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Mineral Metabolism in Acute Renal Failure

  • Michael Freundlich
  • Gaston Zilleruelo
  • José Strauss
Chapter
Part of the Developments in Nephrology book series (DINE, volume 7)

Abstract

Disturbances in divalent ion metabolism are well known consequences of chronic renal failure (CRF). An in-depth review of the recent extensive literature about these disturbances is beyond the scope and goals of this chapter. However, in brief, hyperparathyroidism secondary to CRF apparently develops through two major mechanisms (both with lowered serum ionized calcium): hyperphosphatemia and acquired vitamin D resistance. It has been suggested (1) that hyperphosphatemia resulting from decreased glomerular filtration rate is one of the main causes of the hypocalcemia and secondary hyperparathyroidism of CRF. The second mechanism, vitamin D resistance (truly a reduced generation of active vitamin D due to a diminished functional renal mass), decreases intestinal absorption of calcium resulting in hypocalcemia, secondary hyperparathyroidism, and delayed mineralization of osteoid (2). Furthermore, skeletal resistance to the calcemic action of both exogenous and endogenous parathyroid hormone (PTH) has been demonstrated in patients with CRF (3), partly due to deficiency of 1,25-dihydroxyvitamin D (l,25(OH)2D) (4). Studies dealing with alterations of mineral metabolism in acute renal failure (ARF) are rather scanty, and limited almost exclusively to patients in the adult age group. Pertinent information from these studies follows.

Keywords

Acute Renal Failure Chronic Renal Failure Serum Calcium Parathyroid Gland Secondary Hyperparathyroidism 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Martinus Nijhoff Publishing, Boston 1984

Authors and Affiliations

  • Michael Freundlich
  • Gaston Zilleruelo
  • José Strauss

There are no affiliations available

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