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Uremic acidosis and intracellular buffering.

S Del Canale, E Fiaccadori, E Coffrini

Scandinavian Journal of Urology and Nephrology

|January 1, 1986

Summary

Chronic renal failure (CRF) patients with metabolic acidosis exhibit intracellular acidosis in skeletal muscle, depleting buffers and impairing energy metabolism. This intracellular acidosis may cause the cell energy derangement seen in uremia.

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Area of Science:

Nephrology
Biochemistry
Physiology

Background:

Chronic renal failure (CRF) is associated with metabolic acidosis.
Uremia can lead to derangements in cellular energy metabolism.
The impact of untreated metabolic acidosis on skeletal muscle intracellular environment in CRF is not fully understood.

Purpose of the Study:

To investigate intracellular acid-base balance, water compartments, electrolytes, and energy metabolism in skeletal muscle of non-dialyzed CRF patients with untreated metabolic acidosis.

Main Methods:

Skeletal muscle biopsies were obtained from 16 controls and 15 CRF patients.
Intracellular pH (pHi) and bicarbonate (HCO3i) were measured using the muscle total carbon dioxide method.
Muscle water compartments, electrolytes, ATP, and lactate were determined.

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Main Results:

CRF patients showed significantly reduced pHi (6.82 ± 0.13 vs. 7.04 ± 0.05) and HCO3i (6.28 ± 2.07 vs. 11.86 ± 0.87) compared to controls (p < 0.001).
Increased total muscle and extracellular water, along with elevated muscle sodium and chloride, were observed in CRF patients.
Muscle ATP and lactate levels were significantly decreased in CRF patients.

Conclusions:

Chronic acid retention in CRF leads to a depleted muscle buffer pool and intracellular acidosis.
Intracellular acidosis in skeletal muscle may be the primary cause of impaired cellular energy metabolism in uremia.