Page 108 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

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(salt-losing kidney), cellular swelling and cell Sodium chloride is reabsorbed in the early
+
death occurs. distal tubules via a Na -Cl – cotransporter
2+
The Ca reabsorption is accomplished in the (→ C17). Thiazides cause renal loss of sodium
proximal tubules and loop of Henle, in part by and potassium by inhibiting the carrier (see
paracellular transport (→ AB11), by Ca 2+ chan- above). They increase the gradient for the
+
nels in the luminal membrane (→ AC12), and 3Na /Ca 2+ exchanger by reducing the intracel-
+
+
by 3Na /Ca 2+ exchangers in the peritubular lular Na concentration and in this way pro-
membrane (→ AC13). Increased intracellular mote the renal reabsorption of Ca 2+ (see above
+
+
Na concentration reduces the Na gradient and → D1). A genetic defect of the transporter
2+
+
for the 3Na /Ca reabsorption. Parathyroid hor- results in Gitelman’s syndrome, a mild variant
exchanger (→ A13) and thus
Kidney, Salt and Water Balance calciuria. The paracellular shunt (→ B11) is nels (→ C18) and the basolateral Na /K -AT-
2+
of Bartter’s syndrome.
impairs Ca
2+
+
mone (PTH) stimulates Ca
Na is reabsorbed in the late distal tubules
reabsorption; con-
+
versely, hypoparathyroidism results in hyper-
and the collecting ducts via luminal Na chan-
+
+
+
2+
Pase. The influx of Na depolarizes the luminal
blockedbya high Ca concentration(hypercal-
cemia). This impairs not only the reabsorption
cell membrane and thus promotes the secre-
+
2+
2+
+
+
of Ca
(loss of magnesium)
tion of K via luminal K channels. If Na reab-
but also of Mg
+
sorption in the proximal tubules, loop of
and of Na (natriuresis, impaired urinary con-
centration; → p.100). Hypercalciuria leads not
Henle, or early distal tubules is inhibited,
+
nephron and it is reabsorbed there in exchange
precipitating in the urine (→ p.120).
+
+
–
+
+
for K . The result is renal loss of K (see above).
cotransporter
Inhibition of Na -K -2 Cl
+
+
+
(→ B14) by loop diuretics stops NaCl reabsorp-
Na channels and Na /K -ATPase are activated
5 only to Ca 2+ deficiency, but also to calcium salts more Na reaches the late distal parts of the
tion in the loop of Henle and thus urinary con- by aldosterone (→ D1). Deficiency of aldoste-
centration (→ p.100). This results in massive rone (hypoaldosteronism) or its reduced effec-
natriuresis and diuresis. Distal tubules and tiveness (pseudohypoaldosteronism, e.g., due
+
+
collecting ducts are overwhelmed by Na and to a defective Na channel) results in the renal
+
+
+
reabsorb Na in exchange for K (see below), loss of Na , decreased extracellular volume,
leading to kaliuresis and hypokalemia. The and low blood pressure. Distal diuretics act by
+
+
Na -K -2 Cl – cotransport needs K + as sub- blocking the aldosterone receptors (aldoste-
+
strate, which must recirculate via K channels rone antagonists) or by directly inhibiting the
+
+
(ROMK; → B15). In K deficiency or hypokale- Na channel. They cause mild natriuresis and
+
+
mia the K channel is closed off and NaCl reab- renal K retention. Conversely, a hyperactive
+
sorption in the loop of Henle is impaired. A ge- Na channel (Liddle’s syndrome) leads to Na +
–
+
+
netic defect in the Na -K -2 Cl cotransporter, retention and hypertension.
–
+
+
Cl or K channel are causes of Bartter’s syn- H secretion in the late distal tubules and in
+
drome which gives rise to impaired urinary the collecting duct is achieved by H -ATPases
+
+
concentration, natriuresis, hypokalemia (ex- (→ C19) and H /K -ATPases (→ C20). A defect
cept in defects of ROMK), and lowered blood results in distal-tubular acidosis (→ D2, E4).
pressure, despite increased renin, angiotensin The affected person can produce only moder-
and aldosterone formation (→ p.114). Because ately acidic urine even when the plasma con-
+
–
of the abnormal Na reabsorption, the kidney centration of HCO 3 is low. Furthermore, they
produces large amounts of prostaglandins suffer from CaHPO 4 stones because phosphate
+
that inhibit Na -reabsorption in more distal is readily precipitated in alkaline urine
nephron segments and thus aggravate NaCl (→ p.120).
loss. Furthermore they cause life-threatening Water can be reabsorbed in the entire neph-
peripheral vasodilation. ron, except the ascending loop of Henle. How-
Finally, the reabsorption of salt in the loop ever, water reabsorption in the distal tubules
of Henle is reduced in hypercalcemia, for ex- and the collecting ducts requires ADH. A lack
ample, by blockage of the paracellular shunt of ADH or decreased sensitivity of the nephron
98 (see above) as well as the activation of a Ca 2+ to ADH causes diabetes insipidus (→ p.100).
receptor (→ B16).
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
All rights reserved. Usage subject to terms and conditions of license.