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.