Nutrition Renal Function and Recovery

Kidney Function Restoration Program

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FIGURE 18-25

A, B, Impact of nutritional interventions on renal function and course of acute renal failure (ARF). Starvation accelerates protein breakdown and impairs protein synthesis in the kidney, whereas refeeding exerts the opposite effects [49]. In experimental animals, provision of amino acids or total parenteral nutrition accelerates tissue repair and recovery of renal function [50]. In patients, however, this has been much more difficult to prove, and only one study has reported on a positive effect of TPN on the resolution of ARF [51].

Infusion of amino acids raised renal cortical protein synthesis as evaluated by 14C-leucine incorporation and depressed protein breakdown in rats with mercuric chloride-induced ARF [49]. On the other hand, in a similar model of ARF, infusions of varying quantities of essential amino acids (EAA) and nonessential amino acids (NEAA) did not provide any protection of renal function and in fact increased mortality [52]. However, in balance available evidence suggests that provision of substrates may enhance tissue regeneration and wound healing, and potentially, also renal tubular repair [49]. (From Toback et al. [50]; with permission.)

FIGURE 18-26

Impact of nutritional interventions on renal function in acute renal failure (ARF). Amino acid infused before or during ischemia or nephrotoxicity may enhance tubule damage and accelerate loss of renal function in rat models of ARF. In part, this therapeutic paradox [53] from amino acid alimentation in ARF is related to the increase in metabolic work for transport processes when oxygen supply is limited, which may aggravate ischemic injury [54]. Similar observations have been made with excess glucose infusion during renal ischemia. Amino acids may as well exert a protective effect on renal function. Glycine, and to a lesser degree alanine, limit tubular injury in ischemic and nephrotoxic models of ARF [55]. Arginine (possibly by producing nitric oxide) reportedly acts to preserve renal perfusion and tubular function in both nephro-toxic and ischemic models of ARF, whereas inhibitors of nitric oxide synthase exert an opposite effect [56,57]. In myoglobin-induced ARF the drop in renal blood flow (black circles, ARF controls) is prevented by L-arginine infusion (black triangles) [57]. (From Wakabayashi et al. [57]; with permission.)

FIGURE 18-27

Impact of endocrine-metabolic interventions on renal function and course of acute renal failure (ARF). Various other endocrine-metabolic interventions (eg, thyroxine, human growth hormone [HGH], epidermal growth factor, insulin-like growth factor 1 [IGF-1]) have been shown to accelerate regeneration after experimental ARF [51]. In a rat model of postischemic ARF, treatment with IGF-1 starting 5 hours after induction of ARF accelerates recovery from ischemic ARF, A, but also reduces the increase in BUN and improves nitrogen balance, B, [58]. (open circles) ARF plus vehicle; (black circles, sham-operated rats plus vehicle; open squares, ARF plus rhIGF-I; black squares, sham operated rats plus rhIGF-I.) Unfortunately, efficacy of these interventions was not uniformly confirmed in clinical studies [59, 60]. (From Ding et al. [58]; with permission.)

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