Amiloride-sensitive and amiloride-insensitive kaliuresis in advanced chronic kidney disease.

YEYATI NL; FELLET A.; ARRANZ C; BALASZCZUK A.; ADROGUE H

JN. JOURNAL OF NEPHROLOGY

Milano : Wichtig Editore

Año: 2008 vol. 21 p. 93 - 98

1121-8428

BACKGROUND.  Salt delivery to the distal nephron and sodium reabsorption in this segment are considered critical factors that modulate kaliuresis in chronic kidney disease (CKD).  Amiloride administration, a drug that blocks Na+ reabsorption in the distal nephron, can help to assess the role of Na+ transport in this segment in the kaliuresis of CKD patients.   METHODS.  A bolus of amiloride (1 mg/kg body weight) followed by an intravenous infusion (1 mg/kg body weight per hour) was administered to six normal subjects and ten patients with CKD undergoing water diuresis.  Serum and urine electrolytes were measured.  Glomerular filtration rate (GFR) was measured with clearance of  135I Iodothalamate.   RESULTS.  Normal subjects and CKD patients had a control FEK+ of 26±11% and 126± 28%, respectively; the corresponding FENa+ were 2.3±0.8% and 15±3%.  In response to amiloride, FENa+ increased significantly to 3.5±0.6% and 20±3% in normal and CKD subjects, respectively, and FEK+ decreased significantly to 6.5±0.6% and 39±8%, respectively.  Amiloride-sensitive and insensitive kaliuresis in normal subjects represented 71.4% and 28.6%, respectively; the corresponding values for CKD patients were 73% and 27%, respectively.  Urine output correlated positively with kaliuresis in CKD. CONCLUSIONS.  The very high FEK+ observed in CKD occurs in the absence of hyperkalemia and is largely amiloride-sensitive; therefore maintenance of potassium balance by the kidney in CKD is mostly dependent on sodium reabsorption through channels along the distal nephron.  The high urinary flow of CKD further promotes potassium excretion.