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Comparative Study
. 2013 Feb;34(7):540-548a.
doi: 10.1093/eurheartj/ehs197. Epub 2012 Jul 6.

Inflammatory and injury signals released from the post-stenotic human kidney

Alfonso Eirin  1 , Monika L Gloviczki, Hui Tang, Mario Gössl, Kyra L Jordan, John R Woollard, Amir Lerman, Joseph P Grande, Stephen C Textor, Lilach O Lerman
Affiliations
Comparative Study

Inflammatory and injury signals released from the post-stenotic human kidney

Alfonso Eirin et al. Eur Heart J. 2013 Feb.

Abstract

Aims: The mechanisms mediating kidney injury and repair in humans with atherosclerotic renal artery stenosis (ARAS) remain poorly understood. We hypothesized that the stenotic kidney releases inflammatory mediators and recruits progenitor cells to promote regeneration.

Methods and results: Essential hypertensive (EH) and ARAS patients (n=24 each) were studied during controlled sodium intake and antihypertensive treatment. Inferior vena cava (IVC) and renal vein (RV) levels of CD34+/KDR+ progenitor cells, cell adhesion molecules, inflammatory biomarkers, progenitor cell homing signals, and pro-angiogenic factors were measured in EH and ARAS, and their gradient and net release compared with systemic levels in matched normotensive controls (n= 24). Blood pressure in ARAS was similar to EH, but the glomerular filtration rate was lower. Renal vein levels of soluble E-Selectin, vascular cell adhesion molecule-1, and several inflammatory markers were higher in the stenotic kidney RV vs. normal and EH RV (P < 0.05), and their net release increased. Similarly, stem-cell homing factor levels increased in the stenotic kidney RV. Systemic CD34+/KDR+ progenitor cell levels were lower in both EH and ARAS and correlated with cytokine levels. Moreover, CD34+/KDR+ progenitor cells developed a negative gradient across the ARAS kidney, suggesting progenitor cell retention. The non-stenotic kidney also showed signs of inflammatory processes, which were more subtle than in the stenotic kidney.

Conclusion: Renal vein blood from post-stenotic human kidneys has multiple markers reflecting active inflammation that portends kidney injury and reduced function. CD34+/KDR+ progenitor cells sequestered within these kidneys may participate in reparative processes. These inflammation-related pathways and limited circulating progenitor cells may serve as novel therapeutic targets to repair the stenotic kidney.

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Figures

Figure 1
Figure 1
The net release of cytokines in essential hypertension, stenotic kidney, and contralateral kidney of atherosclerotic renal artery stenosis patients. *P< 0.05 vs. essential hypertension, ‡P< 0.05 vs. contralateral kidney.
Figure 2
Figure 2
(A) Representative flow cytometric dot plots for CD34+/KDR+ progenitor cells in study patients. Systemic and renal vein (RV) levels (B) and gradients (C) of CD34+/KDR+ progenitor cells in normal, essential hypertensive, stenotic kidney and contralateral kidney of atherosclerotic renal artery stenosis patients. Renal vein CD34+/KDR+ progenitor cell levels were reduced in the stenotic kidney-atherosclerotic renal artery stenosis kidney, leading to a negative CD34+/KDR+ progenitor cell gradient across it, greater than across the contralateral kidney. *P< 0.05 vs. normal, #P< 0.05 vs. essential hypertension, †P< 0.05 vs. systemic, ‡P< 0.05 vs. contralateral kidney.
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