Abstract
Sodium balance is reasonably well maintained in chronic kidney disease (CKD) patients until renal function is extensively diminished. Patients do not usually develop either edema or sodium depletion during the early stages of CKD. The adaptive response to decreasing glomerular filtration rate (GFR) in the face of a constant (or high) sodium intake is an increase in the fractional excretion of sodium (FENa). This, in turn, requires a reduction in sodium reabsorption per nephron. In most circumstances, this is protective and prevents or limits sodium retention and extracellular fluid volume expansion. However, if dietary sodium intake is suddenly or greatly reduced, the chronically diseased kidney cannot immediately adjust. Distal nephron tubular function is not permanently impaired because the kidney can adequately adjust to decreases in sodium intake if the changes occur slowly. Hypertension is very common in CKD patients. Control of extracellular fluid volume through diet, and dialysis prescription in the case of end-stage renal disease, is the most effective means of controlling blood pressure. The KDOQI Clinical Practice Guidelines recommends that dietary sodium intake be limited to no more than 2.4g/day.
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