Page 118 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Acute Renal Failure
Numerous and diverse disorders can lead to ! Obstruction of the glomerular filter by fi-
more or less sudden impairment of renal func- brin and erythrocyte aggregates.
tion (→ A1): ! Seeping away of filtered fluid in the dam-
Obstruction of the urinary tract, for exam- aged tubules.
ple, by urinary stones (→ p.120) can stop uri- ! Obstruction of the tubular lumen by des-
nary excretion, even though the kidney re- quamated tubular cells, by crystals, or due to
mains intact—at least at first. swelling of the tubular cells.
In hemolysis and in the destruction of mus- ! Intravascular stasis (“sludge”) that cannot
Kidney, Salt and Water Balance especially because their tubular concentration no urine (anuria) or only a little volume of
be flushed out of the network between renal
cle cells (myolysis) hemoglobin or myoglobin,
medulla and cortex, even if the perfusion pres-
respectively, is filtered through the glomeruli
sure rises.
and precipitated in the acidic tubular lumen,
In the first three days of acute renal failure
is increased by fluid absorption. The resulting
poorly concentrated urine (oliguria) is excret-
obstruction leads to urine formation being in-
terrupted.
ed as a rule (oliguric phase; → A2). However,
Renal function can also cease as a result of
urinary volume alone is a very poor indicator
of the functional capacity of the kidney in
rapidly progressing renal diseases (e.g., glo-
port processes are severely restricted and the
the kidney.
Loss of blood and fluid impairs renal perfu-
reabsorption of filtered fluid is thus reduced.
Despite normal-looking urine volume, renal
sion and glomerular filtration because in cen-
5 merulonephritis; → p.102) or toxic damage to acute renal failure, because the tubular trans-
tralization of the circulation (→ p. 230) the excretion of all those substances that must
kidney is treated like a peripheral organ, i.e., normally be excreted in the urine may be
sympathetic activation produces renal vascu- markedly impaired. In this case determination
lar constriction via α-adrenoceptors. The re- of the plasma and urine creatinine concentra-
sult is acute ischemic renal failure. tion provides information on the true func-
Several pathophysiological mechanisms can tional state of the kidneys.
prevent the recovery of GFR or restoration of Recovery after the oliguric phase will lead
normal excretion of substances filtered by the to a polyuric phase characterized by the grad-
glomeruli, even after the state of shock has ual increase of the GFR while the reabsorption
been overcome and blood pressure has been function of the epithelial nephron is still im-
normalized (→ A1): paired (salt-losing kidney; → A3). If the renal
! Constriction of the vasa afferentia: tubules are damaged (e.g., by heavy metals),
+
+
– Energy deficiency impairs Na /K -ATPase; polyuric renal failure occurs as a primary re-
the resulting increase in intracellular con- sponse, i.e., large volumes of urine are excreted
+
+
centration of Na also causes, via the 3Na / despite a markedly decreased GFR.
Ca 2+ exchanger, a rise in intracellular Ca 2+ The dangers of acute renal failure lie in the
concentration (→ p.10,12) and thus vaso- inability of the kidney to regulate the water
constriction. and electrolyte balance. The main threat in
– The ischemia promotes the release of renin the oliguric phase is hyperhydration (especial-
both primarily and via an increased NaCl ly with infusion of large volumes of fluid) and
supply in the macula densa (reduced Na + hyperkalemia (especially with the simulta-
+
absorption in the ascending tubules) and neous release of intracellular K , as in burns,
thus the intrarenal formation of angioten- contusions, hemolysis, etc.). In the polyuric
–
+
sin II, which has a vasoconstrictor action. phase the loss of Na , water, HCO 3 , and espe-
+
– If there is a lack of energy supply, adenosine cially of K may be so large as to be life-threat-
is freed from ATP. It acts on the kidney—in ening.
contrast to the other organs—as a marked
108 vasoconstrictor.
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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