Interaction Between Stenotic and Contralateral Kidneys: Unique Features of Each in Unilateral Disease

Juncos, Luis A.; Chandrashekar, Kiran; Lopez‐Ruiz, Arnaldo; Juncos, Luis I.

doi:10.1007/978-1-4471-2810-6_11

Cited by 1 publication

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“…Putative interactions between the STK and CLK affected by neurohormonal pathways are thought to produce dysregulation of the CLK, affecting sodium excretion, kidney hypertrophy, and persistent elevations of BP. Observational studies indicate structural consequences affecting both STK and CLK not easily explained by hemodynamics alone, suggesting functional interactions or crosstalk between the two (6). The sequence and reversibility of hemodynamic and cytokine pathways affecting STKs and CLKs and leading to loss of function in ARAS are incompletely understood.…”

Section: Introductionmentioning

confidence: 99%

Differences in GFR and Tissue Oxygenation, and Interactions between Stenotic and Contralateral Kidneys in Unilateral Atherosclerotic Renovascular Disease

Herrmann

Saad

Eirin

et al. 2016

Clinical Journal of the American Society of Nephrology

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Background and objectives Atherosclerotic renal artery stenosis (ARAS) can reduce renal blood flow, tissue oxygenation, and GFR. In this study, we sought to examine associations between renal hemodynamics and tissue oxygenation with single-kidney function, pressor hormones, and inflammatory biomarkers in patients with unilateral ARAS undergoing medical therapy alone or stent revascularization.Design, setting, participants, & measurements Nonrandomized inpatient studies were performed in patients with unilateral ARAS (.60% occlusion) before and 3 months after revascularization (n=10) or medical therapy (n=20) or patients with essential hypertension (n=32) under identical conditions. The primary study outcome was change in single-kidney GFR. Individual kidney hemodynamics and volume were measured using multidetector computed tomography. Tissue oxygenation (using R 2 * as a measure of deoxyhemoglobin) was determined by blood oxygen level-dependent magnetic resonance imaging at 3 T. Renal vein neutrophil gelatinase-associated lipocalin (NGAL), monocyte chemoattractant protein-1 (MCP-1), and plasma renin activity were measured.Results Total GFR did not change over 3 months in either group, but the stenotic kidney (STK) GFR rose over time in the stent compared with the medical group (12.2[21.8 to 10.5] versus 25.3[27.3 to 20.3] ml/min; P=0.03). Contralateral kidney (CLK) GFR declined in the stent group (43.6619.7 to 36.6619.5 ml/min; P=0.03). Fractional tissue hypoxia fell in the STK (fraction R 2 * .30/s: 22.1%620% versus 14.9%618.3%; P,0.01) after stenting. Renal vein biomarkers correlated with the degree of hypoxia in the STK: NGAL(r=0.3; P=0.01) and MCP-1(r=0.3; P=0.02; more so after stenting). Renal vein NGAL was inversely related to renal blood flow in the STK (r=20.65; P,0.001). Biomarkers were highly correlated between STK and CLK, NGAL (r=0.94; P,0.001), and MCP-1 (r=0.96; P,0.001).Conclusions These results showed changes over time in single-kidney GFR that were not evident in parameters of total GFR. Furthermore, they delineate the relationship of measurable tissue hypoxia within the STK and markers of inflammation in human ARAS. Renal vein NGAL and MCP-1 indicated persistent interactions between the ischemic kidney and both CLK and systemic levels of inflammatory cytokines.

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Section: Introductionmentioning

confidence: 99%