الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
CKD is a global public health problem and the burden of chronic kidney disease is rising worldwide, as shown by increases in attributable deaths and incidence and prevalence of end-stage renal failure. chronic kidney disease and its complications, which involve most organ systems, can be prevented by restriction of dietary protein intake which remains a common practice for CKD.
The pathophysiology of CKD is complex and in large part dependent on the primary cause. The loss of kidney function is characterized by a progressive decline in the number of surviving nephrons .The kidneys adapt to loss of nephrons by recruitment of the surviving nephrons to recoup much of the function lost. However, once the number of surviving nephrons declines below some critical mass, surviving nephrons continue to be damaged and lost even if the primary kidney disease is no longer active which leads to additional nephron loss and a progressive decline in renal function.
Inflammation is also a key component in the progression of kidney disease. AngII recruits T cells and mac¬rophages by stimulating endothelin-1 (ET-1) and increases production of nuclear factor κ-light-chain-enhancer of acti¬vated B cells (Nf-κB); these molecules release cytokines creating more inflammation also creates cellular recruitment. Finally, free radical oxy¬gen species lead to additional injury, which enables further inflammation and fibrosis.
Dietary protein restriction is an important treatment for CKD; GFR is the most useful measurement of kidney function. GFR represents the volume of plasma ultra-filtrate presented to the nephrons per unit time in the process of urine formation.
The kidneys generate ammonia via metabolism of glutamine to glutamate and alpha-ketoglutarate in the renal tubules .However, as the number of functioning renal tubules becomes limited ,as CKD progresses, metabolic acidosis develops primarily because the ability to increase renal ammonia production, and thus excrete hydrogen ions, is limited by loss of functional renal mass. Decreased medullary recycling of ammonia due to structural renal damage may also contribute to impaired ammonium excretion.
Chronic metabolic acidosis may promote a variety of adverse clinical effects including anorexia, nausea, vomiting, lethargy, weakness, muscle wasting, and weight loss. In addition, it can increase urinary calcium excretion and promote progressive bone demineralization and malnutrition. chronic metabolic acidosis may impair adaptation to protein restriction ,which has been proposed for metabolic purposes ,and promote protein malnutrition in patients with CKD.(50)
Protein catabolism is increased in patients with acidosis to provide a source of nitrogen for hepatic glutamine synthesis, glutamine being the substrate for renal ammonia genesis .The combined effects of reduced protein synthesis due to uremia and accelerated proteolysis due to acidosis promote elevations in blood urea nitrogen, increased nitrogen excretion, and negative nitrogen balance typical of uremic acidosis. Metabolic acidosis blocks the metabolic responses to dietary protein restriction in two ways. First, it stimulates irreversible degradation of the essential, branched chain amino acids and second, it stimulates degradation of protein in muscle.(60)Thus, acidosis may limit the ability of patients to adapt to dietary protein restriction. Metabolic acidosis also suppresses albumin synthesis in humans and may reduce the concentration of serum albumin.