Acidosis and renal bone disease

David A. Bushinsky

in The Spectrum of Mineral and Bone Disorders in Chronic Kidney Disease

Second edition

Published on behalf of Oxford University Press

Published in print June 2010 | ISBN: 9780199559176
Published online November 2012 | e-ISBN: 9780191753350 | DOI:

Series: Oxford Clinical Nephrology Series

Acidosis and renal bone disease

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In humans the daily cellular metabolism of dietary amino acids leads to production of ∼1mmol/kg of acid (protons, H+), so called endogenous acid production. Additional endogenous acid production occurs during pathophysiological conditions including diabetic ketoacidosis and lactic acidosis. This additional acid results in a reduction of systemic pH, secondary to a reduction in blood bicarbonate concentration [HCO3-], which is termed metabolic acidosis. The physiological response to metabolic acidosis is to rapidly increase in extracellular fluid pH toward the physiologic neutral of 7.40 in order to maintain optimal cellular function. This homeostatic response to metabolic acidosis involves first buffering of the acid, then increasing respiratory rate to lower the partial pressure of carbon dioxide (PCO2) and finally renal excretion of the additional acid. The initial step, buffering of the additional acid, is critical to the immediate restoration toward neutral pH allowing the preservation of life. The final step, renal excretion of the acid, begins hours after the acid challenge and is complete only days later. Renal acid excretion relies upon normal kidney function; as we age our ability to excrete acid declines and humans become slightly, but significantly, more acidemic.

Chapter.  5982 words.  Illustrated.

Subjects: Rheumatology ; Nephrology

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