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

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Fabian N. Berru ◽  
Sarah E. Gray ◽  
Trace Thome ◽  
Ravi A. Kumar ◽  
Zachary R. Salyers ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Tibialis Anterior Muscle ◽  
Force Production ◽  
Capillary Density ◽  
Arterial Disease ◽  
Peripheral Arterial ◽  
Muscle Force Production ◽  
The Impact ◽  
Ischemic Muscle

Abstract 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.

Abstract 20579: Chronic Kidney Disease is Associated With Increased Mortality and Major Adverse Cardiovascular Events in Patients With Peripheral Arterial Disease

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Gregory G Westin ◽  
Ehrin J Armstrong ◽  
Debbie C Chen ◽  
John R Laird
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Peripheral Arterial Disease ◽  
Cardiovascular Events ◽  
Cox Model ◽  
Univariate Analysis ◽  
Arterial Disease ◽  
Major Adverse Cardiovascular Events ◽  
Ckd Stage ◽  
Peripheral Arterial

Introduction: Chronic kidney disease (CKD) is common in patients with peripheral arterial disease (PAD), but patients with severe CKD have been excluded from many trials and no objective performance goals exist for patients with PAD and CKD. We sought to analyze the association between severity of CKD and cardiovascular and limb-related outcomes among patients with PAD. Methods: We reviewed records of all patients at our institution who underwent lower extremity angiography between 2006 and 2013. We analyzed outcomes including mortality, major adverse cardiovascular event (MACE) rate, and major adverse limb event (MALE) rate according to clinical stage of CKD, determined by calculating each patient’s glomerular filtration rate using the Cockcroft-Gault equation. We used Cox proportional hazard modeling to account for covariates, along with Bonferroni correction for multiple comparisons. Results: Of 773 patients, 45% had CKD stage 3-5. The patients had a median age of 67, were 58% male, 51% diabetic, and 57% presented with critical limb ischemia (CLI). During a median follow-up time of 3.2 years, patients with higher stages of CKD had an increased rate of death (Figure 1, p<0.001). CKD stages 4 and 5 were significant predictors of mortality in a multivariate model (HR 3.2 and 2.4 vs. CKD 1, P<0.001 and P<0.01, respectively). An analysis of MACE by CKD stage demonstrated similar results (CKD 4 HR 2.2, p<0.01; CKD 5 HR 2.0, p<0.01). CKD stage also predicted MALE in a univariate analysis (p<0.01), driven by increased limb events among patients with CKD stage 5 (p<0.01). However, CKD stage did not demonstrate a significantly increased hazard of MALE in a multivariate Cox model. Conclusions: Patients with PAD who also have CKD have increased rates of adverse outcomes. This relationship seems to be more robust for major cardiovascular events and overall mortality than for major limb events. Future studies should investigate how management of PAD should differ for patients with CKD.

scholarly journals Subclinical peripheral arterial disease in patients with chronic kidney disease: Prevalence and related risk factors

2005 ◽  
Vol 67 ◽  
pp. S44-S47 ◽  
Author(s):  
Soledad Garcia de Vinuesa ◽  
Mayra Ortega ◽  
Patricia Martinez ◽  
Marian Goicoechea ◽  
Francisco Gomez Campdera ◽  
...  
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Peripheral Arterial Disease ◽  
Arterial Disease ◽  
Disease Prevalence ◽  
Chronic Kidney Disease Prevalence ◽  
Related Risk ◽  
Peripheral Arterial

scholarly journals MO762RELATIONSHIP BETWEEN INFLAMMATION AND PERIPHERAL ARTERIAL DISEASE MEASURED BY ANKLE-BRACHIAL INDEX IN CHRONIC HEMODIALYSIS PATIENTS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Yanet Parodis ◽  
Tania Monzon ◽  
Francisco Valga ◽  
Gloria Anton-Perez
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Peripheral Arterial Disease ◽  
Point Group ◽  
Ankle Brachial Index ◽  
Arterial Disease ◽  
Chronic Hemodialysis ◽  
Lymphocyte Ratio ◽  
Markers Of Inflammation ◽  
Peripheral Arterial

Abstract Background and Aims Peripheral arterial disease (PAD) is very common in patients with chronic kidney disease. There are predisposing factors such as high blood pressure, diabetes mellitus, and dyslipidemia that are highly prevalent in this population. The ankle-brachial index (ABI) is a widely validated diagnostic method for the diagnosis of PAD. A value below 0.9 is suggestive of this pathology. On the other hand, inflammation is a phenomenon that favors development of atherosclerosis and therefore could be another predisposing factor for PAD. There are emerging markers of inflammation such as the neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR) and systemic immune-inflammation index (SII) that have an excellent correlation with classic markers such as C-reactive protein (CRP). The objective of our study was to determine whether there is a relationship between ABI values and the degree of inflammation in patients. Method A retrospective observational cross-sectional study was conducted in our prevalent hemodialysis population between April-May 2019. ABI was measured through the Microlife WatchBP Office ABI™ device. The sample was divided into two groups using 0.9 as a cut-off point: group 1 (ABI &lt;0.9) and group 2 (ABI&gt; 0.9). Inflammatory ratios (NLR, PLR and SII) and other parameters of bone kidney disease such as serum calcium, bicarbonate, phosphorus, parathyroid hormone (PTH), magnesium and vitamin D were determined. Results 100 patients with chronic kidney disease on chronic hemodialysis belonging to our Avericum Negrin center were analyzed. 42% (N = 42) of the sample were women and 42% (N = 42) were diabetic. The etiology of kidney disease was: 12% (N = 12) renal nephroangiosclerosis, 35% (N = 35) diabetic nephropathy, 14% (N = 14) chronic glomerulonephritis, 8% (N = 8) polycystic kidney disease, 17% (N = 17) unknow and 14% (N = 14) others. 19% (N = 19) had a central venous catheter as vascular access. The mean values of inflammatory and renal bone disease parameters are described in Table 1. The values of PLR and SII index were significantly higher in patients with ABI &lt;0.9. (Figures 1 and 2). Conclusion Patients with peripheral arterial disease (ABI &lt;0.9) had higher PLR and SII values

scholarly journals Prevalence and Prognostic Significance of Apparent Treatment Resistant Hypertension in Chronic Kidney Disease

Hypertension ◽  
2016 ◽  
Vol 67 (2) ◽  
pp. 387-396 ◽  
Author(s):  
George Thomas ◽  
Dawei Xie ◽  
Hsiang-Yu Chen ◽  
Amanda H. Anderson ◽  
Lawrence J. Appel ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Arterial Disease ◽  
Treatment Resistant ◽  
Mortality Hazard ◽  
All Cause Mortality ◽  
Peripheral Arterial ◽  
Mortality Hazard Ratio

The association between apparent treatment resistant hypertension (ATRH) and clinical outcomes is not well studied in chronic kidney disease. We analyzed data on 3367 hypertensive participants in the Chronic Renal Insufficiency Cohort (CRIC) to determine prevalence, associations, and clinical outcomes of ATRH in nondialysis chronic kidney disease patients. ATRH was defined as blood pressure ≥140/90 mm Hg on ≥3 antihypertensives, or use of ≥4 antihypertensives with blood pressure at goal at baseline visit. Prevalence of ATRH was 40.4%. Older age, male sex, black race, diabetes mellitus, and higher body mass index were independently associated with higher odds of having ATRH. Participants with ATRH had a higher risk of clinical events than participants without ATRH—composite of myocardial infarction, stroke, peripheral arterial disease, congestive heart failure (CHF), and all-cause mortality (hazard ratio [95% confidence interval], 1.38 [1.22–1.56]); renal events (1.28 [1.11–1.46]); CHF (1.66 [1.38–2.00]); and all-cause mortality (1.24 [1.06–1.45]). The subset of participants with ATRH and blood pressure at goal on ≥4 medications also had higher risk for composite of myocardial infarction, stroke, peripheral arterial disease, CHF, and all-cause mortality (hazard ratio [95% confidence interval], (1.30 [1.12–1.51]) and CHF (1.59 [1.28–1.99]) than those without ATRH. ATRH was associated with significantly higher risk for CHF and renal events only among those with estimated glomerular filtration rate ≥30 mL/min per 1.73 m 2 . Our findings show that ATRH is common and associated with high risk of adverse outcomes in a cohort of patients with chronic kidney disease. This underscores the need for early identification and management of patients with ATRH and chronic kidney disease.

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