ABSTRACT
PURPOSE: In chronic renal failure (CRF), extracellular fluid (ECF) volume is maintained close to normal, often until end-stage renal disease is imminent. This remarkable feat is accomplished by an increase in fractional excretion of sodium (FENa) in inverse proportion to the decline in glomerular filtration rate (GFR). Many researchers have carried out to try to indentify in animal study but human study was not done in Korea. METHODS: The study is an investigation of the changes of plamsa and urine electrolytes and FENa and fractional excretion of potassium (FEK) in 19 patients (13 men and 6 women) with chronic renal failure. Ages of 19 patients were average 54.6 year-old (range, 29-74 years). Underlying renal disease of the CRF was 42.1% in diabetic nephropathy, 31.6% in chronic glomerulonephritis, 10.5% in hydronephrosis with ureter reflux, and 5.3% in IgA nephropathy. RESULTS: In CRF, plasma Na+ is decreased significantly from normal control 141 +/- 2.1 mEq/L to 139.9 +/- 3.2 mEq/L and GFR from 75.9 +/- 42.9 mL/min to 9.7 +/- 6.3 mL/min, but plasma K+ is increased significantly from 4.2 +/- 0.4 mEq/L to 4.7 +/- 0.8 mEq/L. In CRF however, urine Na+ is decreased significantly from normal control 175.4 +/- 68.5 mEq/L to 89.9 +/- 31.6 mEq/L and osmolality from 610.6 +/- 210.9 mOsm/kg to 397.7 +/- 119.1 mOsm/kg, but urine K+ is decreased tendency from control 32.1 +/- 22.7 mEq/L to 24.3 +/- 14.8 mEq/L. FENa, FEK, and transtubular potassium gradient (TTKG) on CRF were 3.4 +/- 5.4%, 15.4 +/- 20.8% 7.1 +/- 6.9% each and 0.6 +/- 0.6%, 2.2 +/- 2.3% 3.2 +/- 2.8% on normal persons. The difference between CRF and normal control in FENa, FEK, TTKG and osmolar clearance were statistically significant. CONCLUSION: These results suggest that renal tubular cells of CRF were responsible for the decreased Na+ and K+ reabsorption and enhance K+ secretion.