Overlapping clinical definitions of the causes and characteristics of intradialytic hypertension make it a frustrating condition to diagnose and treat
Intradialytic hypertension (IDH) is another shadowy culprit that appears to be responsible for increased mortality risk in kidney disease patients. But it is also a risk factor over which physicians can at least try to exercise some control as continuing studies identify ways that they might tweak dialysate recipes or prescribe medication therapy.
Mark J. Sarnak, MD, a researcher at Tufts Medical Center and an active investigator on the topic of IDH, gave a presentation at Renal Week 2010, the 43rd Annual Meeting and Scientific Exposition of the American Nephrology Society, that highlighted the problematic issues of teasing out appropriate IDH diagnoses from a plethora of varying clinical definitions, as well as finding proper mitigation measures for it.
In general terms, (IDH) is defined by blood pressure (BP) values during and at the end of dialysis sessions that exceed BP values at the onset of dialysis. The complication occurs in an estimated 10% of hemodialysis patients and has been associated with increased mortality. Using more specific terms, Sarnak believes it makes sense to go by the clinical definition supported by the largest current observational studies: an increase of 10 mm Hg diastolic pressure from pre- to post-dialysis.
A second stew of possibilities awaits the nephrologist who hopes to accurately identify the manifest characteristics of IDH in dialysis patients. These include measurements of pre-dialysis BP, dry weight, body mass index, and interdialytic weight gain. The patient’s levels of albumin and zero creatinine also stand as possible manifestations. But Sarnak noted that some studies posit these metrics in a way that begs the question of whether the patients already were sicker than other recipients of dialysis at the outset of treatment.
He said that the pathophysiologic mechanisms that appear to give the strongest clues to a viable IDH treatment plan include volume overload, sympathetic neural activity, endothelin and nitric oxide levels in plasma, and the factors associated with dialysis itself, including sodium levels in the dialysate and whether or not IDH-causal medications were administered to or taken away from the patient during treatment.
With regard to dialysis-centric complications, there is more than one area in which the clinician can err. “There are some potential effects of the dialysate calcium in how it affects the blood pressure during dialysis,” Sarnak explained. He cited one study that revealed higher systolic BP and higher stroke volume for patients who were subjected to high calcium dialysate, thereby increasing their cardiac output.
Evidence suggests that improper sodium levels can further poison a patient’s dialysate. This can occur when sodium intake ends at a higher level during the treatment, which promotes thirst and subsequent volumetric overload. In a contrary scenario, thirst may be promoted by use of a dialysate that removes sodium.
Sarnak said that blood pressure may also rise in cases where certain beta blockers or ACE inhibitors are taken away from the patient. He summed up his talk with the following conclusions: