Page 120 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Chronic Renal Failure: Abnormal Functions
A number of renal diseases can ultimately lead function (nausea, peptic ulcer, diarrhea), and
to the destruction of renal tissue (→ p.102ff., of blood cells (hemolysis, abnormal leukocyte
114). If the residual renal tissue is not in a posi- function, abnormal blood clotting) are due to
tion to adequately fulfill its tasks, the picture this.
of renal failure evolves. While uric acid can be precipitated at high
Reduced renal excretion is particularly sig- concentrations, especially in the joints, and
nificant. The decreased GFR leads to an in- thus cause gout (→ p. 250), sufficiently high
versely proportional rise in the plasma level concentrations of uric acid are only rarely
Kidney, Salt and Water Balance renal tubular reabsorption is impaired in renal ic acid, methylguanidine, indoles, phenols,
achieved in renal failure. The role of reduced
of creatinine (→ A, top; see also p. 94). The
elimination of so-called uremia toxins (e.g.,
plasma concentration of reabsorbed sub-
acetone, 2,3-butyleneglycol, guanidinosuccin-
stances also rises, but less markedly, because
+
failure. The reabsorption of Na and water is
aliphatic and aromatic amines, etc.) as well as
of so-called middle molecules (lipids or pep-
inhibited in renal failure by a variety of factors,
such as natriuretic hormone, PTH, and van-
tides with a molecular weight of 300–
2000 Da) in producing the symptoms of renal
adate (→ p.112). The reduced reabsorption of
+
failure remains the subject of considerable de-
Na in the proximal tubules also directly or in-
substances, such as phosphate, uric acid,
lize proteins and bring about cell shrinkage.
2+
–
HCO 3 , Ca , urea, glucose, and amino acids.
But its effect is partly canceled by the cellular
The reabsorption of phosphate is also inhibited
uptake of stabilizing osmolytes (especially be-
5 directly decreases the reabsorption of other bate. High concentrations of urea can destabi-
by PTH. taine, glycerophosphorylcholine).
Reduced NaCl reabsorption in the ascending The impaired renal production of erythro-
limb compromises the concentrating mecha- poietin leads to the development of renal ane-
nism (→ p.100). The large supply of volume mia (→ p. 30ff.), while the reduced formation
and NaCl from parts of the proximal nephron of calcitriol contributes to abnormalities of
+
promotes the reabsorption of Na distally and mineral metabolism (→ p.112). Depending on
+
+
aids in the secretion of K and H in the distal the cause and course of the disease, the intra-
nephron and in the collecting duct. As a result, renal formation of renin and of prostaglandins
the plasma concentration of electrolytes can can be raised (→ p.114) or reduced (death of
remain practically normal even if GFR is mark- renin- or prostaglandin-producing cells). In-
edly reduced (compensated renal insufficien- creased formation of renin promotes, while its
cy). Disorders occur only once GFR has fallen reduced formation inhibits, the development
to less than a quarter of the normal level. How- of hypertension, a frequent occurrence in renal
ever, this compensation is carried out at the failure (→ p.112ff.). Prostaglandins, on the
cost of the regulatory range, in that the dam- other hand, are more likely to cause vasodila-
aged kidney is unable adequately to increase tion and a fall in blood pressure (→ p. 296).
+
+
+
the excretion of water, Na , K , H , phosphate, The loss of renal inactivation of hormones
etc. (e.g., if oral intake is increased). (→ p. 92) may slow down hormonal regulatory
It is probably the disruption in renal water cycles. It is not clear, however, what the role of
and electrolyte excretion that is responsible, these changes is in the development of symp-
at least partially, for the development of most toms.
of symptoms of chronic renal failure. Excess The reduced consumption of fatty acids by
volume and the changed electrolyte concentra- the kidney contributes to hyperlipidemia,
tions lead to edemas, hypertension, osteoma- while reduced gluconeogenesis favors the de-
lacia, acidosis, pruritus, and arthritis, either di- velopment of hypoglycemia.
rectly or via the activation of hormones
(→ p.112). Also, abnormalities of the excitato-
110 ry cells (polyneuropathy, confusion, coma, sei-
zures, cerebral edemas), of gastrointestinal
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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