Other biochemical, functional and morphological changes associated with renal failure:
Change
Mechanism
Acidosis
Decreased tubular excretion of H
+
; impaired reabsorption of bicarbonate;
increased retention of volatile acids; reduced capacity of distal convoluted
tubules and collecting tubules to produce ammonia.
Anemia
In acute renal failure, decreased erythrocyte life span due to a malfunctioning
of the membrane Na
+
-K
+
-ATPase pump; in chronic renal failure, reduced
synthesis of erythropoietin by the kidney and possible bone marrow
depression by accumulated metabolic waste products.
Heart failure
Electrolyte imbalances, including decreased tubular excretion of K
+
; possible
contribution of uremia-induced endocarditis.
Hypertension
Retention of fluid; activation of the renin-angiotensin system.
Dehydration
Impaired reabsorption of water (polyuria / polydipsia).
Edema and ascites
Hypoproteinemia from loss of protein in urine.
Depression
Toxins and waste products reaching the CNS; uncommonly, a spongiform
encephalopathy may develop.
Fibrous osteodystrophy
“Secondary renal hyperparathyroidism” (overproduction of parathormone in
an attempt to reestablish calcium/phosphorus balance
➝
excessive resorption
of calcium from bones), resulting from several factors including excessive
retention of phosphorus (hyperphosphatemia) and decreased activation of
vitamin D
3
by renal proximal tubular epithelial cells (more specifically,
decreased synthesis of calcitriol from its precursor, 25-hydroxyvitamin D
3
).
Thrombosis
Loss of antithrombin-3, a small protein molecule (associated with increased
permeability of glomerular filtration membrane); degeneration of endothelium
and subendothelial connective tissue.
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