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Should We Still Prescribe A Reduction In Protein Intake For Chronic Kidney Disease (Ckd) Patients

Should We Still Prescribe A Reduction In Protein Intake For Chronic Kidney Disease (Ckd) Patients
Ria Bandiara
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Indonesia
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The medical community most use all safe therapeutic strategies to improve the overall health of CKD patients, slow the progression of their renal insufficiency and stall the need for renal replacement therapy. Dietary management is an integral strategy in managing patients with CKD.

For many years patients with chronic kidney disease (CKD) have been advised to control the protein content of their diet. This advise has been given on the basis of a number of reported metabolic effects of lowering protein intake. The implementation of a protein-restricted diet has been shown to yields improvements in blood pressure control, uraemic symptoms and the harmful metabolic profiles seen with advanced kidney failure. The low protein and phosphorus intake has a crucial role for the prevention and reversal of hyperphosphatemia and secondary hyperparathyroidism, which are major causes of the vascular calcifications and mortality risk of uremic patients. A reduction of nitrogenous waste products and lowering of serum PTH levels may also contribute to ameliorate insulin sensitivity and metabolic control in diabetic patients, as well as to increase the responsiveness to erythropoietin therapy, thus allowing a better control anemia. Protein-restricted diets may have also anti-inflammatory and anti-oxidant properties. Dietary protein restriction also leads to lower glomerular capillary pressure and decreases both albuminuria and fractional clearance of immunoglobulin-G in rats with the remnant kidney model of chronic renal failure. In humans, several clinical studies have confirmed that restricted protein intake had a striking effect on the rate of urinary protein excretion. There are suggestive results indicating that low-protein diets may slow the progression of kidney failure in some subjects.

A protein-restricted diet is safe and does not lead to diminished muscle mass, fatigue or malnutrition, as some would suspect. The term malnutrition is used erroneously when describing these findings in patients with CKD. In fact, more recent experimental data show that the muscle atrophy and decreased protein stores associated with CKD are due to activation of proteolytic pathways and not to diminished caloric/protein intake. More studies are necessary to reveal other pathways associated with the anorexia pf CKD or dialysis-related muscle catabolism.

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