ArticleThe international journal of cardiovascular imaging2022
Subclinic arterial and left ventricular systolic impairment in autosomal dominant polycystic kidney disease with preserved renal functions.
Article in The international journal of cardiovascular imaging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Autosomal dominant polycystic kidney disease: an overview of recent genetic and clinical advances.Renal failure · 2025Review
- Cardiovascular Manifestations and Management in ADPKD.Kidney international reports · 2023Review
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Subclinical atherosclerosis and cardiovascular events are common even in young normotensive patients with autosomal dominant polycystic kidney disease (ADPKD). Our aim was to examine the relationship between serum fibroblast growth factor-23 (FGF-23) levels, left ventricular global longitudinal strain (LV-GLS), arterial stiffness (AS), and carotid intima-media thickness (CIMT) in patients with ADPKD with preserved kidney function. The relationship between albuminuria, AS, LV-GLS, CIMT, 24-hour ambulatory blood pressure measurement, and FGF-23 was examined in 52 normotensive and hypertensive patients with ADPKD and a matched control group of 35 subjects. AS was assesed with brachial-ankle pulse wave velocity, LV-GLS was measured with speckle-tracking echocardiography. FGF-23 was measured with enzyme-linked immunosorbent assay. The microalbumin/creatinine ratio was significantly higher in the ADPKD group than in the control group (p?<?0.001). Serum FGF-23 levels were similar between the study and control group. LV-GLS value tended to be impaired and CIMT to be higher in the ADPKD group compared to controls (?18.1?±?2.6 vs. -19.4?±?3.1?%, p?=?0.08; 0.75?±?0.1 vs. 0.68?±?0.1 mm, p?=?0.09, respectively). The augmentation index was significantly higher in the ADPKD group than in the control group (26.2?±?12.5 vs. 16.4?±?11.2 mmHg/mmHg, p?=?0.01). Our study supports subclinical impairment in arterial and cardiac functions in the early period of ADPKD. However, none of these factors was found to be associated with serum FGF-23 levels.
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