TY - JOUR
T1 - Renal osteodystrophy
AU - Barzel, Uriel S.
AU - Hruska, Keith A.
PY - 1995/11/23
Y1 - 1995/11/23
N2 - To the Editor: In their otherwise comprehensive review of the mechanisms of renal osteodystrophy, Hruska and Teitelbaum (July 20 issue)1 do not mention the role of acidosis. The high-phosphate diet of the average adult American generates approximately 100 mmol of hydrogen ions daily. The inability of the failing kidney to excrete this endogenously produced acid results in metabolic acidosis, which stimulates osteoclastic bone resorption.2,3 Thus, the skeleton, the principal source of alkali buffer, is slowly consumed in the defense against metabolic acidosis. This acid-induced bone resorption is present from the earlier stages of chronic renal failure but is overshadowed.
AB - To the Editor: In their otherwise comprehensive review of the mechanisms of renal osteodystrophy, Hruska and Teitelbaum (July 20 issue)1 do not mention the role of acidosis. The high-phosphate diet of the average adult American generates approximately 100 mmol of hydrogen ions daily. The inability of the failing kidney to excrete this endogenously produced acid results in metabolic acidosis, which stimulates osteoclastic bone resorption.2,3 Thus, the skeleton, the principal source of alkali buffer, is slowly consumed in the defense against metabolic acidosis. This acid-induced bone resorption is present from the earlier stages of chronic renal failure but is overshadowed.
UR - http://www.scopus.com/inward/record.url?scp=0028798978&partnerID=8YFLogxK
U2 - 10.1056/NEJM199511233332116
DO - 10.1056/NEJM199511233332116
M3 - Letter
C2 - 7477140
AN - SCOPUS:0028798978
SN - 0028-4793
VL - 333
SP - 1428
JO - New England Journal of Medicine
JF - New England Journal of Medicine
IS - 21
ER -