Since wasting and malnutrition are common problems in patients with renal failure, it is important to develop techniques for the longitudinal assessment of nutritional status. This paper reviews available methods for assessing the nutritional status; their possible limitations when applied to uremic patients are discussed. If carefully done, dietary intake can be estimated by recall interviews augmented with dietary diaries. Also, in a stable patient with chronic renal failure, the serum urea nitrogen (N)/creatinine ratio and the rate of urea N appearance reflect dietary protein intake. A comparison of N intake and urea N appearance will give an estimate of N balance. Anthropometric parameters such as the relationship between height and weight, thickness of subcutaneous skinfolds, and midarm muscle circumference are simple methods for evaluating body composition. Other methods for assessing body composition, such as densitometry and total body potassium, may not be readily applicable in patients with renal failure. More traditional biochemical estimates of nutritional status such as serum protein, albumin, transferrin, and selected serum complement determinations show that abnormalities are common among uremic patients. Certain anthropometric and biochemical measurements of nutritional status are abnormal in chronically uremic patients who appear to be particularly robust; thus, factors other than altered nutritional intake may lead to abnormal parameters in such patients. Serial monitoring of selected nutritional parameters in the same individual may improve the sensitivity of these measurements to detect changes. Standards for measuring nutritional status are needed for patients with renal failure so that realistic goals can be established optimal body nutriture.

A sensitive radioreceptor assay for 1alpha,25-dihydroxyvitamin D3 (1alpha,25-(OH)2D3) is utilized to quantitate the circulating concentration of this sterol in experimental animals and humans. When weanling rats are grown for 2 weeks on low calcium or low phosphate diets, limited availability of either ion elicits a five-fold increase in the plasma level of 1alpha,25-(OH)2D3. The enhancement of 1alpha,25-(OH)2D3 in calcium deficiency is dependent upon the presence of the parathyroid and/or thyroid glands, which is consistent with parathyroid hormone (PTH) mediation of this effect. In contrast, the response to phosphate deficiency is independent of these glands and may result from a direct action of low phosphate on the renal synthesis of 1alpha,25-(OH)2D3. Studies in humans indicate that the normal level of 1alpha,25-(OH)2D is 2.1--4.5 ng/100 ml plasma. Patients with chronic renal failure have markedly lower circulating 1alpha,25-(OH)2D and this kidney hormone is undetectable in anephric subjects, but returns to normal within 1 day after successful renal transplantation. Hypoparathyroidism and pseudohypoparathyroidism are associated with reduced plasma 1alpha,25-(OH)2D while patients with primary hyperparathyroidism have significantly elevated sterol hormone levels. Thus, from measurements in rats and humans, it appears that circulating 1alpha,25-(OH)2D3 is regulated by PTH and/or phosphate and that abnormal plasma 1alpha,25-(OH)2D3 is a part of the pathophysiology of renal osteodystrophy and parathyroid disorders.

Tolerance and physical dependence development to morphine in mice can be prevented by concomitant administration of cycloheximide. The fact that the rate of synthesis of brain 5-hydroxytryptamine (5HT) increases with tolerance to morphine suggests that the protein involved may be associated with 5HT synthesis. Inhibition of this synthesis with p-chlorophenylalanine markedly decreases tolerance and physical dependence development to morphine.

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