Oxidative stress in hemodialysis patients: Is NADPH oxidase complex the culprit?

Moréna, Marion; Cristol, Jean‐Paul; Senécal, Lynne; Leray‐Moragues, Hélène; Krieter, Detlef H.; Canaud, Bernard

doi:10.1046/j.1523-1755.61.s80.20.x

Cited by 69 publications

(53 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Previous reports suggest that, in addition to proteinuria and hypertension, hyperlipidemia is the third important risk factor for CKD (43). Abnormal lipid metabolism and deposition are associated with microinflammation and oxidative stress (44). The current study demonstrated that PTH is positively correlated with the expression levels of serum TG, TC and LDL-C in patients with CKD, suggesting that hyperlipidemia is closely associated with SHPT.…”

Section: % CI ------------------------------Variablesupporting

confidence: 61%

Risk factors associated with secondary hyperparathyroidism in patients with chronic kidney disease

Wei

Lin

Yang

et al. 2016

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

Abstract. Secondary hyperparathyroidism (SHPT) is common in patients with chronic kidney disease (CKD), and its development and progression are affected by various factors. The aim of the present study was to identify the risk factors for SHPT in patients with CKD. A retrospective study was performed in 498 patients (305 males and 193 females) with CKD, observed in the The First Hospital of Jilin University between January 2008 and December 2012. The demographic, clinical and laboratory data were collected. Patients were divided into the SHPT group (n=424) with elevated serum parathyroid hormone (PTH) expression levels and the control group (n=74) with normal serum PTH expression levels. Univariate and multivariate regression analyses were employed to explore the risk factors for SHPT. Serum PTH expression levels in women with CKD were significantly higher than in men (P= 0.047). Serum PTH expression levels were positively correlated with the expression levels of serum creatinine (P<0.01), phosphorus (P<0.01), C-reactive protein (P<0.05), triglyceride (P<0.05), cholesterol (P<0.05) and low-density lipoprotein cholesterol (P<0.05), but were negatively correlated with the expression levels of hemoglobin (P<0.05), calcium (P<0.01) and CO 2 combining power (P<0.01) in patients with CKD. Multivariate analysis showed that the serum expression levels of creatinine [µmol/l; odds radio (OR), 1.003; 95% confidence interval (CI), 1.002-1.004; P=0.001] and phosphorus (mmol/l; OR, 2.19; 95% CI, 1.254-3.826; P=0.006) in patients with CKD significantly influenced serum PTH expression levels. The SHPT risk factors include female gender, low calcium, high phosphorus, acidosis, anemia, hypertension, hyperlipidemia and micro-inflammation, with blood phosphorus and creatinine being independent risk factors. IntroductionThe incidence of chronic kidney disease (CKD) is rapidly increasing, posing a serious health problem worldwide. More than 16 million adults are affected by end stage CKD in the USA (1,2). Abnormal serum calcium, phosphorus and parathyroid hormone (PTH) expression levels are common challenges in the management of CKD (3,4). These biochemical abnormalities, together with the dysregulation of vitamin D metabolism and bone turnover, constitute a systemic syndrome termed CKD mineral and bone disorder (CKD-MBD) (5).Secondary hyperparathyroidism (SHPT) is a common complication of patients with CKD, which is characterized by increased blood PTH levels, and abnormal mineral and bone metabolism (6). It is associated with increased morbidity and mortality, and adversely influences the quality of life of patients with CKD (3,6). The incidence of SHPT is reported to increase with the stage of CKD: 40% in stage 3, 70% in stage 4 and >80% in stage 5 (4,7).The kidneys are vital organs regulating calcium and phosphorous homeostasis (8). SHPT is an adaptive pathophysiological process in response to deteriorating renal insufficiency (6). The fundamental mechanism of PTH in kidneys is to suppress the reabsorption of phosphate in the pro...

show abstract

Section: % CI ------------------------------Variablesupporting

confidence: 61%

Risk factors associated with secondary hyperparathyroidism in patients with chronic kidney disease

Wei

Lin

Yang

et al. 2016

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

show abstract

“…40 Most reports prove that oxidative stress is present in end-stage renal disease patients, and oxidative stress would be a strong cofactor for the development of cardiovascular complications. 41 Considering the high prevalence of LVH in hemodialysis patients, our findings emphasize the need for clinical studies to determine the potential beneficial effects of MR blockade in patients with chronic renal failure.…”

Section: Perspectivesmentioning

confidence: 78%

Mineralocorticoid Receptor Antagonism Attenuates Cardiac Hypertrophy and Prevents Oxidative Stress in Uremic Rats

et al. 2008

View full text Add to dashboard Cite

Abstract-Chronic renal failure causes left ventricular hypertrophy, but the molecular mechanisms involved remain unknown. We, therefore, investigated whether the mineralocorticoid receptor is implicated in the cardiac hypertrophy observed in uremic rats and whether mineralocorticoid receptor blockade could be protective in chronic renal failure. Experimental groups were: control rats, uremic rats (NPX) with 5/6 nephrectomy (5 weeks), and NPX rats fed with spironolactone for 5 weeks. Systolic blood pressure was increased in both NPX rats and NPX rats fed with spironolactone for 5 weeks. Echocardiography revealed concentric left ventricular hypertrophy in uremia, which was attenuated by spironolactone. Enlarged cardiomyocyte size was observed in both left and right ventricles of NPX rats, an effect that was prevented by spironolactone. Mineralocorticoid receptor antagonism attenuated the increase of ventricular brain natriuretic peptide mRNA levels induced by nephrectomy. Left ventricular gene expressions of aldosterone synthase, mineralocorticoid receptor, and hydroxysteroid dehydrogenase type 2 were the same in the 3 groups, whereas gene expression of the glucocorticoid receptor was significantly diminished in chronic renal failure rats. No significant differences in cardiac aldosterone were observed between control rats and NPX rats, although NPX rats fed with spironolactone for 5 weeks showed increased plasma aldosterone levels. However, a significant increase in serum and glucocorticoid-inducible kinase-1 mRNA expression and protein was present in the NPX group; spironolactone treatment significantly reduced serum and glucocorticoid-inducible kinase-1 mRNA and protein in the left ventricle. Uremic rats exhibited a significant increase of superoxide production and reduced nicotinamide-adenine dinucleotide phosphate oxidase subunits expression (NOX-2, NOX-4, and p47 phox ) in the left ventricle, which was prevented by the mineralocorticoid receptor antagonist. Our findings provide evidence of the beneficial effects of spironolactone in cardiac hypertrophy and cardiac oxidative stress in chronic renal failure. (Hypertension. 2008;52:295-300.) Key Words: aldosterone Ⅲ mineralocorticoid receptor Ⅲ cardiac hypertrophy Ⅲ SGK1 Ⅲ oxidative stress Ⅲ hydroxysteroid dehydrogenase type 2

show abstract

“…The significantly enhanced priming of HD PMNL versus CKD not on RRT occurred despite blood withdrawal before HD session and may reflect accumulating nondialyzed uremic toxins as well as possible accumulating side effects of the extracorporeal treatment (23)(24)(25). From this and other studies (6), it seems that uremia per se is a major contributor to PMNL priming: PMNL priming was almost twofold higher in CKD patients who were not on RRT, compared with NC, whereas hemodialysis further increased the priming of PMNL by only 25%.…”

Section: Discussionmentioning

confidence: 99%

Primed Peripheral Polymorphonuclear Leukocyte

Sela¹,

Shurtz-Swirski²,

Cohen-Mazor³

et al. 2005

Journal of the American Society of Nephrology

175

126

View full text Add to dashboard Cite

This study characterizes the causal relationship between peripheral polymorphonuclear leukocyte (PMNL) priming, systemic oxidative stress (OS), and inflammation in patients with varying degrees of renal insufficiency (chronic kidney disease [CKD] not on renal replacement therapy [RRT]: continuous ambulatory peritoneal dialysis or hemodialysis [HD]) and healthy control subjects. Rate of superoxide release was measured after stimulation of PMNL with phorbol 12-myristate 13-acetate or zymosan. Priming was estimated by the rate of superoxide release after phorbol 12-myristate 13-acetate stimulation. Systemic OS was related to PMNL priming and intracellular myeloperoxidase activity. Inflammation was linked to peripheral white blood cells and PMNL counts, PMNL apoptosis, and PMNL ex vivo survival in autologous and heterologous sera. PMNL priming and counts were related to the severity of renal failure in CKD not on RRT. Compared with control subjects, PMNL from all CKD patients showed increased priming, highest in HD, with a significant decrease in their response to zymosan. PMNL myeloperoxidase activity and apoptosis were increased in all renal failure patients. Decreased ex vivo cell survival and elevated leukocyte counts were found in all patients, highest in HD. Both PMNL priming and counts correlated negatively with the GFR. A positive significant correlation was shown between PMNL counts and their priming in all groups, suggesting that the increased PMNL count in peripheral blood is an adaptive response to PMNL priming. Hence, PMNL priming is a key mediator of low-grade inflammation and OS associated with renal failure, occurring before the onset of RRT and further augmented in chronic HD.

show abstract

Oxidative stress in hemodialysis patients: Is NADPH oxidase complex the culprit?

Cited by 69 publications

References 34 publications

Risk factors associated with secondary hyperparathyroidism in patients with chronic kidney disease

Risk factors associated with secondary hyperparathyroidism in patients with chronic kidney disease

Mineralocorticoid Receptor Antagonism Attenuates Cardiac Hypertrophy and Prevents Oxidative Stress in Uremic Rats

Primed Peripheral Polymorphonuclear Leukocyte

Contact Info

Product

Resources

About