Abstract—We have postulated that the diminished renal capacity to excrete sodium causes nocturnal blood pressure (BP) elevation, which enhances pressure natriuresis in compensation for impaired daytime natriuresis. If such a mechanism holds, high BP during sleep at night may continue until excess sodium is sufficiently excreted into urine. This study examined whether the duration, defined as "dipping time," until nocturnal mean arterial pressure began to fall to <90% of daytime average became longer as renal function deteriorated. Ambulatory BP measurements and urinary sodium excretion rates were evaluated for daytime and nighttime to estimate their circadian rhythms in 65 subjects with chronic kidney disease. Dipping time showed an inverse relationship with creatinine clearance (C_cr; =-0.61; P<0.0001) and positive relationships with night/day ratios of mean arterial pressure (=0.84; P<0.0001) and natriuresis (=0.61; P<0.0001), both of which were also inversely correlated with C_cr (mean arterial pressure: r=-0.58, P<0.0001; natriuresis: r=-0.69, P<0.0001). When divided into tertiles by C_cr (mL/min), hazard ratios of nocturnal BP dip adjusted for age, gender, and body mass index were 0.37 (95% CI: 0.17 to 0.79; P=0.01) for the second tertile (C_cr: 50 to 90) and 0.20 (95% CI: 0.08 to 0.55; P=0.002) for the third tertile (C_cr: 5 to 41) compared with the first tertile (C_cr: 91 to 164). These findings demonstrate that patients with renal dysfunction require a longer duration until BP falls during the night. The prolonged duration until BP dip during sleep seems an essential component of the nondipper pattern of the circadian BP rhythm.