Skeletal growth in experimental uremia

Abstract

Although in recent years experimental work on growth in uremia has clarified many issues, many key questions cannot be answered with available experimental data. In our own studies on subtotally nephrectomized rats, uremic animals consumed less food and grew less. However, although low energy intake diminishes growth, it has not been established that high protein energy intake will normalize growth. We showed that uremia reduced growth (and net protein synthesis) even under conditions of controlled food intake. In renal failure the optimal dietary protein level for growth or for efficiency of utilization has not been established, particularly since protein intake has an independent injurious effect on long-term renal function. Calcium and vitamin D supplements improved growth in uremic rats, but the data cannot easily be extrapolated to humans. The growth-promoting action of 1,25(OH)2D3 was not superior to that of equipotent doses of vitamin D3. Correction of anemia and physical exercise did not improve growth. Diminished stimulation of growth cartilage cyclic AMP with PTH and augmented stimulation with calcitonin was noted in uremic animals. Growth hormone in supraphysiological doses improved growth and raised IGF carrier protein in uremic animals. Spermine, a potential uremic toxin, inhibited growth cartilage 3H-thymidine incorporation, but only in concentrations higher than that encountered in uremia.