Ischemic nephropathy: Clinical characteristics and treatment

Alcázar, Jose María Morillas; Rodicio, José L.

doi:10.1053/ajkd.2000.19077

Cited by 35 publications

(17 citation statements)

References 78 publications

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“…We thus introduced a second experimental kidney model that is characterized by an inflammatory component. Since renal ischemia is a major cause of acute and end-stage renal failure [28], producing serious morbidity and mortality, renal ischemia/reperfusion (I/R) injury was chosen to evaluate whether Ang-(1–7) and Mas was involved in the primary mechanisms determining ischemia-mediated renal failure.…”

Section: Resultsmentioning

confidence: 99%

Angiotensin-(1–7) and the G Protein-Coupled Receptor Mas Are Key Players in Renal Inflammation

Esteban¹,

et al. 2009

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Angiotensin (Ang) II mediates pathophysiologial changes in the kidney. Ang-(1–7) by interacting with the G protein-coupled receptor Mas may also have important biological activities.In this study, renal deficiency for Mas diminished renal damage in models of renal insufficiency as unilateral ureteral obstruction and ischemia/reperfusion injury while the infusion of Ang-(1–7) to wild-type mice pronounced the pathological outcome by aggravating the inflammatory response. Mas deficiency inhibited NF-κB activation and thus the elevation of inflammation-stimulating cytokines, while Ang-(1–7) infusion had proinflammatory properties in experimental models of renal failure as well as under basal conditions. The Ang-(1–7)-mediated NF-κB activation was Mas dependent but did not involve Ang II receptors. Therefore, the blockade of the NF-κB-activating properties of the receptor Mas could be a new strategy in the therapy of failing kidney.

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Section: Resultsmentioning

confidence: 99%

Angiotensin-(1–7) and the G Protein-Coupled Receptor Mas Are Key Players in Renal Inflammation

Esteban¹,

et al. 2009

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“…The mean patient age in published series of renal revascularization has risen from the mid-50s to above 71 yr over the past two decades (34). The level of preintervention GFR tends to predict the likely recovery potential after revascularization, as those with serum creatinine Ͼ3.0 mg/dl less commonly improve (35,36). Clinical observations confirm that the rate of loss of GFR just before renal revascularization correlates with the potential for recovery of renal function in the year after endovascular stent placement (37).…”

Section: Pathophysiology Of "Critical" Ras and "Ischemic Nephropathy"mentioning

confidence: 99%

Ischemic Nephropathy

Textor

2004

Journal of the American Society of Nephrology

148

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Abstract. Identification and reversing the loss of kidney function beyond occlusive disease of the renal arteries poses a major clinical challenge. Recent studies indicate that atherosclerotic renal artery stenosis develops as a function of age and is commonly associated with other microvascular disease, including nephrosclerosis and diabetic nephropathy. The risks of renal artery stenosis are related both to declining kidney function and to accelerated cardiovascular disease, with increased morbidity and mortality. Newer drugs, including agents that block the renin-angiotensin system, have improved the level of BP control for renovascular hypertension. Progressive renovascular disease during medical therapy can produce refractory hypertension, congestive heart failure, and renal failure with tubulointerstitial fibrosis. Recent studies indicate a complex interplay of oxidative stress, endothelial dysfunction, and activation of fibrogenic cytokines as a result of experimental atherosclerosis and renal hypoperfusion. Advances in imaging and interventional devices offer major new opportunities to prevent progressive loss of kidney function. Recent series indicate that although 25 to 30% of patients with impaired renal function can recover glomerular filtration after revascularization, many have no apparent change in kidney function and 19 to 25% experience a significant loss of kidney function, in some cases as a result of atheroemboli. To select patients who are most likely to benefit from vascular intervention, clinicians should understand the pathophysiology of developing ischemic nephropathy and the potential hazards of revascularization in the setting of diffuse atherosclerotic disease. Further research should be directed toward identification of critical disease, regulation of fibrogenesis, and the interaction with other atherosclerotic processes.

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“…4 Eventually, occlusive disease leads to tissue fibrosis that becomes irreversible and can lead to end-stage kidney disease, which some authors designate "ischemic nephropathy." [5][6][7] Whether the sequence of events leading to fibrosis and kidney injury actually entails reduced oxygenation and regional tissue ischemia in humans is not yet known. Some authors estimate that basal oxygen requirements are met with less than 10% of blood flow.…”

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confidence: 99%

The Use of Magnetic Resonance to Evaluate Tissue Oxygenation in Renal Artery Stenosis

Textor

Glockner

Lerman

et al. 2008

Journal of the American Society of Nephrology

155

114

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Vascular occlusive disease poses a threat to kidney viability, but whether the events leading to injury and eventual fibrosis actually entail reduced oxygenation and regional tissue ischemia is unknown. Answering this question has been difficult because of the lack of an adequate method to assess tissue oxygenation in humans. BOLD (blood oxygen-level-dependent) magnetic resonance imaging detects changes in tissue deoxyhemoglobin during maneuvers that affect oxygen consumption, therefore this technique was used to image and analyze cortical and medullary segments of 50 kidneys in 25 subjects undergoing magnetic resonance (MR) angiography to diagnose renal artery stenosis (RAS). Magnetic rate of relaxation (R2*) positively correlates with deoxyhemoglobin levels and was therefore used as a surrogate measure of tissue oxygenation. Furosemide was administered to examine the effect of inhibiting energy-dependent electrolyte transport on tissue oxygenation in subjects with renovascular disease. In 21 kidneys with normal nephrograms, administration of furosemide led to a 20% decrease in medullary R2* (P Ͻ 0.01) and an 11.2% decrease in cortical R2*. In normal-size kidneys downstream of high-grade renal arterial stenoses, R2* was elevated at baseline, but fell after furosemide. In contrast, atrophic kidneys beyond totally occluded renal arteries demonstrated low levels of R2* that did not change after furosemide. In kidneys with multiple arteries, localized renal artery stenoses produced focal elevations of R2*, suggesting areas of deoxyhemoglobin accumulation. These results suggest that BOLD MR coupled with a method to suppress tubular oxygen consumption can be used to evaluate regional tissue oxygenation in the human kidney affected by vascular occlusive disease.

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Ischemic nephropathy: Clinical characteristics and treatment

Cited by 35 publications

References 78 publications

Angiotensin-(1–7) and the G Protein-Coupled Receptor Mas Are Key Players in Renal Inflammation

Angiotensin-(1–7) and the G Protein-Coupled Receptor Mas Are Key Players in Renal Inflammation

Ischemic Nephropathy

The Use of Magnetic Resonance to Evaluate Tissue Oxygenation in Renal Artery Stenosis

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