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Skeletal muscle biopsies were performed in 16 controls and 15 non-dialysed end-stage chronic renal failure (CRF) patients presenting untreated metabolic acidosis. Intracellular bicarbonate, pH, water compartments and electrolytes were determined. In 8 of 15 patients muscle ATP and lactate were measured. Intracellular bicarbonate (HCO3i) and pH (pHi) were obtained by means of muscle total carbon dioxide method: a significant (p less than 0.001) reduction in both intracellular acid--base indexes was found in all patients (pHi 6.82 +/- 13 vs. 7.04 +/- 0.05; HCO3i 6.28 +/- 2.07 vs. 11.86 +/- 0.87). Total muscle as well as extracellular water was increased. Muscle sodium and chloride contents were also increased, while no change in potassium and magnesium was detected. A significant decrease of both muscle ATP and lactate was found. The data lead to the conclusion that chronic retention of acids in CRF results in a depletion of the muscle buffer pool and consequently in intracellular acidosis: the latter could be the main cause of the cell energy metabolism derangement described in uremia.

Muscle specimens by means of quadriceps femoris needle biopsy and blood samples were obtained in 32 patients consecutively admitted to a pulmonary ICU for chronic obstructive pulmonary disease and acute respiratory failure, and in 30 age and sex-matched healthy control subjects. Muscle magnesium (Mg) and potassium (K) content was assessed by atomic absorption spectrophotometry; serum electrolytes were also measured. The presence of clinical and biochemical correlates of low serum and muscle Mg was investigated. Three (9.4%) out of 32 patients had hypomagnesemia (Mgs less than or equal to 0.7 mmol/L) with normal muscle Mg values, whereas low muscle Mg values were found in 15 (47%) of 32 patients, with no alterations of serum Mg levels. Muscle Mg was decreased significantly in pulmonary ICU patients as compared to control subjects. No significant correlation was present between serum and muscle Mg, or between serum and muscle K. Significant relationships between muscle Mg and both muscle and intracellular K concentrations were also found. Lower values for muscle and intracellular K and a higher incidence of both more prolonged ICU stays and ventricular extrasystolic beats characterized the ICU patients with altered muscle Mg levels. We conclude that, given the serious complications of Mg metabolism derangements, the presence of altered cell Mg content should be taken into account in pulmonary ICU patients. Moreover, in these patients, serum Mg levels are of little value in the diagnosis of intracellular Mg deficits.

In 90 patients with hypercapnic-hypoxemic chronic obstructive pulmonary disease (COPD), noninvasive anthropometric and biochemical nutritional indices were measured to assess the prevalence and features of malnutrition in COPD and to analyze the relationship between nutritional depletion and the severity of the disease. A significant inverse relationship was found between PaCO2 and body weight; a parallel decrease of both somatic proteins and body-energy stores of fat appears to be paired with decreasing body weight. Deterioration of nutritional status occurred in the COPD patients considered despite seemingly adequate calorie and protein intakes, although in patients with more severe impairment of pulmonary gas exchange, calorie intake was significantly lower compared with basal energy expenditure. In the course of hypercapnic-hypoxemic COPD malnutrition is common, it is related to the severity of the disease as judged by the need for hospitalization and degree of impairment of gas exchange, and it may be present despite apparently adequate nutrient intake.