Page 126 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Kidney Disease in Pregnancy
In a normal pregnancy (→ A) the placenta Damage to the glomeruli could explain the
forms vasodilating prostaglandins (especially proteinuria. Corresponding damage to the pe-
PGE 2 ) and possibly other substances that re- ripheral vessels leads to the development of
duce the reactivity of vessels to vasoconstric- edemas at the expense of the plasma volume,
tor stimuli. As a result, the peripheral vascular which is reduced.
resistance (R) is decreased and blood pressure The placenta of patients with preeclampsia
falls. In the kidney, too, the vascular resistance, also has a reduced ability to form vasodilating
the RPF, and the GFR rise markedly. prostaglandins (and other vasodilators?)
Kidney, Salt and Water Balance proximal tubules (IsK). The resulting depolar- the one hand, to peripheral vasoconstriction
+
Na reabsorption in the proximal tubules
(→ B2). The sensitivity of the vessels to vaso-
constrictor influences (e.g., angiotensin II) is
does not keep in step with a high GFR. In addi-
+
therefore markedly increased. This leads, on
tion, estrogens inhibit the K channel in the
–
and hypertension and, on the other hand, to
ization retains HCO 3 in the cell, and the intra-
+
+
cellular acidosis inhibits the Na /H exchanger
an increase in the resistance of renal vessels
(→ B3); RPF and GFR are reduced. As a conse-
(→ p. 97 A). The depolarization also inhibits
the electrogenic transport processes for glu-
quence of volume deficiency an increased
+
amount of Na is reabsorbed in the proximal
cose, amino acids, etc. Due to the reduced re-
+
time with the reabsorbing epithelium is pro-
concentrated within the lumen and thus also
less of it is reabsorbed. Among the conse-
longed, and reabsorption of uric acid is thus
quences of reduced proximal tubular reab-
raised. The plasma level of uric acid is in-
5 absorption of Na and fluid, uric acid is less tubules, luminal flow is reduced, the contact
sorption are a fall in the renal threshold for creased, providing a valuable diagnostic indi-
glucose (tendency toward glycosuria) and for cation.
bicarbonate (fall in plasma bicarbonate con- It is not quite clear whether or not the plas-
centration). ma concentration of renin and angiotensin II is
It is possible that the release of renin is increased in preeclampsia. Stimulation of re-
stimulated by the increased supply of NaCl to nin secretion in the kidney could be explained
the macula densa. The plasma level of renin by the reduction in renal perfusion. In any
and thus also of angiotensin II and aldosterone case, the vasoconstrictor action of angiotensin
are raised. Aldosterone increases the distal re- II is greatly increased in preeclampsia by the
+
absorption of Na . All in all, NaCl and water are raised vascular reactivity (see above). In addi-
retained in pregnancy, despite a rise in GFR, tion to an increase in peripheral resistance, the
and extracellular and plasma volumes in- raised vascular reactivity also leads to the de-
crease. However, because of the low reactivity velopment of local vascular spasms. These are
of peripheral vessels to vasoconstrictor stimu- thought to occur in various organs (including
li, no hypertension develops, despite the high the brain), where in a few cases they can cause
angiotensin level and hypervolemia. convulsions and coma (eclampsia). Occasion-
Edema, proteinuria, and hypertension (EPH) ally, vascular narrowing can be seen in the
occur in ca. 5% of all pregnant women (pre- ocular fundi even a few days before the onset
eclampsia, toxemia of pregnancy, or EPH-ges- of eclampsia.
tosis). The symptoms point to renal damage,
hence the term nephropathy of pregnancy
(→ B). The pathogenesis of toxemia of preg-
nancy with EPH is still not adequately known.
Release of thrombokinase in the placenta
may be a pathophysiologically relevant factor.
Stimulation of blood clotting (→ B1) causes fi-
brin to be desposited, for example, in the glo-
116 meruli, leading to thickening of the basement
membrane and injury to the endothelial cells.
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
All rights reserved. Usage subject to terms and conditions of license.