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Dialysis and Hypertension: Worthy of Investigation?

Should future research and funding be devoted to the study of dialysis hypertension? There are a number of perspectives on such a question. From the most provincial and naive point of view the answer is certainly yes. Hemodialysis was once a temporary measure rescuing individuals from uremic coma, but today it is the standard of renal replacement therapy. People with irreversible, intractable uremia survive years and decades through regular hemodialysis. Indeed, dialysis patients seldom die of uremia; rather, as illustrated in Figure 1, they die because of cardiovascular disease and infection (1 ). Certainly, providing longer survival with less morbidity would be a worthy goal. Scribner recently asked why the role of hypertension is overlooked when we discuss reducing dialysis patient mortality (2). This is an intriguing question, particularly in light of the Health Care Financing Administration’s (HCFA’s) decision to eliminate preand postdialysis blood pressure data from the Hemodialysis Core Indicators data set. Clearly, blood pressure has two key features desirable in a performance indicator: it is measurable and it is modifiable. This has been demonstrated in both dialysis and nondialysis populations (3-5). Further, crosssectional studies conclude that both hypertension and predialysis systolic blood pressure are predictors of excess patient morbidity (6-lo), though the United States Renal Data Service (USRDS) reports that among prevalent hemodialysis patients low rather than high blood pressure is associated with an increased risk of death (11). Parfrey and Foley have reported on 432 patients followed for an average of 41 months after the initiation of dialysis. They find the average predialysis blood pressure to be correlated with an increased risk of developing left ventricular hypertrophy, left ventricular dilatation, angina, and new-onset heart failure (Table 1) ( 1 2). Cannella et al. have furthered these observations by demonstrating that not only can left ventricular hypertrophy be prevented through blood pressure control but hypertensive dialysis patients with established left ventricular hypertrophy can normalize their ventricular structure following prolonged pharmacologic blood pressure normalization (13). Neither Cannella’s report nor Palfrey’s counters the USRDS finding that low rather