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Abstract: SA-PO341

Poststenotic Dilatation (PSD) in Human Renal Artery Stenosis (RAS)

Session Information

Category: Hypertension and CVD

  • 1602 Hypertension and CVD: Clinical

Authors

  • Al Saeedi, Mina H., Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States
  • Arabi, Tarek Ziad, Mayo Foundation for Medical Education and Research, Rochester, United States
  • Nyvad, Jakob, Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States
  • Bajpai, Shivam, Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States
  • Oudih, Mouaz, Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States
  • Xing, Li, Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States
  • Lu, Bo, Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States
  • Zhang, Lei, Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States
  • Tang, Hui, Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States
  • Zhu, Xiang yang, Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States
  • Misra, Sanjay, Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States
  • Lerman, Amir, Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States
  • Lerman, Lilach O., Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States

Group or Team Name

  • Nephrology and Hypertension.
Background

A hemodynamically significant RAS may cause renal inflammation and development of PSD. However, beyond local remodeling, the functional significance of PSD, its link to renal function and inflammation, or its reversibility remain unclear. We hypothesized that PSD-RAS is associated with renal dysfunction and inflammatory marker levels in the stenotic renal vein (STK-RV) and would regress after percutaneous transluminal renal angioplasty (PTRA)

Methods

RAS patients with PSD (n=31, Table 1) underwent multidetector CT scanning and STK-RV sampling. In 3D CT images, PSD dilatation diameter ratio (DDR) was defined as the ratio between the maximal PSD diameter and the non-diseased segment proximal to RAS (Fig1). In 7 patients, studies were repeated 3 months after PTRA

Results

Patients had kidney dysfunction and hypertension (Table 1). DDR directly correlated with elevated serum creatinine, STK-RV levels of neutrophil gelatinase-associated lipocalin (NGAL), interleukin-6 (IL-6), and interferon-gamma (INF-γ) (Fig2), and 24h urinary protein levels. After PTRA renal function improved, inflammatory biomarkers declined, and PSD regressed (Fig3)

Conclusion

Development of PSD is reversible but associated with kidney dysfunction and inflammation and may reflect the severity of kidney injury in RAS. Detection of PSD may be beneficial in guiding treatment decisions

Table1 Demographics
VariablesMean±SD
Age, Yrs.71±7
MAP, mmHg93±11
S.Cr, mg/dl1.4±0.4
eGFR, ml/min/1.73m248.2±18.7
Ras Severity, %71±11

MAP: Mean Arterial Pressure, S. Cr: Serum Creatinine, eGFR: Estimated Glomerular Filtration Rate.

Funding

  • NIDDK Support