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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 . . . [Full Text of this Article]

AUTHOR INFORMATION
Iddo Z. Ben-Dov, MD; Michael Bursztyn, MD

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