (see also p.36). Unlike the Na+ metabolism, the calcium metabolism is regulated mainly by absorption of Ca2+ in the gut (^ p.290ff.) and, secondarily, by renal excretory function. Total plasma calcium (bound calcium + ionized Ca2+) is a mean 2.5 mmol/L. About 1.3 mmol/L of this is present as free, ionized Ca2+, 0.2 mmol/L forms complexes with phosphate, citrate, etc., and the rest of 1 mmol/ L is bound to plasma proteins and, thus, not subject to glomerular filtration (^ p. 154). Fractional excretion ofCa2+ (FEca) in the urine is 0.5%—3% (^ A1).

Ca2+ reabsorption occurs practically throughout the entire nephron (^ A1,2). The reabsorption of filtered Ca2+ occurs to about 60% in the proximal tubule and about 30% in the thick ascending limb (TAL) of the loop of

Henle and is paracellular, i.e., passive A4a and p. 163 B5, B7). The lumen-positive trans-epithelial potential (LPTP) provides most of the driving force for this activity. Since Ca2+ reabsorption in TAL depends on NaCl reabsorption, loop diuretics (^ p. 172) inhibit Ca2+ reabsorption there. PTH promotes Ca2+ reabsorption in TAL as well as in the distal convoluted tubule, where Ca2+ is reabsorbed by transcellu-lar active transport (^ A4b). Thereby, Ca2+ influx into the cell is passive and occurs via luminal Ca2+ channels, and Ca2+ efflux is active and occurs via Ca2+-ATPase (primary active Ca2+ transport) and via the 3Na+/l Ca2+ antiporter (secondary active Ca2+ transport). Acidosis inhibits Ca2+ reabsorption via unclear mechanisms.

Urinary calculi usually consist of calcium phosphate or calcium oxalate. When Ca2+, Pi or oxalate levels are increased, the solubility product will be exceeded but calcium complex formers (e.g., citrate) and inhibitors of crystallization (e.g., nephrocalcin) normally permit a certain degree of supersaturation. Stone formation can occur if there is a deficit of these substances or if extremely high urinary concentrations of Ca2+, Pi and oxalate are present (applies to all three in pronounced antidiuresis).

Magnesium metabolism and reabsorption.

Since part of the magnesium in plasma (0.7-1.2 mmol/L) is protein-bound, the Mg2+ conc. in the filtrate is only 80% of the plasma magnesium conc. Fractional excretion of Mg2+, FEMg, is 3-8% (^ A1,2). Unlike Ca2+, however, only about 15% of the filtered Mg2+ ions leave the proximal tubule. About 70% of the Mg2+ is subject to paracellular reabsorption in the TAL (^ A4 and p. 163 B5, B7). Another 10% of the Mg2+ is subject to transcellular reabsorption in the distal tubule (^ A4b), probably like Ca2+ (see above).

Mg2+ excretion is stimulated by hypermag-nesemia, hypercalcemia, hypervolemia and loop diuretics, and is inhibited by Mg2+ deficit, Ca2+ deficit, volume deficit, PTH and other hormones that mainly act in the TAL.

The kidney has sensors for divalent cations like Ca2+ and Mg2+ (^ p. 36). When activated, the sensors inhibit NaCl reabsorption in the TAL which, like loop diuretics, reduces the driving force for paracellular cation resorption, thereby diminishing the normally pronounced Mg2+ reabsorption there.

Distal tubule
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