Acute correction of metabolic acidosis increases serum procollagen type I carboxyterminal propeptide in patients with chronic renal failure

Pauling Chu, Kuo Cheng Lu, Yuh Feng Lin

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3 Citations (Scopus)

Abstract

Background and Purpose: Previous in vitro study has shown that an acidic medium increases osteoclastic and inhibits osteoblastic activity. The present study sought to determine the role of alkali therapy in osteoblast function in patients with chronic renal failure by assessing the serum concentration of procollagen type I carboxyterminal propeptide (PICP), a marker of bone formation, before and after bicarbonate infusion. Patients and Methods: Eighteen patients with chronic renal failure (creatinine clearance 12 ± 6.6 mL/min) associated with mild to moderate metabolic acidosis were enrolled in this study. None had undergone dialysis. Metabolic acidosis was corrected by continuous bicarbonate infusion while plasma ionized calcium was clamped at the preinfusion level by calcium gluconate infusion throughout the procedure. Results: After bicarbonate infusion, there were significant increases in plasma pH (7.31 ± 0.04 to 7.40 ± 0.03, p <0.001), bicarbonate concentration (18.46 ± 2.49 to 23.66 ± 2.72, p <0.001), serum total calcium concentration (2.01 ± 0.24 to 2.12 ± 0.24 mmol/L, p <0.001), and PICP concentration (137.3 ± 56.25 to 159.6 ± 57.30 μg/L, p <0.05), whereas serum parathyroid hormone concentrations assessed by radioimmunoassay decreased significantly (153.7 ± 88.6 to 111.5 ± 78.7, p <0.001). Serum ionized calcium concentrations showed no significant difference before and after bicarbonate infusion. Conclusion: These results suggest that acute correction of metabolic acidosis improves osteoblast function and appear to underline the importance of maintaining normal acid-base homeostasis in chronic renal failure.

Original languageEnglish
Pages (from-to)748-752
Number of pages5
JournalJournal of the Formosan Medical Association = Taiwan yi zhi
Volume100
Issue number11
Publication statusPublished - 2001
Externally publishedYes

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Bicarbonates
Collagen Type I
Acidosis
Chronic Kidney Failure
Serum
Calcium
Osteoblasts
Calcium Gluconate
Alkalies
Parathyroid Hormone
Osteogenesis
Radioimmunoassay
Dialysis
Creatinine
Homeostasis
Acids
Therapeutics

Keywords

  • Bone formation
  • Carboxy-terminal propeptide
  • Chronic renal failure
  • Ionized calcium clamp
  • Metabolic acidosis
  • Type I procollagen

ASJC Scopus subject areas

  • Medicine(all)

Cite this

@article{e7f19f90b8fc48328a6bd1de3bb3c2a3,
title = "Acute correction of metabolic acidosis increases serum procollagen type I carboxyterminal propeptide in patients with chronic renal failure",
abstract = "Background and Purpose: Previous in vitro study has shown that an acidic medium increases osteoclastic and inhibits osteoblastic activity. The present study sought to determine the role of alkali therapy in osteoblast function in patients with chronic renal failure by assessing the serum concentration of procollagen type I carboxyterminal propeptide (PICP), a marker of bone formation, before and after bicarbonate infusion. Patients and Methods: Eighteen patients with chronic renal failure (creatinine clearance 12 ± 6.6 mL/min) associated with mild to moderate metabolic acidosis were enrolled in this study. None had undergone dialysis. Metabolic acidosis was corrected by continuous bicarbonate infusion while plasma ionized calcium was clamped at the preinfusion level by calcium gluconate infusion throughout the procedure. Results: After bicarbonate infusion, there were significant increases in plasma pH (7.31 ± 0.04 to 7.40 ± 0.03, p <0.001), bicarbonate concentration (18.46 ± 2.49 to 23.66 ± 2.72, p <0.001), serum total calcium concentration (2.01 ± 0.24 to 2.12 ± 0.24 mmol/L, p <0.001), and PICP concentration (137.3 ± 56.25 to 159.6 ± 57.30 μg/L, p <0.05), whereas serum parathyroid hormone concentrations assessed by radioimmunoassay decreased significantly (153.7 ± 88.6 to 111.5 ± 78.7, p <0.001). Serum ionized calcium concentrations showed no significant difference before and after bicarbonate infusion. Conclusion: These results suggest that acute correction of metabolic acidosis improves osteoblast function and appear to underline the importance of maintaining normal acid-base homeostasis in chronic renal failure.",
keywords = "Bone formation, Carboxy-terminal propeptide, Chronic renal failure, Ionized calcium clamp, Metabolic acidosis, Type I procollagen",
author = "Pauling Chu and Lu, {Kuo Cheng} and Lin, {Yuh Feng}",
year = "2001",
language = "English",
volume = "100",
pages = "748--752",
journal = "Journal of the Formosan Medical Association",
issn = "0929-6646",
publisher = "Elsevier Science Publishers B.V.",
number = "11",

}

TY - JOUR

T1 - Acute correction of metabolic acidosis increases serum procollagen type I carboxyterminal propeptide in patients with chronic renal failure

AU - Chu, Pauling

AU - Lu, Kuo Cheng

AU - Lin, Yuh Feng

PY - 2001

Y1 - 2001

N2 - Background and Purpose: Previous in vitro study has shown that an acidic medium increases osteoclastic and inhibits osteoblastic activity. The present study sought to determine the role of alkali therapy in osteoblast function in patients with chronic renal failure by assessing the serum concentration of procollagen type I carboxyterminal propeptide (PICP), a marker of bone formation, before and after bicarbonate infusion. Patients and Methods: Eighteen patients with chronic renal failure (creatinine clearance 12 ± 6.6 mL/min) associated with mild to moderate metabolic acidosis were enrolled in this study. None had undergone dialysis. Metabolic acidosis was corrected by continuous bicarbonate infusion while plasma ionized calcium was clamped at the preinfusion level by calcium gluconate infusion throughout the procedure. Results: After bicarbonate infusion, there were significant increases in plasma pH (7.31 ± 0.04 to 7.40 ± 0.03, p <0.001), bicarbonate concentration (18.46 ± 2.49 to 23.66 ± 2.72, p <0.001), serum total calcium concentration (2.01 ± 0.24 to 2.12 ± 0.24 mmol/L, p <0.001), and PICP concentration (137.3 ± 56.25 to 159.6 ± 57.30 μg/L, p <0.05), whereas serum parathyroid hormone concentrations assessed by radioimmunoassay decreased significantly (153.7 ± 88.6 to 111.5 ± 78.7, p <0.001). Serum ionized calcium concentrations showed no significant difference before and after bicarbonate infusion. Conclusion: These results suggest that acute correction of metabolic acidosis improves osteoblast function and appear to underline the importance of maintaining normal acid-base homeostasis in chronic renal failure.

AB - Background and Purpose: Previous in vitro study has shown that an acidic medium increases osteoclastic and inhibits osteoblastic activity. The present study sought to determine the role of alkali therapy in osteoblast function in patients with chronic renal failure by assessing the serum concentration of procollagen type I carboxyterminal propeptide (PICP), a marker of bone formation, before and after bicarbonate infusion. Patients and Methods: Eighteen patients with chronic renal failure (creatinine clearance 12 ± 6.6 mL/min) associated with mild to moderate metabolic acidosis were enrolled in this study. None had undergone dialysis. Metabolic acidosis was corrected by continuous bicarbonate infusion while plasma ionized calcium was clamped at the preinfusion level by calcium gluconate infusion throughout the procedure. Results: After bicarbonate infusion, there were significant increases in plasma pH (7.31 ± 0.04 to 7.40 ± 0.03, p <0.001), bicarbonate concentration (18.46 ± 2.49 to 23.66 ± 2.72, p <0.001), serum total calcium concentration (2.01 ± 0.24 to 2.12 ± 0.24 mmol/L, p <0.001), and PICP concentration (137.3 ± 56.25 to 159.6 ± 57.30 μg/L, p <0.05), whereas serum parathyroid hormone concentrations assessed by radioimmunoassay decreased significantly (153.7 ± 88.6 to 111.5 ± 78.7, p <0.001). Serum ionized calcium concentrations showed no significant difference before and after bicarbonate infusion. Conclusion: These results suggest that acute correction of metabolic acidosis improves osteoblast function and appear to underline the importance of maintaining normal acid-base homeostasis in chronic renal failure.

KW - Bone formation

KW - Carboxy-terminal propeptide

KW - Chronic renal failure

KW - Ionized calcium clamp

KW - Metabolic acidosis

KW - Type I procollagen

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