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Hypertension (Dallas, Tex. : 1979)

August 24, 2026 · via Europe PMC

Hemodynamics and Renin Profiles of Renal Artery Variations in Hypertensive CKD.

Ma H, Jin K, Xu X, +8 more, Zhang W.

Journal ArticleAbstract only — full text under license

AI summary — for doctors, generated from the abstract only

In hypertensive CKD, accessory renal arteries showed small pressure gradients and segmental renin hypersecretion, unlike early-branching variants.

What was studied

A prospective cohort of 38 hypertensive CKD patients with unilateral renal artery variations (24 accessory, 14 early branching) undergoing pressure-wire assessment and segmental renal vein renin sampling, with 2-year follow-up in 35.

Key findings

  • Mean pressure gradient higher in variant artery than main artery (1.10 vs -0.15 mm Hg), limited to accessory arteries
  • Plasma renin activity elevated in accessory-artery-supplied segments (1.77 vs 1.24 ng/mL/h)
  • Variant artery pressure gradient associated with segmental and peripheral renin activity (exploratory)
  • eGFR declined 5.2 mL/min/1.73 m2 within the accessory group, but group-by-time interaction was not significant

Clinical relevance

Suggests accessory renal arteries may contribute to renin-mediated hypertension in some patients, but the small sample makes these preliminary signals.

Who should care

Vascular Surgery

Limitations

Very small sample (38) with exploratory associations; between-group differences in eGFR change were not significant.

Accessory renal arteries may be functionally relevant in hypertensive kidney disease and merit larger studies.

This is an AI-generated summary of the published abstract, not a clinical recommendation. It may not reflect the full text or subsequent updates — verify against the original source before acting on it.

Abstract

Background

The functional implications of renal artery variations-including accessory renal artery (ARA) and early branching-in hypertensive chronic kidney disease remain poorly understood.

Methods

This prospective cohort study enrolled 38 patients with hypertensive chronic kidney disease and unilateral solitary renal artery variation (24 ARA, 14 early branching) undergoing pressure wire-based hemodynamic evaluation and selective segmental renal vein renin sampling; 35 patients completed 2-year follow-up.

Results

Mean pressure gradient was higher in variant artery than in ipsilateral main (1.10±3.39 versus -0.15±2.21 mm Hg, P=0.04) and contralateral renal artery (versus -0.10±1.56 mm Hg, P=0.04) in the overall cohort, a difference limited to the ARA subgroup. Plasma renin activity was elevated in ARA-supplied segments compared with the ipsilateral main trunk (1.77±1.86 versus 1.24±1.40 ng/(mL·h), P=0.004) and contralateral artery-supplied segments (versus 1.24±1.37, P=0.002), whereas no significant difference was observed in the early branching subgroup. After multivariable adjustment, variant artery systolic pressure gradient was positively associated with variant-supplied segmental (β=0.41, P=0.02) and peripheral (β=0.37, P=0.04) plasma renin activity, angiotensin II, and nighttime mean arterial pressure. Peripheral aldosterone was associated with lower estimated glomerular filtration rate and higher urinary protein. All adjusted associations represent exploratory signals given limited sample size. Over 2 years, an intragroup estimated glomerular filtration rate decline was observed within the ARA subgroup (-5.2 mL/[min·1.73 m2]; P=0.02) while the early branching subgroup remained stable (P=0.47); however, the group-by-time interaction was not significant (P=0.06), indicating these preliminary trends require larger validation cohorts.

Conclusions

Renal artery variations may alter intrarenal hemodynamics, with functional impairment and segmental renin hypersecretion observed primarily in ARA. This suggests a potential role for functional evaluation.

DOI

10.1161/hypertensionaha.126.27130

PMID

42634941

Research metadata (titles, abstracts, authors, publication dates) is sourced from Europe PMC, which aggregates content from PubMed/MEDLINE, PubMed Central, and other providers under the U.S. National Library of Medicine (NLM/NCBI). NLM does not claim copyright on abstracts; the original journal publishers or authors may hold rights to the full articles. AI-generated summaries are derived only from the abstract, never the full text, and are always labeled as AI-generated.

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