Background: Renal handling of sodium and water is abnormal in chronic kidney disease (CKD). The aim of this\nstudy was to test the hypothesis that abnormal activity of the aquaporin-2 water channels (AQP2), the\nsodium-potassium-2chloride transporter (NKCC2) and/or the epithelial sodium channels (ENaC) contribute to this\nphenomenon.\nMethods: 23 patients with CKD and 24 healthy controls at baseline and after 3% saline infusion were compared.\nThe following measurements were performed: urinary concentrations of AQP2 (u-AQP2), NKCC2 (u-NKCC2), ENaC\n(u-ENaC?), glomerular filtration rate (GFR) estimated by 51Cr-EDTA clearance, free water clearance (CH2O), urinary\noutput (UO), fractional excretion of sodium (FENa), plasma concentrations of AVP, renin (PRC), Angiotensin II (ANG II),\nAldosterone (Aldo) and body fluid volumes.\nResults: At baseline, GFR was 34 ml/min in CKD patients and 89 ml/ml in controls. There were no significant\ndifferences in u-AQP2, u-NKCC2 or u-ENaC?, but FENa, p-Aldo and p-AVP were higher in CKD patients than controls.\nIn response to hypertonic saline, patients with CKD had an attenuated decrease in CH2O and UO. A greater increase\nin U-AQP2 was observed in CKD patients compared to controls. Furthermore, u-NKCC2 increased in CKD patients,\nwhereas u-NKCC2 decreased in controls. Body fluid volumes did not significantly differ.\nConclusions: In response to hypertonic saline, u-NKCC2 increased, suggesting an increased sodium reabsorption\nvia NKCC2 in patients with CKD. U-AQP2 increased more in CKD patients, despite an attenuated decrease in CH2O.\nThus, though high levels of p-AVP and p-Aldo, the kidneys can only partly compensate and counteract acute\nvolume expansion due to a defective tubular response.
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