Phosphodiesterase-5 inhibitors ameliorate structural kidney damage in a rat model of contrast-induced nephropathy

Iordache, Andrei Mihai; Buga, Ana-Maria; Albulescu, Dana Maria; Vasile, Ramona Constantina; Mitruț, Radu; Georgiadis, George S.; Zisis, Ioannis-Erineos; Mamoulakis, Charalampos; Tsatsakis, Aristidis; Docea, Anca Oana; Calina, Daniela

doi:10.1016/j.fct.2020.111535

Cited by 24 publications

(19 citation statements)

References 51 publications

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“…Other agents such as cardiotrophin-1 and antithrombin III, [53,54] exendin-4, [55] β-receptor antagonist, [56,57] phosphodiesterase-5 inhibitor, [58][59][60][61] an mTOR inhibitor, [62] exogenous sphingosylphosphorylcholine, [63] and sodium bicarbonate; [64] have been investigated in CIN models (Table 4 and Fig. 3).…”

Section: Antioxidants As Interventions To Reduce Cinmentioning

confidence: 99%

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Kusirisin

Chattipakorn

2020

J Transl Med

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Contrast-induced nephropathy (CIN) or contrast-induced acute kidney injury (CI-AKI) is an iatrogenic acute kidney injury observed after intravascular administration of contrast media for intravascular diagnostic procedures or therapeutic angiographic intervention. High risk patients including those with chronic kidney disease (CKD), diabetes mellitus with impaired renal function, congestive heart failure, intraarterial intervention, higher volume of contrast, volume depletion, old age, multiple myeloma, hypertension, and hyperuricemia had increased prevalence of CIN. Although CIN is reversible by itself, some patients suffer this condition without renal recovery leading to CKD or even end-stage renal disease which required long term renal replacement therapy. In addition, both CIN and CKD have been associated with increasing of mortality. Three pathophysiological mechanisms have been proposed including direct tubular toxicity, intrarenal vasoconstriction, and excessive production of reactive oxygen species (ROS), all of which lead to impaired renal function. Reports from basic and clinical studies showing potential preventive strategies for CIN pathophysiology including low- or iso-osmolar contrast media are summarized and discussed. In addition, reports on pharmacological interventions to reduce ROS and attenuate CIN are summarized, highlighting potential for use in clinical practice. Understanding this contributory mechanism could pave ways to improve therapeutic strategies in combating CIN.

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Section: Antioxidants As Interventions To Reduce Cinmentioning

confidence: 99%

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Kusirisin

Chattipakorn

2020

J Transl Med

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“…Sildenafil and tadalafil were reported to ameliorate structural kidney damage in contrast‐induced nephropathy. 23 …”

Section: Introductionmentioning

confidence: 99%

Ameliorative effect of phosphodiesterase 4 and 5 inhibitors in deoxycorticosterone acetate‐salt hypertensive uni‐nephrectomized KKA ^y mice

et al. 2020

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Diabetic nephropathy (DN) is a leading cause of end-stage renal disease (ESRD). Hypertension increases kidney stress, which deteriorates function, and leads to peripheral renal vascular resistance. Long-term hypoperfusion promotes interstitial fibrosis and glomerular sclerosis, resulting in nephrosclerosis. Although hypertension and DN are frequent ESRD complications, relevant animal models remain unavailable. We generated a deoxycorticosterone acetate (DOCA)-salt hypertensive uni-nephrectomized (UNx) KKA y mouse model demonstrating hypertension, hyperglycemia, cardiac hypertrophy, kidney failure, increased urinary albumin creatinine ratio (UACR), and increased renal PDE4D and cardiac PDE5A mRNA levels. We hypothesized that the novel PDE4 selective inhibitor, compound A, and PDE5 inhibitor, sildenafil, exhibit nephroprotective, and cardioprotective effects in this new model. Compound A, sildenafil, and the angiotensin II receptor blocker, irbesartan, significantly reduced ventricular hypertrophy and pleural effusion volume. Meanwhile, compound A and sildenafil significantly suppressed the UACR, urinary kidney injury molecule-1, and monocyte chemoattractant protein-1 levels, as well as that of renal pro-fibrotic marker mRNAs, including collagen 1A1, fibronectin, and transforming growth factor-beta (TGF-β). Moreover, compound A significantly suppressed TGF-β-induced pro-fibrotic mRNA expression in vitro in all major kidney lesions, including within the glomerular mesangial region, podocytes, and epithelial region. Hence, PDE4 and PDE5 inhibitors may be promising treatments, in combination with irbesartan, for DN with hypertension as they demonstrate complementary mechanisms.

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“…The reduction of nephrotoxic exposure is one of the effective tools already used in oncological patients [ 30 ]. The animal models suggest the possibility to prevent AKI with the use of phosphodiesterase-5 inhibitors prior to potentially nephrotoxic treatment [ 31 , 32 ]. Independent of the chosen strategy, the threat of renal injury should urge careful follow-up of the patient in order to avoid additional insults triggering irreversible damage to the kidney.…”

Section: Discussionmentioning

confidence: 99%

Clusterin as a New Marker of Kidney Injury in Children Undergoing Allogeneic Hematopoietic Stem Cell Transplantation—A Pilot Study

Musiał

Augustynowicz

Miśkiewicz-Migoń

et al. 2020

JCM

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Background and aims: The markers of renal damage defining subclinical AKI are not widely used in children undergoing allogeneic hematopoietic stem cell transplantation (alloHSCT). The aim of the study was to evaluate serum and urinary clusterin as indices of kidney injury after alloHSCT in relation to damage (kidney injury molecule (KIM)-1) and functional (cystatin C) markers. Material and methods: Serum and urinary clusterin, KIM-1 and cystatin C concentrations were assessed by ELISA in 27 children before alloHSCT, 24 h, 1, 2, 3 and 4 weeks after alloHSCT and in controls. Results: All parameters were significantly higher in HSCT patients compared to controls even before the transplantation. The serum concentrations increased after HSCT and this rising trend was kept until the third (clusterin) or 4th (KIM-1, cystatin C) week. Urinary clusterin and KIM-1 were elevated until the third week and then decreased yet remained higher than before HSCT. Urinary cystatin C has risen from the second week after HSCT and decreased after the third week but was still higher than before alloHSCT. Conclusions: The features of kidney injury are present even before alloHSCT. Clusterin seems useful in the assessment of subclinical AKI and may become a new early marker of sublethal kidney injury in children.

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Phosphodiesterase-5 inhibitors ameliorate structural kidney damage in a rat model of contrast-induced nephropathy

Cited by 24 publications

References 51 publications

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Ameliorative effect of phosphodiesterase 4 and 5 inhibitors in deoxycorticosterone acetate‐salt hypertensive uni‐nephrectomized KKA ^y mice

Clusterin as a New Marker of Kidney Injury in Children Undergoing Allogeneic Hematopoietic Stem Cell Transplantation—A Pilot Study

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Phosphodiesterase-5 inhibitors ameliorate structural kidney damage in a rat model of contrast-induced nephropathy

Cited by 24 publications

References 51 publications

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches

Ameliorative effect of phosphodiesterase 4 and 5 inhibitors in deoxycorticosterone acetate‐salt hypertensive uni‐nephrectomized KKA y mice

Clusterin as a New Marker of Kidney Injury in Children Undergoing Allogeneic Hematopoietic Stem Cell Transplantation—A Pilot Study

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Ameliorative effect of phosphodiesterase 4 and 5 inhibitors in deoxycorticosterone acetate‐salt hypertensive uni‐nephrectomized KKA ^y mice