Why the study?
Nocturnal hypertension increases renal and cardiovascular risk in CKD, but microcirculatory function and central hemodynamics had not been compared between CKD patients with and without nocturnal hypertension.
Does nocturnal hypertension impair microcirculatory function and central hemodynamics in pre-dialysis CKD patients?
Does nocturnal hypertension impair microcirculatory function and central hemodynamics in pre-dialysis CKD patients?
Nocturnal hypertension in CKD patients is associated with impaired capillary recruitment and higher aortic blood pressure, suggesting an additive detrimental effect on microvascular function.
Nocturnal hypertension may link to microvascular dysfunction in CKD; hypothesis-generating and should not yet change practice.
BACKGROUND: Nocturnal hypertension is associated with an increased risk for renal and cardiovascular events in patients with chronic kidney disease (CKD). Endothelial dysfunction and microvascular damage are highly prevalent in CKD and related to CKD progression and adverse cardiovascular outcomes. The aim of this analysis was to compare for the first time microcirculatory function parameters and central hemodynamics in CKD patients with and without nocturnal hypertension. METHODS: 96 pre-dialysis CKD patients underwent 24-h ABPM (Mobil-O-Graph-NG device) and nailfold video-capillaroscopy, during which capillary density was measured at baseline, after 4-min arterial occlusion (postocclusive reactive hyperemia) and following 2-min venous occlusion (congestion phase). Arterial stiffness and central hemodynamics were captured in office conditions with Sphygmocor. RESULTS: The two groups (with and without nocturnal hypertension) were similar in terms of age, eGFR, BMI, and major comorbidities. Patients with nocturnal hypertension presented significantly lower capillary density at baseline (30.6 ± 3.6 vs. 33.1 ± 3.2 capillaries/mm2; P = 0.003), during postocclusive reactive hyperemia (36.6 ± 4 vs. 39.5 ± 3.9 capillaries/mm2; P = 0.003), and during venous congestion (38.1 ± 4.2 vs. 41 ± 3.5 capillaries/mm2; P = 0.003) compared to those without nocturnal hypertension. Participants with nocturnal hypertension had significantly higher aortic BP; no differences were found in the other parameters of arterial stiffness. The above observations were more prominent in patients with diabetes. CONCLUSIONS: Capillary density during postocclusive hyperemia and after venous congestion is lower in patients with nocturnal hypertension compared to those with normotension, suggesting that nocturnal hypertension is a factor superimposed on the microvascular changes characterizing CKD to further impair capillary recruitment.
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Theodorakopoulou et al. (2025) studied this question.
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