Studies presented today by a Yale researcher at the annual National Kidney Foundation Meeting in Orlando, Florida, show that midodrine hydrochloride, a medication normally used to treat low blood pressure, may also help kidney disease patients avoid some of the serious side effects of dialysis.
"The results of the studies show that midodrine not only effectively blunts the fall in blood pressure during and after dialysis, but it is also well-tolerated and easy to administer," said Mark Perazella, M.D., associate professor of medicine and director of the Acute Dialysis Services at Yale School of Medicine.
About 250,000 patients with end-stage renal disease undergo dialysis, a life-saving procedure that clears toxins and excess fluids from the blood. Between dialysis sessions, the patients accumulate excess fluids, but after the fluids are removed, the vessels are unable to constrict and return blood to the heart, causing intradialytic hypotension (IDH), or very low blood pressure.
This condition affects 20 to 50 percent of dialysis patients and can cause nausea, vomiting, dizziness and even life-threatening symptoms such as abnormal heart rhythms and diminished blood supply to the heart and brain. These side effects often cause patients to stop treatments. Perazella said that most medications used to treat IDH in the past have been either modestly effective or poorly tolerated.
IDH occurs most often in dialysis patients who are older, people with diabetes or heart disease, and people whose bodies cannot automatically compensate for dialysis-induced fluid loss by constricting the blood vessels to maintain blood return to the heart. The number of at-risk patients is growing; at least 20 percent of dialysis patients are over 65, and more than half suffer from other illnesses, such as diabetes or high blood pressure.
"The complications of IDH take a substantial toll on patients health and quality of life, which can force them to discontinue dial
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Contact: Karen N. Peart
karen.peart@yale.edu
203-432-1326
Yale University
23-Apr-2001