Why the study?
How do varying dialysate sodium concentrations and buffers affect plasma aldosterone release during hemodialysis in chronic hemodialysis patients?
How do varying dialysate sodium concentrations and buffers affect plasma aldosterone release during hemodialysis in chronic hemodialysis patients?
Serum potassium and the renin-angiotensin system are the main factors regulating aldosterone release during hemodialysis, with dialysate buffer also playing a role.
Dialysate buffer and sodium may modulate aldosterone during hemodialysis; leaves open effects on outcomes or need for regimen changes.
In order to clarify the influence of serum potassium, serum sodium and plasma angiotensin II concentrations on aldosterone release during hemodialysis (HD), six chronic hemodialysis patients were studied during HD with varying dialysate sodium concentrations and different buffers. Plasma aldosterone concentrations were higher during acetate than bicarbonate HD, during low sodium compared to high sodium HD, and were correlated inversely to serum sodium concentrations. The decline in plasma aldosterone concentrations during HD paralleled the decrease in serum potassium concentrations, and plasma aldosterone concentrations were correlated with serum potassium concentrations. In addition, plasma aldosterone and plasma angiotensin II concentrations were correlated significantly. It is proposed that serum potassium and the renin-angiotensin system are the main factors of aldosterone release during hemodialysis, while serum sodium per se seems to be of less importance. The dialysate buffer employed also plays a role in aldosterone regulation (via the renin-angiotensin system)
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Krämer et al. (1990) studied this question.
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