Muscle intracellular electrolytes in patients with chronic uremia.

We performed 182 percutaneous muscle biopsies in 161 nondialyzed or dialyzed patients with chronic renal failure. Muscle sodium (NaM), potassium (KM), magnesium (MgM) and phosphorus (PM) were determined by neutron activation analysis and atomic absorption spectrophotometry. Intracellular water (H2OI) in muscle was increased in all groups of uremic patients but was not correlated with total muscle water (H2OM) which varied with the content of extracellular water (H2OE). In the nondialyzed patients KM, MgM, and PM were normal in relation to fat free solids (FFS). KM/MgM and KM/PM were also normal. Alkali soluble muscle protein (ASP) was low, and KM/ASP was significantly increased. In hemodialyzed patients and in predialysis peritoneal dialysis patients, KM/FFS and KM/MgM were high. For 22 to 24 hours after peritoneal dialysis, H2OM, H2OE, ClM, NaM, KM, and PM fell significantly, but H2OI was unchanged. The calculated intracellular potassium concentration (KI/H2OI) was significantly reduced in all groups of patients, even though KM was normal or increased. This decrease became more marked when calculating H2OE, H2OI, and KI/H2OI with the chloride method, assuming a reduced muscle transmembrane potential. There was a covariation between KM and PM, KM and H2OI, and KM and plasma potassium, but not between MgM and plasma magnesium or PM and plasma inorganic phosphate. Thus, typical features of chronically uremic muscle are an increase in intracellular water and normal or increased content of potassium in relation to various reference bases representing cell mass. However, the concentration of potassium in intracellular fluid is reduced, presumably because of inhibition of the sodium pump, which reduces transmembrane potential and interferes with the volume regulation of the muscle cells.