Protein Metabolism in Acute Renal Failure

Abstract

The hallmark of metabolic alterations in acute renal failure (ARF) is accelerated protein breakdown which, unfortunately, cannot be suppressed effectively by provision of exogenous nutritional substrates. Causes of excessive protein catabolism are manifold and present a combination of unspecific mechanisms induced by the acute disease process and underlying illness or associated complications, effects induced by the acute loss of renal function and, finally, the type and intensity of renal replacement therapy. Specific uremic toxic effects, insulin resistance, hormonal derangements, metabolic acidosis, circulating proteases, inflammatory mediators, and dialysis-related losses of nutritional substrates all contribute to the activation of protein degradation. Metabolism in ARF is also affected by an impairment of the multiple metabolic and endocrine functions of the kidney. Various amino acids are synthesized or interconverted by the kidneys and may become conditionally indispensable. The kidney is also an important organ in the degradation of peptides, such as peptide hormones. As a consequence of these metabolic aberrations, imbalances in amino acid pools in plasma and in the intracellular compartment occur in ARF and elimination and utilization of infused amino acids is altered. Protein or amino acids requirements are influenced more by the nature of the illness causing ARF, by the extent of hypercatabolism, by associated complications, and by the type and frequency of renal replacement therapy than by renal dysfunction per se. In noncatabolic patients, an intake of 1 g/kg body weight per day may be sufficient, while in critically ill hypercatabolic patients undergoing continuous renal replacement therapy, 1.5 g amino acids/kg body weight per day should be provided to minimize nitrogen losses. For the future, we need to identify safe methods to control the accelerated catabolism in order to improve the efficiency of nutritional interventions in patients with ARF.

Protective Effects of Broccoli (Brassica oleracea) against Oxidative Damage in Vitro and in Vivo

“…Furthermore, excessive urinary excretion of albumin in nephritic states is thought to arise from structural changes in capillary wall permeability (39). Accelerated protein breakdown is a hallmark of metabolic alterations; thus, protein catabolism has been attributed to the acute disease process, uremic toxins, inflammatory mediators, metabolic acidosis, hormonal imbalance, and insulin resistance (39,40). The present results demonstrated that the serum level of albumin in diabetic control rats decreased compared to normal rats, while oral administration of the BuOH fraction to diabetic rats slightly increased the serum level of albumin, indicating that albumin loss induced by urinary elimination under diabetic conditions was attenuated by oral administration of the BuOH fraction.…”

Trends in Acute Renal Failure in Central Anatolia

“…Albumin level is one of the indicators of nutritional status that has been demonstrated as a mortality (20,21). Acute renal failure is one of the conditions that induce protein catabolism due to uremic toxins, infl ammatory mediators, metabolic acidosis, and hormonal imbalance (22). In addition, decreased serum albumin is associated with infl ammatory conditions because it is one of the negative acute phase reactive proteins (23).…”

How to Feed Patients with Renal Dysfunction

“…It has been suggested [4] that in order to achieve a positive nitrogen balance in critically ill patients with renal dysfunction hormonal manipulation is needed in the form of either growth hormone (GH) or insulin-like growth factor-I (IGF-I). Both these agents have a significant anabolic effect.…”