Endothelin-1 and the kidney

Miguel, Carmen De; Speed, Joshua S.; Kasztan, Małgorzata; Gohar, Eman Y.; Pollock, David M.

doi:10.1097/mnh.0000000000000185

Cited by 64 publications

(28 citation statements)

References 63 publications

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“…The association between CKD and ET-1 has been well documented 34 . Excessive ET-l production may drive CKD progression by causing acute ischemic renal injury, renal fibrosis, or podocyte dysfunction 35 . Blockade of ET-1 receptors may prevent renal inflammation and fibrosis 7 .…”

Section: Discussionmentioning

confidence: 99%

Synergistic effect of renalase and chronic kidney disease on endothelin-1 in patients with coronary artery disease ‒ a cross-sectional study

Sheu

Lee

et al. 2018

Sci Rep

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Endothelin-1 (ET-1) is associated with endothelial dysfunction and vasoconstriction. Increased circulating ET-1 levels are associated with long-term cardiovascular mortality. Renalase, released from kidney, metabolizes catecholamines and regulates blood pressure. An increase in circulating renalase levels has been reported in patients with chronic kidney disease (CKD) and is associated with coronary artery disease (CAD). We hypothesized the existence of a synergistic effect of serum renalase levels and CKD on ET-1 levels in patients with CAD. We evaluated 342 non-diabetic patients with established CAD. ET-1 and renalase levels were measured in all patients after an overnight fast. Patients with CKD had higher ET-1 (1.95 ± 0.77 vs. 1.62 ± 0.76 pg/ml, P < 0.001) and renalase levels (46.8 ± 17.1 vs. 33.9 ± 9.9 ng/ml, P < 0.001) than patients without CKD. Patients with both CKD and high renalase levels (>the median of 36.2 ng/ml) exhibited the highest serum ET-1 (P value for the trend <0.001). According to multivariate linear regression analysis, the combination of high serum renalase levels with CKD was a significant risk factor for increased serum ET-1 levels (regression coefficient = 0.297, 95% confidence interval = 0.063‒0.531, P = 0.013). In conclusion, our data suggest a synergistic effect of high serum renalase levels and CKD on increases in ET-1 levels in patients with established CAD.

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Section: Discussionmentioning

confidence: 99%

Synergistic effect of renalase and chronic kidney disease on endothelin-1 in patients with coronary artery disease ‒ a cross-sectional study

Sheu

Lee

et al. 2018

Sci Rep

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“…Endothelin-1 (ET-1), a peptide with potent vasoconstrictive properties, is produced by endothelial cells in response to various insults, including sheer stress, hypoxia, and inflammatory signals. ET-1 mediates endothelial dysfunction by reducing NO bioavailability and induces direct injury to podocytes via the ETA receptor [9,10]. In sickle cell mouse models, ET-1 has been demonstrated to mediate glomerular injury via reactive oxygen species, and ETA receptor antagonism appears to afford renal protection [11,12].…”

Section: Pathophysiology Of Sickle Cell Nephropathymentioning

confidence: 99%

“…Free heme filtered through the glomerulus is directly cytotoxic to renal tubular epithelial cells, which subsequently induces damaging inflammatory responses [10]. A recent study also found that hemoglobin competes with filtered albumin by binding to megalin and cubilin in the proximal tubule.…”

Section: Pathophysiology Of Sickle Cell Nephropathymentioning

confidence: 99%

The spectrum of sickle hemoglobin-related nephropathy: from sickle cell disease to sickle trait

Naik

Derebail

2017

Expert Review of Hematology

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Introduction Renal dysfunction is among the most common complication of sickle cell disease (SCD), from hyposthenuria in children to progression to overt chronic kidney disease (CKD) in young adults. Emerging evidence now suggests that sickle hemoglobin-related nephropathy extends to individuals with sickle cell trait (SCT). Areas covered This review will highlight the pathophysiology, epidemiology, and management recommendations for sickle hemoglobin-related nephropathy in both SCD and SCT. In addition, it will focus on the major demographic and genetic modifiers of renal disease in sickling hemoglobinopathies. Expert commentary Studies have elucidated the course of renal disease in SCD; however, the scope and age of onset of renal dysfunction in SCT has yet to be determined. In SCD, several modifiers of renal disease – such as α-thalassemia, hemoglobin F, APOL1 and HMOX1 – have been described and provide an opportunity for a precision medicine approach to risk stratify patients who may benefit from early intervention. Extrapolating from this literature may also provide insight into the modifiers of renal disease in SCT. Further studies are needed to determine the optimal treatment for sickle hemoglobin-related nephropathy.

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“…It is known that sex hormones affect Endothelin plasma levels, which are increased by testosterone and decreased by oestradiol [ 51 ]. In addition, sex steroids influence almost every component of the ET system [ 52 – 55 ]. Renal ET receptors function somewhat differently between males and females.…”

Section: Discussionmentioning

confidence: 99%

The Role of Endothelin System in Renal Structure and Function during the Postnatal Development of the Rat Kidney

et al. 2016

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Renal development in rodents, unlike in humans, continues during early postnatal period. We aimed to evaluate whether the pharmacological inhibition of Endothelin system during this period affects renal development, both at structural and functional level in male and female rats. Newborn rats were treated orally from postnatal day 1 to 20 with vehicle or bosentan (Actelion, 20 mg/kg/day), a dual endothelin receptor antagonist (ERA). The animals were divided in 4 groups: control males, control females, ERA males and ERA females. At day 21, we evaluated renal function, determined the glomerular number by a maceration method and by morphometric analysis and evaluated possible structural renal alterations by three methods: 〈alpha〉-Smooth muscle actin (α-SMA) immunohistochemistry, Masson's trichrome and Sirius red staining. The pharmacological inhibition of Endothelin system with a dual ERA during the early postnatal period of the rat did not leads to renal damage in the kidneys of male and female rats. However, ERA administration decreased the number of glomeruli, the juxtamedullary filtration surface area and the glomerular filtration rate and increased the proteinuria. These effects could predispose to hypertension or renal diseases in the adulthood. On the other hand, these effects were more pronounced in male rats, suggesting that there are sex differences that could be greater later in life. These results provide evidence that Endothelin has an important role in rat renal postnatal development. However these results do not imply that the same could happen in humans, since human renal development is complete at birth.

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Endothelin-1 and the kidney

Cited by 64 publications

References 63 publications

Synergistic effect of renalase and chronic kidney disease on endothelin-1 in patients with coronary artery disease ‒ a cross-sectional study

Synergistic effect of renalase and chronic kidney disease on endothelin-1 in patients with coronary artery disease ‒ a cross-sectional study

The spectrum of sickle hemoglobin-related nephropathy: from sickle cell disease to sickle trait

The Role of Endothelin System in Renal Structure and Function during the Postnatal Development of the Rat Kidney

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