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Editor's Correspondence |

Nondipping and Impaired Kidney Function: Which Is the Cause?

Iddo Z. Ben-Dov, MD; Michael Bursztyn, MD
Arch Intern Med. 2006;166(19):2158. doi:10.1001/archinte.166.19.2158-a.
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Davidson et al1 have established beyond doubt a link between blood pressure (BP) nondipping (a lack of nocturnal decline in BP) at baseline and declining kidney function among subjects referred to their ambulatory BP-monitoring service. This association withstood rigorous multivariate and subset analyses. Thus, a causal relationship is implied, and the authors further discuss the issue. Indeed, decreasing glomerular filtration rate may reflect hypertensive target organ damage, exacerbated by the nondipping state and the accompanying amplified sympathetic nervous system activity. Alternatively, subtle kidney derangements, destined to deteriorate regardless of BP variability, may be responsible for the nondipping state at the outset of the follow-up period. For example, evidence is available that compared with neuropathy, nephropathy is more strongly associated with nondipping in patients with diabetes.2 This salt-sensitive state was argued to cause BP nondipping through deranged extracellular volume homeostasis. In fact, other salt-sensitive conditions, some mentioned by Davidson et al,1 have also been linked to the nondipping phenotype. Included in this list, in addition to diabetes, are old age, Cushing syndrome, hyperaldosteronism, advanced kidney disease, nephrotic syndrome, liver cirrhosis, and congestive heart failure.3 Assuming that a salt-sensitive state (caused by overt or covert renal abnormalities) was responsible for decreased BP variability among nondippers (patients with nondipping status) in the cohort of Davidson et al,1 a diuretic, rather than a renin-angiotensin antagonist as the authors suggested, would be the logical choice for therapy. Indeed, Uzu and Kimura4 have found that diuretics, as well as sodium restriction, convert hypertensive nondippers to dippers (patients with normal diurnal BP variation). Likewise, in our ambulatory BP database, we found that diuretics were associated with dipping (odds ratio, 1.5; 95% confidence interval, 1.1-2.2), while α-blockers (which may cause salt retention) correlated with nondipping (odds ratio for dipping, 0.6; 95% confidence interval, 0.4-0.9).5 Renin-angiotensin system blockers were not associated with any dipping phenotype. Another look at Table 1 in the article by Davidson et al1 reveals similar trends in their population. While the odds ratio for nondipping among users of β-blockers or renin-angiotensin blockers was significantly greater than 1, it was not so for diuretic-treated subjects. Thus, the important study by Davidson and coworkers1 tightens the link between nondipping BP pattern, impending kidney disease, volume state, and antihypertensive treatment.

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