The effect of chronic renal failure on cardiac function: an experimental study with a rat model

Nakano, Shinya; Masuda, Kasumi; Asanuma, Toshihiko; Nakatani, Satoshi

doi:10.1007/s12574-016-0300-x

Cited by 12 publications

(12 citation statements)

References 29 publications

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“…We have recently used this model and demonstrated that intratracheal instillation of diesel exhaust particles aggravate renal oxidative stress, inflammation, and DNA damage in mice with adenine-induced CKD (Nemmar et al, 2016a ). We and others have also used this model to show the occurrence of gastrointestinal or cardiovascular complications after the induction of CKD with adenine (Ali et al, 2013 , 2014b ; Diwan et al, 2013 ; Nakano et al, 2016 ). However, as far as we are aware, no study to date has investigated the in vivo pulmonary consequence of this valid and well-established model of CKD.…”

Section: Discussionmentioning

confidence: 99%

“…While the effect of adenine on the development of CKD has been widely investigated, little is known on the extra-renal impact of such model of CKD. Recently, it has been reported that adenine induce CKD and cardiovascular damage in rats including increased ventricular fibrosis, systolic blood pressure and left ventricular stiffness, left ventricular diastolic dysfunction independent of the presence of hypertension and impaired vascular responses (Diwan et al, 2013 ; Ali et al, 2014a ; Nakano et al, 2016 ). Since it has been reported that CKD is associated with effects on distant organs, including the lungs, in the present study, we wanted to test the hypothesis of the possible occurrence of pulmonary injury in animal model of CKD induced by adenine.…”

Section: Introductionmentioning

confidence: 99%

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Lung Oxidative Stress, DNA Damage, Apoptosis, and Fibrosis in Adenine-Induced Chronic Kidney Disease in Mice

et al. 2017

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It is well-established that there is a crosstalk between the lung and the kidney, and several studies have reported association between chronic kidney disease (CKD) and pulmonary pathophysiological changes. Experimentally, CKD can be caused in mice by dietary intake of adenine. Nevertheless, the consequence of such intervention on the lung received only scant attention. Here, we assessed the pulmonary effects of adenine (0.2% w/w in feed for 4 weeks)-induced CKD in mice by assessing various physiological histological and biochemical endpoints. Adenine treatment induced a significant increase in urine output, urea and creatinine concentrations, and it decreased the body weight and creatinine clearance. It also increased proteinuria and the urinary levels of kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin. Compared with control group, the histopathological evaluation of lungs from adenine-treated mice showed polymorphonuclear leukocytes infiltration in alveolar and bronchial walls, injury, and fibrosis. Moreover, adenine caused a significant increase in lung lipid peroxidation and reactive oxygen species and decreased the antioxidant catalase. Adenine also induced DNA damage assessed by COMET assay. Similarly, adenine caused apoptosis in the lung characterized by a significant increase of cleaved caspase-3. Moreover, adenine induced a significant increase in the expression of nuclear factor erythroid 2–related factor 2 (Nrf2) in the lung. We conclude that administration of adenine in mice induced CKD is accompanied by lung oxidative stress, DNA damage, apoptosis, and Nrf2 expression and fibrosis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Lung Oxidative Stress, DNA Damage, Apoptosis, and Fibrosis in Adenine-Induced Chronic Kidney Disease in Mice

et al. 2017

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“…We combined this model with an oral diet of adenine to induce progression to CKD caused by precipitation of the adenine metabolite 2,8-dihydroxyadenine, which precip-itates into crystals to cause tubular damage (11,39). Although there are several models that simulate CKD, studies demonstrate that the adenine model closely mimics findings associated with CKD including progressive hypertension, uremia, anemia, and abnormal calcium dynamics (6,18,29,45). In addition, this model consistently exhibits renal inflammation and fibrosis as seen in CKD (11,22,28).…”

Section: Introductionmentioning

confidence: 99%

Intermittent hypoxia exacerbates increased blood pressure in rats with chronic kidney disease

Riggs

Pace

Ward

et al. 2018

American Journal of Physiology-Renal Physiology

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Kidney injury and sleep apnea (SA) are independent risk factors for hypertension. Exposing rats to intermittent hypoxia (IH) to simulate SA increases blood pressure whereas adenine feeding causes persistent kidney damage to model chronic kidney disease (CKD). We hypothesized that exposing CKD rats to IH would exacerbate the development of hypertension and renal failure. Male Sprague-Dawley rats were fed a 0.2% adenine diet or control diet (Control) until blood urea nitrogen was >120 mg/dl in adenine-fed rats (14 ± 4 days, mean ± SE). After 2 wk of recovery on normal chow, rats were exposed to IH (20 exposures/h of 5% O2-5% CO2 7 h/day) or control conditions (Air) for 6 wk. Mean arterial pressure (MAP) was monitored with telemeters, and plasma and urine samples were collected weekly to calculate creatinine clearance as an index of glomerular filtration rate (GFR). Prior to IH, adenine-fed rats had higher blood pressure than rats on control diet. IH treatment increased MAP in both groups, and after 6 wk, MAP levels in the CKD/IH rats were greater than those in the CKD/Air and Control/IH rats. MAP levels in the Control/Air rats were lower than those in the other three groups. Kidney histology revealed crystalline deposits, tubule dilation, and interstitial fibrosis in both CKD groups. IH caused no additional kidney damage. Plasma creatinine was similarly increased in both CKD groups throughout whereas IH alone increased plasma creatinine. IH increases blood pressure further in CKD rats without augmenting declines in GFR but appears to impair GFR in healthy rats. We speculate that treating SA might decrease hypertension development in CKD patients and protect renal function in SA patients.

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“…Patients with CRF have an increased risk of cardiovascular diseases (CVD) (Couser and Riella 2011) such as cardiac fibrosis, hypertrophy, and dysfunction, i.e., uremic cardiomyopathy (Drummond et al 2016) with a higher risk of cardiovascular mortality (10 to 20-fold) than controls without kidney disease (Foley et al 1998). Although the mechanistic pathways employed in CRF impact on cardiac functions are not fully understood, hypertension, oxidative stress, and volume overload are considered common contributors (Garcia-Trejo et al 2016;Nakano et al 2016). The sodium/potassium-adenosine-triphosphatase (Na + /K + -ATPase) plays a key role in myocardial contractility through regulating the concentration of ions inside and outside cells.…”

Section: Introductionmentioning

confidence: 99%

Garlic (Allium sativum) exhibits a cardioprotective effect in experimental chronic renal failure rat model by reducing oxidative stress and controlling cardiac Na+/K+-ATPase activity and Ca2+ levels

Gomaa

Abdelhafez

Aamer

2018

Cell Stress and Chaperones

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Gentamicin (GNT)-induced nephrotoxicity culminates into renal failure with a possible cardiovascular impact. Garlic extract (GE) is a cardiovascular protectant with limited mechanistic data. Therefore, we assessed the disturbance in specific cardiac parameters and the potential protective effect of GE supplementation against them in a rat model of GNT-induced chronic renal failure (CRF). Adult male rats (n = 24) were randomly assigned into four groups (n = 6 each): normal controls (CON), garlic extract controls (GE; 250 mg kg, orally), GNT-induced CRF (GNT; 100 mg kg, i.p.), and GNT + GE (GNT and GE in the same previous doses) groups. GNT and GE were given daily for 3 weeks. Animals co-treated with GNT and GE exhibited improved renal functions, body weight (BW), and heart weight (HW)/BW ratio; declined blood pressure; lowered plasma levels of lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), and total peroxides (TP); and elevated total antioxidant capacity (TAC) levels. Moreover, the heart tissue contained raised levels of TAC and Na/K-ATPase activity and lowered levels of TP and Ca. Findings provide evidence that administration of GE in experimental CRF model helped protect the heart through reducing oxidative stress and controlling cardiac Na/K-ATPase activity and Ca levels.

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The effect of chronic renal failure on cardiac function: an experimental study with a rat model

Abstract: The adenine-induced CRF rat model developed renal dysfunction and left ventricular diastolic dysfunction independent of the presence of hypertension.

Cited by 12 publications

References 29 publications

Lung Oxidative Stress, DNA Damage, Apoptosis, and Fibrosis in Adenine-Induced Chronic Kidney Disease in Mice

Lung Oxidative Stress, DNA Damage, Apoptosis, and Fibrosis in Adenine-Induced Chronic Kidney Disease in Mice

Intermittent hypoxia exacerbates increased blood pressure in rats with chronic kidney disease

Garlic (Allium sativum) exhibits a cardioprotective effect in experimental chronic renal failure rat model by reducing oxidative stress and controlling cardiac Na+/K+-ATPase activity and Ca2+ levels

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