Structural and Functional Capillary Integrity, Arterial Stiffness and Central Hemodynamics in CKD Patients With and Without Nocturnal Hypertension.

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.