Role of the Renin-Angiotensin-Aldosterone System in the Regulation of Plasma Potassium in Chronic Renal Disease

Abstract

The relationship between plasma potassium concentration and the renin-angiotensin-aldosterone system was evaluated in ten patients with chronic renal failure (creatinine clearance 10–56 ml/min). Under basal conditions and following various stimulation maneuvers, normokalemic patients demonstrated normal plasma renin and aldosterone levels. Five of six patients with hyperkalemia had diminished function of the renin-angiotensin-aldosterone system; their ability to conserve sodium during salt depletion was less than that of normokalemic patients. The data suggest that the maintenance of plasma potassium levels in these patients is dependent on the presence of a normally functioning renin-angiotensin-aldosterone system; aldosterone activity may be an important determinant of sodium conservation in patients with renal failure.

Functional profile of the isolated uremic nephron: potassium adaptation in the rabbit cortical collecting tubule.

“…In vitro studies on the isolated perfused CCT of the rabbit have demonstrated the existence of active potassium secretion in this segment (23)(24)(25)(26)(27). The ability of patients and experimental animals with renal disease to maintain potassium homeostasis despite significant reductions on functioning renal mass (1,4,(14)(15)(16)(17)(18)(19)(20)(21)(22)(28)(29)(30)(31)(32) suggests that nephron sites which normally secrete potassium are able to augment this secretion to maintain potassium balance in chronic uremia. The site of this "potassium adaptation" has recently been the subject of a number of studies.…”

Influence of Basal Insulin and Glucagon Secretion on Potassium and Sodium Metabolism

“…The possible clinical importance of the relationship between basal insulin secretion and potassium homeostasis is underscored by several recent reports of hyperkalemia in diabetic patients in the absence of uremia or acidosis (25,26). In some of the patients hyporeninemic-hypoaldosteronism has been identified as the major factor responsible for hyperkalemia (27,28).…”

Salt-Losing Nephropathy

“…However, the degree of renal failure was usually not severe enough to cause hyperkalemia [50], and many of the patients showed sustained hyperkalemia even after improvement of kidney function, and correc tion of acidosis. In addition, there is good evidence that hyperkalemia can induce acidosis by depressing ammo nia synthesis and hence net acid excretion [51], e.g.…”