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Cutaneous microcirculation is impaired in early autosomal dominant polycystic kidney disease. | LitMetric

AI Article Synopsis

  • The study investigates endothelial dysfunction and microvascular reactivity in early-stage autosomal dominant polycystic kidney disease (ADPKD) before hypertension and renal impairment occurs.
  • Fifteen normotensive ADPKD patients were tested for microcirculation and various plasma parameters, showing significant differences when compared to healthy controls and hypertensive patients.
  • Results highlighted lower microvascular reactivity in ADPKD patients and elevated levels of Lp(a), suggesting that these factors may play a role in increased cardiovascular risks associated with ADPKD.

Article Abstract

Background/aims: An endothelial dysfunction has been described in autosomal dominant polycystic kidney disease (ADPKD) before the development of hypertension and renal impairment. The aim of this work was to verify the existence of a microvascular reactivity in the early stages of ADPKD.

Methods: Fifteen ADPKD normotensive patients with normal renal function underwent laser Doppler examination of the cutaneous microcirculation in basal conditions and after the warm test, as well as evaluation of plasma concentrations of some endothelial activation parameters [total cholesterol and fractions, fibrinogen, von Willebrand factor, Lp(a)]. The results were compared with those in 15 healthy subjects, 15 essential hypertensive patients and 15 hypertensive ADPKD patients with normal renal function.

Results: Both basal and post-warm-test values were significantly lower in normotensive ADPKD subjects than controls (3.2 +/- 1 vs. 5.8 +/- 1.3 AU, p = 0.0001; 35.2 +/- 10.9 vs. 50.5 +/- 10.8 AU, p = 0.005, respectively). All evaluated parameters were within normal limits and comparable between normotensive ADPKD subjects and controls, except for LDL cholesterol (125 +/- 18 vs. 101 +/- 22 mg/dl, p = 0.01) and Lp(a), which was significantly higher in the ADPKD subjects (52.2 +/- 36 vs. 6.0 +/-4 mg/dl, p = 0.0006).

Conclusion: Our study confirms the existence of a systemic microcirculation defect in ADPKD. The presence of high levels of Lp(a) could contribute to causing the high incidence of cardiovascular events in ADPKD.

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Source
http://dx.doi.org/10.1159/000228537DOI Listing

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