Effects of endothelin receptor antagonist on cyclosporine-induced vasoconstriction in isolated rat renal arterioles.

Lanese, Diane M.; Conger, John D.

doi:10.1172/jci116440

Cited by 208 publications

(98 citation statements)

References 22 publications

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“…CNI cause afferent arteriolar vasoconstriction by sympathetic stimulation and by upregulation of the local renin-angiotensin-aldosterone system. (10,11) CNI also decrease vasodilator prostaglandins and nitric oxide and increase vasoconstrictor cytokines (12,13). Glucocorticoids contribute to HTN by causing sodium and water retention.…”

Section: Cvd Risk Factors For Which There Is An Evidentiary Basis Formentioning

confidence: 98%

Cardiovascular Disease in Transplant Recipients

Gill¹

2008

Clinical Journal of the American Society of Nephrology

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A cardiovascular disease event in a transplant recipient may be the result of a pretransplantation disease process, a direct effect of immunosuppressant medications, or the result of exposure to a variety of traditional and nontraditional risk factors after transplantation. Although the understanding of posttransplantation cardiovascular disease remains incomplete, there is evidence that the impact of posttransplantation cardiovascular disease has been decreased, through increased attention to this problem. In the absence of controlled studies to guide therapy, this review summarizes treatment of cardiovascular disease risk factors for which there is strong evidence of benefit in the nontransplantation setting, observational evidence of a similar risk in transplant recipients, and evidence that treatment can be safely administered to transplant recipients. Putative risk factors for posttransplantation cardiovascular disease for which the current level of evidence is insufficient to support specific treatment recommendations are also discussed. Potential new strategies to decrease the risk for cardiovascular disease events after transplantation in the future, including aggressive pretransplantation risk reduction, individualized treatments to prevent different types of cardiovascular disease, dedicated efforts to reduce cardiovascular disease events during transitions between dialysis and transplantation, and manipulation of immunosuppressant protocols, are also introduced.Clin J Am Soc Nephrol 3: S29 -S37, 2008. doi: 10.2215/CJN.02690707A lthough increased awareness of cardiovascular disease (CVD) has resulted in a reduction in CVD-related deaths over time (1,2), CVD remains the major known cause of death in transplant recipients (3) and is a significant barrier to improving long-term outcomes in kidney transplantation. The high risk for CVD in transplant recipients is in part explained by the high prevalence of conventional CVD risk factors (e.g., diabetes, hypertension, dyslipidemia) in this patient population; however, a significant portion of CVD risk in transplant recipients is unexplained by these factors (4) and may be related to pretransplantation exposure to chronic kidney disease (CKD)-related risk factors, ongoing exposure to CKD-related risk factors as a result of impaired allograft function, or to transplant-specific risk factors including those related to the use of immunosuppressant medications or infection. Given the relative absence of randomized, controlled trials in transplant recipients, this review summarizes treatments for which there is strong evidence of benefit in the nontransplantation setting, observational evidence of a similar risk in transplant recipients, and evidence that treatment can be safely administered to transplant recipients. The review also summarizes putative risk factors for posttransplantation CVD, for which the current level of evidence is insufficient to support specific treatment recommendations. Finally, the review introduces new strategies to decrease the risk for...

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Section: Cvd Risk Factors For Which There Is An Evidentiary Basis Formentioning

confidence: 98%

Cardiovascular Disease in Transplant Recipients

Gill¹

2008

Clinical Journal of the American Society of Nephrology

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“…It has been demonstrated that vasoconstriction is induced by activation of the renin-angiotensin system (RAS) and increase in levels of the vasoconstricting factors, endothelin and thromboxane, as well as suppression of synthesis of vasodilating prostacyclin, prostaglandin E2, and nitric oxide (NO) [9][10][11] . Interindividual susceptibility to cyclosporine-induced vasoconstriction also plays an important role 12 .…”

Section: Acute Arteriolopathymentioning

confidence: 99%

Calcineurin Inhibitor-Induced Renal Allograft Nephrotoxicity

Krejčí¹,

Tichý²,

Bachleda³

et al. 2010

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Background. The introduction of the calcineurin inhibitors (CI) cyclosporine and tacrolimus into immunosuppressive protocols initiated a new era in organ transplantation with excellent short-term graft survival. Nevertheless, the chronic nephrotoxicity of these drugs represents a significant adverse factor limiting their long-term use. Patients treated with a CI can be at risk for developing renal failure and this problem is especially pronounced in patients after renal transplantation.Methods and Results. In a review paper we summarize the clinical aspects, histological manifestations and pitfalls of diagnostics of acute and chronic CI nephrotoxicity in patients after kidney transplantation. We look in detail at the disputed relationship between blood concentrations of cyclosporine and tacrolimus and histological manifestation of toxicity and summarize data showing that for toxic effects, local renal exposure to CI and their metabolites can play a more significant role than systemic exposure. We also include recent views on the pathophysiologic and molecular mechanisms underlying these changes; factors influencing local susceptibility to CI nephrotoxicity are discussed, including variability of expression and activity of P-glycoprotein and cytochrome P450. Last but not least we summarize our own experience with clinically manifest and subclinical forms of nephrotoxicity and their impact on the progression of chronic graft changes.Conclusions. Owing to their unique effects, CI remain the cornerstone of most immunosuppressive protocols for renal transplantation. Together with optimization of local kidney exposure to CI and their metabolites, efforts to reduce systemic levels as much as possible are the most important preventive measure for reducing toxic renal graft damage.

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“…It is widely acknowledged that patients treated with the Cyclosporine and Cisplatin are at a high risk of developing nephrotoxicity [9,10]. Studies have demonstrated that Cyclosporine causes vasoconstriction of the afferent and efferent glomerular arterioles and reductions in renal blood flow and glomerular filtration rate [11,12]. Cisplatin is an important antineoplastic drug used for the treatment of cancers.…”

Section: Introductionmentioning

confidence: 99%

Molecular Mechanisms Underlying the Nephrotoxicity of Cisplatin, Lead Acetate and Cyclosporine: Key Roles of Myc and Smad4

Askari¹,

Abdullahi²,

Poortahmasebi³

et al. 2017

Biol syst Open Access

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It is well documented that use of Cisplatin, Lead acetate and Cyclosporine in the chemotherapy and medical interventions is highly associated with nephrotoxicity and interrelated comorbidities. Here, we proposed the possible molecular mechanisms responsible for nephrotoxicity of these compounds. We utilized the microarray dataset GSE59913 consisting of approximately 600 different compounds profiled in up to 8 different tissues. After analysis with GEO2R, gene expression profiles of three aforementioned compounds were integrated with protein-protein interactions (PPI) networks and topological properties of the networks were measured using Cytoscape software. We found several key genes and signaling pathways that seem to be involved in nephrotoxicity of the examined compounds. Myc and Smad4 were identified as principal players of three compounds' nephrotoxicity through various pathways. Our results revealed the critical functions of Il2, Jak-Stat, Mapk-Pi3k, TGFβ and Ca 2+ signaling pathways as well as novel biomarkers that may mediate the nephrotoxicity of Cisplatin, Lead acetate and Cyclosporine. The significantly altered genes in the compound-treated samples were substantially correlated with regulation of cell proliferation, apoptosis, inflammatory responses and homeostatic processes. This study reveals the important hub genes, biological networks and key pathways as well as novel biomarkers involved in nephrotoxicity of Cisplatin, Lead acetate and Cyclosporine.

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Effects of endothelin receptor antagonist on cyclosporine-induced vasoconstriction in isolated rat renal arterioles.

Cited by 208 publications

References 22 publications

Cardiovascular Disease in Transplant Recipients

Cardiovascular Disease in Transplant Recipients

Calcineurin Inhibitor-Induced Renal Allograft Nephrotoxicity

Molecular Mechanisms Underlying the Nephrotoxicity of Cisplatin, Lead Acetate and Cyclosporine: Key Roles of Myc and Smad4

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