Activation of renin-angiotensin system does not cause skeletal muscle cramps during hemodialysis

Abstract

Activation of the renin-angiotensin system usually occurs during hemodialysis and in hemodialyzed normal dogs parallels reductions in blood flow to a tissue group that is largely composed of skeletal muscle. To determine if excessive activation of this system might cause dialysis-associated skeletal muscle cramps in some patients, we conducted a double-blind, randomized and balanced trial in which 5 patients with frequent dialysis-associated cramps were each given either a 25 mg oral dose of captopril or placebo 1 h before 8 consecutive dialyses. Captopril increased the frequency of dialyses complicated by skeletal muscle cramps in 1 patient and did not affect cramp frequency in the other 4 patients. Predialysis plasma renin activity (PRA) averaged 3.9 ng/ml/h (+/- SD) and was the same as in unselected hemodialysis patients. Following captopril, PRA increased by an average of 2.2 +/- 0.7 times, similar to the 2.6-fold increase that was reported when this drug was used to prevent dialysis-associated hypertensive crises. However, hemodialysis by itself did not activate the renin-angiotensin system as consistently in patients with frequent dialysis-associated skeletal muscle cramps as in unselected hemodialysis patients and the ratio of post- to predialysis PRA averaged 1.0 +/- 0.6. We conclude that the renin-angiotensin system does not mediate, and that its activation during hemodialysis may actually help prevent, dialysis-associated skeletal muscle cramps.