English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

Prof. Michele Buemi, Via Salita Villa Contino 30, I-98100 Messina (Italy) Dear Sir, Autosomal dominant polycystic kidney disease (ADPKD) can be frequently complicated by chronic renal failure and hypertension [1]· In the literature there is little consensus on the pathogenesis of hypertension in patients with ADPKD. In fact, although it would seem obvious that the incidence of hypertension would increase as renal insufficiency becomes more severe, it has also been demonstrated that there is no correlation between the severity of hypertension and the severity of renal involvement, and that 15-20% of subjects with ADPKD without renal function impairment have hypertension and that blood pressure alterations can be found in ADPKD patients without renal function impairment before puberty [2]. Importantly, the genetic trait appears to be dominant. The main genie locus responsible for ADPKD is PKD-1, localized on the short arm of chromosome 16, which presents a 100% penetration [3]. However, another locus is involved in the disease. Called PKD-2, it is linked to chromosome 4, which is altered in 10% of patients, and modifications in it could give rise to an altered cellular membrane structure, and therefore to anomalous functioning of the ionic transport systems [4, 5]. Recently Vareesangthip et al. [6] identified altered Na/Li countertransport in ADPKD patients, and Rutherford et al. [7] found that patients with essential hypertension had an altered ionic transport system. However, this alteration is present in the erythrocytes of all ADPKD patients, and so it does not explain why hypertension develops in only 15-20% of such patients without renal function impairment. We therefore evaluated induced Ca2+/K+ flow in the erythrocytes of ADPKD subjects in order to ascertain whether ADPKD patients with hypertension but without renal function impairment also had alterations in other ionic transport systems. Our study was conducted on 40 subjects divided into four groups that were matched for age and gender as follows; 10 healthy controls (5 M, 5 F; mean age 52 ± 7 years); 10 with essential

Alterations in Induced Potassium Calcium Efflux in the Erythrocytes of Patients with Autosomal Dominant Polycystic Kidney Disease and Hypertension