Renocardiac Syndrome Induced by Renal Ischemia and Reperfusion: Vibrational Markers

Abstract Renal injury caused by renal ischemia and reperfusion is capable to change heart morphology, electrophysiology, and redox unbalance. The so-called cardio-renal syndrome is an important class of dysfunction since heart and kidneys are responsible for hemodynamic stability and organ perfusion through a complex network. In the present work we investigate the Fourier-Transform Raman vibrational spectral features of cardiac hypertrophy induced by renal ischemic reperfusion. C57BL/6J mice were subjected to unilateral occlusion of the renal pedicle for 60 minutes and reperfused for 5 days, 8 days, and 15 days. It was observed that bands around 540, 1100, 1300, 1450, 1650, and 2500 cm-1 dominates the spectra. They are associated to stretching of S-S in Cysteine amino acid, stretching of C-C in lipids, twisting of CH2 in collagen and phospholipids, bending modes of CH3 in lipids and amino acids side chains, Amide I vibration of proteins. The intensities of these vibrations are modulated during renocardiac syndrome. We find that tyrosine, tryptophan, cystine/cysteine, fibroblast growth factors, collagen III alterations from homeostasis were the metabolites associate with these changes. These findings are clinically relevant once the presented bands can be used as molecular markers of preventing cardiac diseases’ development in patients with renal injury.

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A1 adenosine receptor knockout mice exhibit increased renal injury following ischemia and reperfusion

AJP Renal Physiology ◽

10.1152/ajprenal.00185.2003 ◽

2004 ◽

Vol 286 (2) ◽

pp. F298-F306 ◽

Cited By ~ 104

Author(s):

H. Thomas Lee ◽

Hua Xu ◽

Samih H. Nasr ◽

Jurgen Schnermann ◽

Charles W. Emala

Keyword(s):

Renal Function ◽

Knockout Mice ◽

Adenosine Receptor ◽

Renal Injury ◽

Renal Ischemia ◽

Myeloperoxidase Activity ◽

Ischemia And Reperfusion ◽

Wild Type Littermate ◽

Renal Histology

Controversy exists regarding the effect of A1 adenosine receptor (AR) activation in the kidney during ischemia and reperfusion (I/R) injury. We sought to further characterize the role of A1 ARs in modulating renal function after I/R renal injury using both pharmacological and gene deletion approaches in mice. A1 AR knockout mice (A1KO) or their wild-type littermate controls (A1WT) were subjected to 30 min of renal ischemia. Some A1WT mice were subjected to 30 min of renal ischemia with or without pretreatment with 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) or 2-chrolo-cyclopentyladenosine (CCPA), selective A1 AR antagonist and agonist, respectively. Plasma creatinine and renal histology were compared 24 h after renal injury. A1KO mice exhibited significantly higher creatinines and worsened renal histology compared with A1WT controls following renal I/R injury. A1WT mice pretreated with the A1 AR antagonist or agonist demonstrated significantly worsened or improved renal function, respectively, after I/R injury. In addition, A1WT mice pretreated with DPCPX or CCPA showed significantly increased or reduced markers of renal inflammation, respectively (renal myeloperoxidase activity, renal tubular neutrophil infiltration, ICAM-1, TNF-α, and IL-1β mRNA expression), while demonstrating no differences in indicators of apoptosis. In conclusion, we demonstrate that endogenous or exogenous preischemic activation of A1 ARs protects against renal I/R injury in vivo via mechanisms leading to decreased necrosis and inflammation.

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Tyrosine and Tryptophan vibrational bands as markers of kidney injury: a renocardiac syndrome induced by renal ischemia and reperfusion study

Scientific Reports ◽

10.1038/s41598-021-93762-z ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Gabrielle Nepomuceno ◽

Carolina Victoria Cruz Junho ◽

Marcela Sorelli Carneiro-Ramos ◽

Herculano da Silva Martinho

Keyword(s):

Raman Spectroscopy ◽

Kidney Injury ◽

Cardiorenal Syndrome ◽

Renal Ischemia ◽

Ischemia And Reperfusion ◽

Collagen Iii ◽

Ft Raman Spectroscopy ◽

Ft Raman

AbstractRenal injury caused by renal ischemia and reperfusion strongly influences heart morphology, electrophysiology, and redox unbalance. The so-called cardiorenal syndrome is an important class of dysfunction since heart and kidneys are responsible for hemodynamic stability and organ perfusion through a complex network. In the present work we investigate the vibrational spectral features probed by Fourier-Transform Raman (FT-Raman) spectroscopy due to physiological alterations induced by renal ischemic reperfusion aiming to detect molecular markers related to progression of acute to chronic kidney injury and mortality predictors as well. C57BL/6J mice were subjected to unilateral occlusion of the renal pedicle for 60 min and reperfusion for 5, 8, and 15 days. Biopsies of heart and kidney tissues were analyzed. Our findings indicated that cysteine/cystine, fatty acids, methyl groups of Collagen, α-form of proteins, Tyrosine, and Tryptophan were modulated during renal ischemia and reperfusion process. These changes are consistent with fibroblast growth factors and Collagen III contents changes. Interestingly, Tyrosine and Tryptophan, precursor molecules for the formation of uremic toxins such as indoxyl sulfate and p-cresyl sulfate were also modulated. They are markers of kidney injury and their increase is strongly correlated to cardiovascular mortality. Regarding this aspect, we notice that monitoring the Tyrosine and Tryptophan bands at 1558, 1616, and 1625 cm−1 is a viable and and advantageous way to predict fatality in cardiovascular diseases both “in vivo” or “in vitro”, using the real-time, multiplexing, and minimally invasive advantages of FT-Raman spectroscopy.

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Faculty Opinions recommendation of Renal ischemia and reperfusion assessment with three-dimensional hyperpolarized 13 C,15 N2-urea.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.729704797.793552863 ◽

2018 ◽

Author(s):

Joshua Thurman

Keyword(s):

Three Dimensional ◽

Renal Ischemia ◽

Ischemia And Reperfusion

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Kidney ischemia and reperfunsion syndrome: effect of lidocaine and local postconditioning

Revista do Colégio Brasileiro de Cirurgiões ◽

10.1590/0100-69912016005012 ◽

2016 ◽

Vol 43 (5) ◽

pp. 348-353 ◽

Cited By ~ 1

Author(s):

IGOR NAGAI YAMAKI ◽

RUY VICTOR SIMÕES PONTES ◽

FELIPE LOBATO DA SILVA COSTA ◽

VITOR NAGAI YAMAKI ◽

RENAN KLEBER COSTA TEIXEIRA ◽

...

Keyword(s):

Ischemia Reperfusion ◽

Serum Levels ◽

Saline Group ◽

Renal Ischemia ◽

Ischemic Postconditioning ◽

Control Group ◽

Ischemia And Reperfusion ◽

Lidocaine Group ◽

Group 5 ◽

Group 2

ABSTRACT Objective: to evaluate the effects of blocking the regulation of vascular tone on the ischemia and reperfusion syndrome in rats through the use of lidocaine in the postconditioning technique. Methods: we randomized 35 rats into seven groups of five animals: Group 1- Control; Group 2- Ischemia and Reperfusion; Group 3- Ischemia, Reperfusion and Saline; Group 4- Ischemic Postconditioning; Group 5- Ischemic Postconditioning and Saline; Group 6- Lidocaine; Group 7- Ischemic Postconditioning and Lidocaine. Except for the control group, all the others were submitted to renal ischemia for 30 minutes. In postconditioning groups, we performed ischemia and reperfusion cycles of five minutes each, applied right after the main ischemia. In saline and lidocaine groups, we instilled the substances at a rate of two drops per minute. To compare the groups, we measured serum levels of urea and creatinine and also held renal histopathology. Results: The postconditioning and postconditioning + lidocaine groups showed a decrease in urea and creatinine values. The lidocaine group showed only a reduction in creatinine values. In histopathology, only the groups submitted to ischemic postconditioning had decreased degree of tubular necrosis. Conclusion: Lidocaine did not block the effects of postconditioning on renal ischemia reperfusion syndrome, and conferred better glomerular protection when applied in conjunction with ischemic postconditioning.

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In vivo spectroscopic monitoring of renal ischemia and reperfusion in a rat model

10.1117/12.645344 ◽

2006 ◽

Author(s):

Rajesh N. Raman ◽

Christopher D. Pivetti ◽

Dennis L. Matthews ◽

Christoph Troppmann ◽

Stavros G. Demos

Keyword(s):

Rat Model ◽

Renal Ischemia ◽

Ischemia And Reperfusion ◽

Spectroscopic Monitoring

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TonEBP/OREBP is activated by hypoxia: Role in renal Ischemia and Reperfusion

The FASEB Journal ◽

10.1096/fasebj.25.1_supplement.lb628 ◽

2011 ◽

Vol 25 (S1) ◽

Author(s):

CARLOS E IRARRAZABAL ◽

Sandra Villanueva ◽

Luis Michea ◽

Juan E Carreno ◽

Mauricio Lozano ◽

...

Keyword(s):

Renal Ischemia ◽

Ischemia And Reperfusion

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Matching Human Unilateral AKI, a Reverse Translational Approach to Investigate Kidney Recovery after Ischemia

Journal of the American Society of Nephrology ◽

10.1681/asn.2018080808 ◽

2019 ◽

Vol 30 (6) ◽

pp. 990-1005 ◽

Cited By ~ 8

Author(s):

Danielle E. Soranno ◽

Hyo-Wook Gil ◽

Lara Kirkbride-Romeo ◽

Christopher Altmann ◽

John R. Montford ◽

...

Keyword(s):

Glomerular Filtration Rate ◽

Glomerular Filtration ◽

Renal Injury ◽

Filtration Rate ◽

Human Study ◽

Renal Ischemia ◽

Research Approach ◽

Urine Biomarkers ◽

Injured Kidney

BackgroundThe duration of renal ischemia that is associated with (or leads to) renal injury in patients is uncertain, and a reverse translational research approach has been proposed to improve animal models of AKI to facilitate clinical translatability. We developed a two murine models of unilateral renal ischemia to match a recently published human study that investigated renal injury after unilateral renal ischemia during partial nephrectomy.MethodsEight 10-week-old C57BL/6 male mice underwent left UiAKI or sham procedure, with or without intra-operative ice packs. Functional, histological, and biomarker outcomes were followed at 2, 6 and 24 hours, or 14 or 28 days later. The 14 and 28 day cohorts were duplicated such that contralateral nephrectomy could be performed 3 days prior to sacrifice with functional measurements obtained to isolate the glomerular filtration rate of the injured kidney.ResultsThe short-term outcomes correlated with the human study findings with urine and serum biomarkers of injury peaking around 24 hours and then normalizing, and reassuring immediate histological outcomes. Functional and histological outcomes at the later time-points (14 and 28 days) demonstrate an increase in fibrosis markers, and a reduction in glomerular filtration rate in the injured kidney, corresponding to the duration of ischemia, while serum and urine biomarkers remained reassuring.ConclusionsOur findings suggest that clinically available biomarkers of renal function are falsely reassuring against long-term injury following UiAKI, and that the duration of ischemia correlates with impaired function and increased fibrosis.

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