Discovery and rediscovery of low protein diet.
The basis of conservative treatment in chronic uremia is the restriction of protein, which lowers blood urea and diminishes nausea, vomiting and other uremic symptoms. Protein restriction to less than 25-30 g per day in adult patients may lead to negative nitrogen balance and protein depletion, which can be prevented by supplementing the diet with essential amino acids or a mixture of essential keto acid analogues and amino acids. The traditional view has been that low protein diet affords symptomatic relief in chronic uremia but does not effect the progression of renal failure. However, recent clinical results, mostly retrospective, suggest that protein restriction may retard or halt progression. This has led to a renewed interest in therapy with low protein diet and essential amino acids or keto analogues, since this form of treatment may postpone the time when the patient has to be started on dialysis, or even make dialysis unnecessary. It is not settled by which mechanism protein restriction effects progression of renal failure. According to one hypothesis, hyperphosphatemia (high Ca X P product) is harmful for the diseased kidneys; protein restriction is beneficial, since a low protein diet is generally also low in phosphate. An alternative hypothesis suggests that glomerular hyperfiltration in the remaining nephrons of the diseased kidneys is harmful and leads to glomerulosclerosis; low protein intake protects the kidney by abolishing glomerular hyperfiltration.
D000596:Amino Acids / Q000008:administration & dosage; D004044:Dietary Proteins / Q000008:administration & dosage* / Q000494:pharmacology; D005919:Glomerular Filtration Rate; D006801:Humans; D007676:Kidney Failure, Chronic / Q000178:diet therapy*
D000596:Amino Acids; D004044:Dietary Proteins