Loss of kidney function in patients with critical limb ischemia treated endovascularly or surgically

Sigterman, Tim A.; Bolt, Lars J.J.; Krasznai, A; Snoeijs, Maarten G.; Heijboer, Roel J.J.; Schurink, Geert-Willem; Bouwman, Lee H.

doi:10.1016/j.jvs.2016.03.409

Cited by 14 publications

(8 citation statements)

References 20 publications

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“…Probably, the increased comorbidity, vessel calcification, and isolated below-knee atherosclerotic disease that are often present in CKD led the treating physicians to an endovascular-first approach. Of note, Sigterman et al 33 recently reported that endovascular revascularization is associated with greater loss of renal function compared with patients treated surgically. On the other hand, bypass surgery remained the treatment of choice for complex anatomical lesions despite numerous studies reporting on endovascular revascularization of TASC II C/D disease.…”

Section: Discussionmentioning

confidence: 99%

One-Year Results of First-Line Treatment Strategies in Patients With Critical Limb Ischemia (CRITISCH Registry)

et al. 2018

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Section: Discussionmentioning

confidence: 99%

One-Year Results of First-Line Treatment Strategies in Patients With Critical Limb Ischemia (CRITISCH Registry)

et al. 2018

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“…Thoracic and abdominal aortic procedures (endovascular as well as open surgical repair (OSR)) carry a higher risk of AKI than peripheral vascular operations. Peripheral vascular procedures have some of the lowest rates, from 4% for patients undergoing infrainguinal lower extremity bypass, up to 19% for endovascular revascularization of critical limb ischemia [26,[30][31][32].…”

Section: Risk Factors Of Post-contrast Akimentioning

confidence: 99%

Acute Renal Failure/Acute Kidney Injury (AKI) Associated with Endovascular Procedures

et al. 2020

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AKI is one of the most common yet underdiagnosed postoperative complications that can occur after any type of surgery. Contrast-induced nephropathy (CIN) is still poorly defined and due to a wide range of confounding individual variables, its risk is difficult to determine. CIN mainly affects patients with underlying chronic kidney disease, diabetes, sepsis, heart failure, acute coronary syndrome and cardiogenic shock. Further research is necessary to better understand pathophysiology of contrast-induced AKI and consequent implementation of effective prevention and therapeutic strategies. Although many therapies have been tested to avoid CIN, the only potent preventative strategy involves aggressive fluid administration and reduction of contrast volume. Regardless of surgical technique—open or endovascular—perioperative AKI is associated with significant morbidity, mortality and cost. Endovascular procedures always require administration of a contrast media, which may cause acute tubular necrosis or renal vascular embolization leading to renal ischemia and as a consequence, contribute to increased number of post-operative AKIs.

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“…In addition to increasing risk of mortality and amputation, CKD also increases the failure rate of endovascular/revascularization surgical interventions in PAD 3,12,13 . Complicating the mortality and surgical failure risk, administration of contrast dyes during endovascular/revascularization surgeries has been shown to induce acute kidney injury that increases future risk of developing CKD 14,15 . Despite strong epidemiological data linking CKD to worsened PAD health outcomes, the biological mechanisms are unknown.…”

Section: Introductionmentioning

confidence: 99%

Chronic kidney disease exacerbates ischemic limb myopathy in mice via altered mitochondrial energetics

Berru¹,

Gray²,

Thome³

et al. 2019

Sci Rep

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Chronic kidney disease (CKD) substantially increases the severity of peripheral arterial disease (PAD) symptomology, however, the biological mechanisms remain unclear. The objective herein was to determine the impact of CKD on PAD pathology in mice. C57BL6/J mice were subjected to a diet-induced model of CKD by delivery of adenine for six weeks. CKD was confirmed by measurements of glomerular filtration rate, blood urea nitrogen, and kidney histopathology. Mice with CKD displayed lower muscle force production and greater ischemic lesions in the tibialis anterior muscle (78.1 ± 14.5% vs. 2.5 ± 0.5% in control mice, P < 0.0001, N = 5–10/group) and decreased myofiber size (1661 ± 134 μm2 vs. 2221 ± 100 μm2 in control mice, P < 0.01, N = 5–10/group). This skeletal myopathy occurred despite normal capillary density (516 ± 59 vs. 466 ± 45 capillaries/20x field of view) and limb perfusion. CKD mice displayed a ~50–65% reduction in muscle mitochondrial respiratory capacity in ischemic muscle, whereas control mice had normal mitochondrial function. Hydrogen peroxide emission was modestly higher in the ischemic muscle of CKD mice, which coincided with decreased oxidant buffering. Exposure of cultured myotubes to CKD serum resulted in myotube atrophy and elevated oxidative stress, which were attenuated by mitochondrial-targeted therapies. Taken together, these findings suggest that mitochondrial impairments caused by CKD contribute to the exacerbation of ischemic pathology.

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Loss of kidney function in patients with critical limb ischemia treated endovascularly or surgically

Abstract: Endovascular procedures for critical limb ischemia are associated with clinically relevant permanent long-term loss of kidney function. This loss of renal function is greater than in comparable patients who were treated with open surgery.

Cited by 14 publications

References 20 publications

One-Year Results of First-Line Treatment Strategies in Patients With Critical Limb Ischemia (CRITISCH Registry)

One-Year Results of First-Line Treatment Strategies in Patients With Critical Limb Ischemia (CRITISCH Registry)

Acute Renal Failure/Acute Kidney Injury (AKI) Associated with Endovascular Procedures

Chronic kidney disease exacerbates ischemic limb myopathy in mice via altered mitochondrial energetics

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