Journal Name:
- Türk Nefroloji, Diyaliz ve Transplantasyon Dergisi
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Abstract (2. Language):
Chronic renal failure (CRF) is consistently associated with major metabolic disorders. There are two reasons io design and implement a low- protein diet (LPD) for the successful managment of patients with chronic renal failure: I) to improve uremic symploms and the metabolic abnormalities associated with renal insufficiency; and 2) to slow the loss of residual renal function. The former reason has been standard clinical practice for more than 130 years ago while the latter is more controversial (1). Controversy about the efficacy of the latter reason is based principally on results of the U.S., NIH-sponsored MDRD Study but there are several reasons why this study can not be accepted as the "last word" about the efficacy of LPD in slowing the loss of the remaining kidney function (2, 3). Even though a LPD does improve metabolism with little or no risk, properly designed diets are not systematically prescribed in many nephrological units and questions are raised about its safety in reviews (4). On the other hand, a systematic examination of the available literature and several meta- analyses have shown this "simple" type of intervention can slow the progression of renal failure and exert other positive effects (3, 5-8). In accordance with criteria of Evidence Based Medicine LPDs have to be regarded a type A recommendation for both nön-diabetic and diabetic patients with CKE.
The major effects of LPDs is to correct metabolic abnormalities and to delay the time until dialysis has to be started. This is not a trivial period of time (9, 10) and viewed from a worldwide public health point of view, LPDs are desirable given the increasing costs of dialysis therapy and the risk of death after patients begin dialy-sis. On average beginning dialysis therapy can be delayed more than one year (9-11). There also is abundant evidence that LPDs are associated with an improvement of a broad range of signs and symptoms of uremic syndrome, including amelioration of hyperparathyroidism, increased insulin sensitivity, reduced incidence of metabolic acidosis, reduced proteinuria, improved management of hypertension and last but not least an improvement in subjective well being (1, 9-12).
Initially, supplements of amino acids and of keto acids (KA), the nitrogen free amino acid analogues respectively, were introduced so that protein intake could be reduced to minimal amounts in order to augment the positive effects exerted by LPDs while avoiding the development of malnutrition - the only real potential complication of LPDs. If KA are used an even lower protein intake of as low as 0.3 g/kg LiW/day can be achieved without increasing the dangers of malnutrition (9, 10). KA are the nitrogen free analogues of amino acids, and are transaminated to form the respective amino acid in the body. This improves nitrogen balance at a lower nitrogen intake because essential amino acid requirements are met with a lower nitrogen intake with reduced waste product formation and relief of the symptoms of uremia while maintaining good nutrition.
The keto amino acid therapy contains a dietary protein restriction as well as a supplementation of ke*to and amino acids essential for patients with CRF. Keto acids are the nitrogen-free analogs of amino acids, which can be converted (transaminated) in the human btxly into the corresponding amino acids by about 70%.
Keto acids not only substitute for their respective amino acid and maintain nitrogen balance bul also exert other desirable properties:
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