Page 191 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

Reabsorption and Excretion of Henle and is paracellular, i.e., passive (! A4a
Phosphate, Ca 2+ and Mg 2+ and p. 163 B5, B7). The lumen-positive trans-
epithelial potential (LPTP) provides most of
2+
Phosphate metabolism. The plasma the driving force for this activity. Since Ca re-
phosphate conc. normally ranges from absorption in TAL depends on NaCl reabsorp-
2+
0.8–1.4 mmol/L, and a corresponding amount tion, loop diuretics (! p. 172) inhibit Ca reab-
2+
of ca. 150–250 mmol/day of inorganic phos- sorption there. PTH promotes Ca reabsorption
2 – –
phate P i (HPO 4 H 2PO 4 ) is filtered each in TAL as well as in the distal convoluted
2+
day, a large part of which is reabsorbed. + tubule, where Ca is reabsorbed by transcellu-
Kidneys, Salt, and Water Balance excess (elevated P i levels in plasma) and falls occurs via Ca -ATPase (primary active Ca 2+
in-
lar active transport (! A4b). Thereby, Ca
2+
The fractional excretion (! A1), which ranges
flux into the cell is passive and occurs via lumi-
between 5 and 20%, functions to balance P i, H ,
2+
2+
efflux is active and
channels, and Ca
nal Ca
2+
andCa .P i excretionrisesinthepresenceofaP i
2+
2+
+
transport) and via the 3 Na /1 Ca
antiporter
during a P i deficit. Acidosis also results in
(secondary active Ca
phosphaturia and increased H excretion (ti-
transport). Acidosis in-
2+
+
hibits Ca
tratable acidity, ! p. 174ff.). This also occurs in
2+
reabsorption via unclear mecha-
phosphaturia of other causes. Hypocalcemia
nisms.
and parathyrin also induce a rise in P i excretion
Urinary calculi usually consist of calcium phosphate
(! A3 and p. 290f.).
2+
P i is reabsorbed at the proximal tubule
increased, the solubility product will be exceeded
but calcium complex formers (e.g., citrate) and in-
+
type 3 Na -P i symport carrier (NaPi-3). The car-
hibitors of crystallization (e.g., nephrocalcin) nor-
7 (! A2,3). Its luminal membrane contains the or calcium oxalate. When Ca , Pi or oxalate levels are
–
mally permit a certain degree of supersaturation.
2 –
rier accepts H 2PO 4 and HPO 4 and cotrans-
ports it with Na by secondary active transport Stone formation can occur if there is a deficit of these
+
(! p. 26ff.). substances or if extremely high urinary concentra-
2+
Regulation of P i reabsorption. P i deficits, al- tions of Ca , Pi and oxalate are present (applies to all
three in pronounced antidiuresis).
kalosis, hypercalcemia, and low PTH levels re-
sult in the increased incorporation of NaPi-3 Magnesium metabolism and reabsorption.
transporters into the luminal membrane, Since part of the magnesium in plasma
whereas P i excesses, acidosis, hypocalcemia (0.7–1.2 mmol/L) is protein-bound, the Mg 2+
and increased PTH secretion results in inter- conc. in the filtrate is only 80% of the plasma
nalization (down-regulation) and subsequent magnesium conc. Fractional excretion of Mg ,
2+
2+
lysosomal degradation of NaPi-3 (! A3). FE Mg, is 3–8% (! A1,2). Unlike Ca , however,
Calcium metabolism (see also p. 36). Unlike only about 15% of the filtered Mg 2+ ions leave
+
the Na metabolism, the calcium metabolism the proximal tubule. About 70% of the Mg 2+ is
2+
is regulated mainly by absorption of Ca in the subject to paracellular reabsorption in the TAL
gut (! p. 290ff.) and, secondarily, by renal ex- (! A4 and p. 163 B5, B7). Another 10% of the
2+
cretory function. Total plasma calcium (bound Mg is subject to transcellular reabsorption in
calcium + ionized Ca ) is a mean 2.5 mmol/L. the distal tubule (! A4b), probably like Ca 2+
2+
About 1.3 mmol/L of this is present as free, (see above).
ionized Ca , 0.2 mmol/L forms complexes with Mg 2+ excretion is stimulated by hypermag-
2+
phosphate, citrate, etc., and the rest of 1 mmol/ nesemia, hypercalcemia, hypervolemia and
L is bound to plasma proteins and, thus, not loop diuretics, and is inhibited by Mg 2+ deficit,
subject to glomerular filtration (! p. 154). Ca deficit, volume deficit, PTH and other hor-
2+
Fractional excretion of Ca (FE Ca) in the urine is mones that mainly act in the TAL.
2+
0.5%—3% (! A1). The kidney has sensors for divalent cations like Ca 2+
Ca 2+ reabsorption occurs practically and Mg 2+ (! p. 36). When activated, the sensors in-
throughout the entire nephron (! A1,2). The hibit NaCl reabsorption in the TAL which, like loop di-
reabsorption of filtered Ca 2+ occurs to about uretics, reduces the driving force for paracellular cat-
60% in the proximal tubule and about 30% in ion resorption, thereby diminishing the normally
178 the thick ascending limb (TAL) of the loop of pronounced Mg reabsorption there.
2+
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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