Page 122 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)
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Chronic Renal Failure: Abnormal Regulation
       Reduced renal elimination of water and elec-  When Ca 2+  forms a complex with phos-
       trolytes is particularly important in the devel-  phate, the concentration of Ca 2+  is lowered.
       opment of symptoms of renal failure (see also  The hypocalcemia stimulates the release of
       p.110). The extracellular volume expands if  PTH from the parathyroid gland, mobilizing
       there is an excess of NaCl and water (→ A),  calcium phosphate from bone (→ B). The result
       and hypervolemia as well as edemas develop  is demineralization of bone (osteomalacia).
       (→ p.122); pulmonary edema being the most  Normally PTH makes it possible, by simulta-
       dangerous complication (→ p. 80). If it is pre-  neous inhibition of renal reabsorption of phos-
    Kidney, Salt and Water Balance  ger of cerebral edema (→ p. 358).  +  +  Ca 2+  concentration remains low. The stimulus
                                       phate, for the plasma concentration of phos-
       dominantly water which is in excess, the os-
                                       phate to fall so that, despite mobilization of
       motically driven entry of water increases the
                                       calcium phosphate from bone, the solubility
       intracellular volume (→ A) and there is a dan-
                                                                  2+
                                       product in plasma is not exceeded and Ca
         The hypervolemia results in the release of
                                       concentration can increase. In renal insuffi-
       atrial natriuretic factor (ANF) and probably
                                       ciency, however, renal excretion cannot be en-
       also of ouabain. The latter inhibits Na /K -
                                       hanced, plasma phosphate concentration in-
       ATPase (→ A1). Vanadate (VNO 4 ), which is
                                       creases, CaHPO 4 is precipitated, and plasma
       largely excreted by the kidney, has a similar ef-
                                       this persisting secretory stimulus the para-
       its plasma level is markedly raised in renal fail-
       ure.
                                       thyroid glands hypertrophy and, in a vicious
                     +
                   +
                                       circle, release ever larger amounts of PTH.
         Inhibition of Na /K -ATPase causes reduced
    5  fect. Its clearance is about the same as GFR and  for PTH release therefore continues. Under
         +
       Na reabsorption in the kidney. Additionally,  As the receptors for PTH are, in addition to
                  +
       the intracellular K concentration falls in cells  those in the kidney and bones, in many other
       from diverse tissues and the cells depolarize.  organs (nervous system, stomach, blood cells,
                               +
       The intracellular concentration of Na rises.  gonads) it is assumed that PTH plays a role in
                  +
       This impairs 3Na /Ca 2+  exchange (→ A2), and  the development of abnormalities in these or-
       thus the intracellular concentration of Ca 2+  gans. In fact, removal of the parathyroid glands
       also increases. The consequences of depolar-  is thought to significantly improve numerous
       ization are abnormal neuromuscular excitabil-  symptoms of renal failure.
                          –
       ity, cellular accumulation of Cl , and cell swel-  The formation of calcitriol is reduced in re-
       ling (→ A; see also p.10). The increased Ca 2+  nal failure, which also plays a part in causing
       concentration causes vasoconstriction as well  the abnormalities of mineral metabolism. Nor-
       as increased release of hormones (e.g., gastrin,  mally this hormone stimulates the absorption
       insulin) and increased hormonal effects (e.g.,  of calcium and phosphate in the gut (→ B). Al-
       epinephrine).                   though calcitriol deficiency reduces the intes-
         Abnormalities of mineral metabolism also  tinal absorption of phosphate, it aggravates
       contribute greatly to the symptoms of renal  the hypocalcemia. There are receptors for cal-
       failure (→ B). If the GFR is reduced to less than  citriol in various organs. Calcitriol substitution
       20% of normal rate, less phosphate is filtered  does not necessarily improve the symptoms
       than is absorbed through the gut. Even if the  and endangers the patient with renal failure
       entire amount of filtered phosphate is elimi-  by stimulating the intestinal absorption of
       nated, i.e., there is no reabsorption, renal elim-  phosphate.
       ination cannot keep up with intestinal absorp-
       tion, and the plasma concentration of phos-
       phate rises. When the solubility is exceeded,
       phosphate combines with Ca 2+  to form poorly
       soluble calcium phosphate. The precipitated
       calcium phosphate is deposited in the joints
  112  and skin (causing joint pains or pruritus, re-
       spectively).
       Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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