Donohoe P, Farmer C, Dallyn P, Kingswood JC, Goldsmith D,
Sharpstone P, Pattison JM
Low-sodium dialysis without fluid removal improves BP control
in chronic hemodialysis patients
Am Soc Nephrol
J Am Soc Nephrol (abstract)
(Sep) 7:1511 1996
Hypertension in dialysis patients is usually largely attributed to
volume-dependent mechanisms. Evidence for this is the oft-cited ability of
ultrafiltration to control BP in the majority of patients without
medication. Low-sodium dialysis is well-known to decrease BP, at least
transiently. This occurs as the sodium gradient from blood to dialysate
leads to sodium diffusion in that direction faster than sodium and urea can
be mobilized from the interstitial compartment. The result is a decrease in
plasma osmolality, accompanied by fluid shifts from intravascular to
interstitial and intracellular compartments. Decreasing BP and cramps are
the usual result. Another possible side effect is hyponatremia, since early
in the treatment the lower dialysate osmolality may lead to water shifts
from dialysate to plasma. Such effects of low sodium dialysis are usually
considered undesirable and have led to the common use of higher sodium
concentrations, particularly in patients with frequent hypotension and
cramps.
These authors used ambulatory BP monitoring in a 48 hour inter-dialytic
period after 2 weeks of low sodium (132 meq/L) dialysis to compare
responses to 1 week of normal sodium (137 meq/L) dialysis, in 7
non-diabetic dialysis patients. "Target weight" was unchanged in the 2
periods. Mean daytime BP fell from 139/84 to 132/78 mmHg with low sodium
dialysis, and mean nighttime BP fell from 133/79 to 124/73.
These results were statistically significant. "5/7 patients reported minor
cramps which improved" with administration of quinine and albumin.
"Intradialysis hypotension was no more frequent or severe during low-sodium
dialysis" and "no patients developed hyponatremia". Cardiac output,
systemic vascular resistance and ejection fraction were not altered.
The mechanism by which low-sodium dialysis lowered inter-dialytic BP is not
entirely clear. Since "target weight" was the same, total-body sodium
should be the same, and since equilibration occurs over the course of
dialysis and thereafter, no difference in BP should follow. One explanation
for the observed benefit could be that there were subtle changes in
total-body sodium. More likely, low-sodium dialysis was not followed by the
stimulation of thirst and subsequent weight gain associated with higher
dialysis sodium concentrations.
There is no assurance that the "target weight" is the same as the dry
weight. It's possible that more vigorous seeking of the dry weight with
normal dialysate sodium concentrations might have led to similar BP
reductions without the same symptoms.
In recent years, computerized dialysis machines have led to the widespread
popularization of "programmable sodium" or "sodium modeling" in which
dialysate sodium concentrations start high (150's), and end lower. This
should cause skepticism regarding the surprising tolerance experienced by
patients dialyzed with low sodium dialysate concentrations. Finally the
cramps relieved by quinine are not clearly benign. Quinine is no longer
available in the United States, and had
some potential for abuse and toxicity. (David S. Goldfarb, M.D.,
NYU School of Medicine)
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Am Soc Nephrol
Basic hemodialysis :
Complications (acute)
CRF by organ system :
Cardiovascular/Hypertension