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injections of long-acting vasopressin the administration of urea reduced urine volume further and increased urinary concentrating ability. We believe that it is possible from this data to ascribe the polyuria and the renal concentrating defect in malnutrition to decreased urea concentration in the renal medulla. Effects of malnutrition on acid-base metabolism Acid production. It is now well accepted that there is a dynamic equilibrium between the production and excretion of H In states of renal insufficiency where there is chronic acidosis it is believed that the endogenous production of acid is not necessarily altered, but the renal mechanisms for excretion are impaired [50]. The kidney increases its output of acid under the stimulus of the acidosis produced. In the steady state, the production and excretion of acid will be evenly balanced. The endogenous production of acid, or metabolic H + is derived from two major sources: metabolism of dietary sulpho- and phosphoproteins and in association with organic acids. The sulphurand phosphorus-containing amino acids are oxidized to the appropriate acids, thus promoting H+ production. In states of severe malnutrition, acid production is likely to be reduced. The subject when given protein will retain nitrogen, and even in the most severely malnourished children there is a strongly positive balance immediately when protein is given. Thus there will be fewer amino acids catabolized. In malnutrition there is also an adaptive change in protein metabolism [51]; in muscle there is reduced protein turnover, while in liver protein turnover is little reduced. However, there is an increase in activity of amino acid-activating enzymes of liver and a decrease in urea cycle enzymes, so that amino acids are preferentially incorporated into proteins and there is less wasteful degradation. Little is known about organic acid excretion in malnutrition; although uric acid excretion varies widely, it would be expected that when there is severe potassium deficiency, citrate excretion would be high—but this still has to be proved. We would expect that the net effect of all these adaptations would be to decrease metabolic hydrogen production. Malnourished adults have normal blood pH and bicarbonate [52] and in malnourished children who do not have severe gastroenteritis, there is usually no evidence of metabolic acidosis. In malnourished adults, as we shall discuss later, there is a reduced acid excretion. Thus the fact that there is reduced acid excretion and a normal blood pH supports the contention that endogenous acid production is reduced in malnutrition. Acid excretion. It is of greater importance to determine whether the malnutrition process affects the capacity of the kidney to regulate the internal environment under conditions of stress. A group of subjects were tested when they were malnourished and again after protein repletion [52]. In the malnourished state, basal net acid excretion was reduced but blood pH and bicarbonate was normal. After NH4CI administration there was a greater degree of acidosis in the malnourished subjects. Thus although the kidney of the malnourished adult can cope with reduced acid production, it is unable to handle an increased acid load. When the acid excretion of these subjects is further analyzed, it is clear that although the basal NH secretion is lower, the increment after NH4CI administration is approximately the same in the two states; but the increment in titratable acid in the protein-repleted subjects is four times that which occurred in the malnourished. Malnourished children given NH4C1 do not excrete as much acid as do normal or nutritionally rehabilitated children made similarly acidotic [6]. Here again the fraction of the total acid which increases more is NH, and the fraction of the total hydrion contributed by NH is greater in the malnourished than the well children. Ward has compared the effects of gastroenteritis on the acid base status of malnourished and well children, and found equal degrees of acidosis in both groups.
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