scholarly journals Role of intratubular pressure during the ischemic phase in acute kidney injury

2017 ◽  
Vol 312 (6) ◽  
pp. F1158-F1165 ◽  
Author(s):  
Jin Wei ◽  
Jiangping Song ◽  
Shan Jiang ◽  
Gensheng Zhang ◽  
Donald Wheeler ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Artery ◽  
Kidney Injury ◽  
Renal Ischemia ◽  
Plasma Creatinine ◽  
Renal Veins ◽  
Artery Pressure ◽  
Intratubular Pressure ◽  
Proximal Tubular

Acute kidney injury (AKI) induced by clamping of renal vein or pedicle is more severe than clamping of artery, but the mechanism has not been clarified. In the present study, we tested our hypothesis that increased proximal tubular pressure (Pt) during the ischemic phase exacerbates kidney injury and promotes the development of AKI. We induced AKI by bilateral clamping of renal arteries, pedicles, or veins for 18 min at 37°C, respectively. Pt during the ischemic phase was measured with micropuncture. We found that higher Pt was associated with more severe AKI. To determine the role of Pt during the ischemic phase on the development of AKI, we adjusted the Pt by altering renal artery pressure. We induced AKI by bilateral clamping of renal veins, and the Pt was changed by adjusting the renal artery pressure during the ischemic phase by constriction of aorta and mesenteric artery. When we decreased renal artery pressure from 85 ± 5 to 65 ± 8 mmHg, Pt decreased from 53.3 ± 2.7 to 44.7 ± 2.0 mmHg. Plasma creatinine decreased from 2.48 ± 0.23 to 1.91 ± 0.21 mg/dl at 24 h after renal ischemia. When we raised renal artery pressure to 103 ± 7 mmHg, Pt increased to 67.2 ± 5.1 mmHg. Plasma creatinine elevated to 3.17 ± 0.14 mg·dl·24 h after renal ischemia. Changes in KIM-1, NGAL, and histology were in the similar pattern as plasma creatinine. In summary, we found that higher Pt during the ischemic phase promoted the development of AKI, while lower Pt protected from kidney injury. Pt may be a potential target for treatment of AKI.

scholarly journals Renalase and Biomarkers of Contrast-Induced Acute Kidney Injury

2015 ◽  
Vol 6 (1) ◽  
pp. 25-36 ◽  
Author(s):  
Maciej T. Wybraniec ◽  
Katarzyna Mizia-Stec
Keyword(s):  
Acute Kidney Injury ◽  
Renal Injury ◽  
Amine Oxidase ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Creatinine Concentration ◽  
Invasive Cardiology ◽  
Proximal Tubular ◽  
Novel Biomarkers

Background: Contrast-induced acute kidney injury (CI-AKI) remains one of the crucial issues related to the development of invasive cardiology. The massive use of contrast media exposes patients to a great risk of contrast-induced nephropathy and chronic kidney disease development, and increases morbidity and mortality rates. The serum creatinine concentration does not allow for a timely and accurate CI-AKI diagnosis; hence numerous other biomarkers of renal injury have been proposed. Renalase, a novel catecholamine-metabolizing amine oxidase, is synthesized mainly in proximal tubular cells and secreted into urine and blood. It is primarily engaged in the degradation of circulating catecholamines. Notwithstanding its key role in blood pressure regulation, renalase remains a potential CI-AKI biomarker, which was shown to be markedly downregulated in the aftermath of renal injury. In this sense, renalase appears to be the first CI-AKI marker revealing an actual loss of renal function and indicating disease severity. Summary: The purpose of this review is to summarize the contemporary knowledge about the application of novel biomarkers of CI-AKI and to highlight the potential role of renalase as a functional marker of contrast-induced renal injury. Key Messages: Renalase may constitute a missing biochemical link in the mutual interplay between kidney and cardiac pathology known as the cardiorenal syndrome.

Successful Repair of Acute Type B and Retrograde Type A Aortic Dissection With Kidney Ischemia

2017 ◽  
Vol 51 (5) ◽  
pp. 342-345 ◽  
Author(s):  
Jeko M. Madjarov ◽  
Michael G. Katz ◽  
Hector Crespo-Soto ◽  
Svetozar Madzharov ◽  
Timothy Roush ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Aortic Dissection ◽  
Renal Artery ◽  
Kidney Injury ◽  
Renal Ischemia ◽  
Left Renal Artery ◽  
Acute Type ◽  
Type B ◽  
Type A Aortic Dissection

Acute dissection of thoracic aorta carries a risk of renal ischemia followed by the development of a kidney failure. The optimal surgical and nonsurgical management of these patients, timing of intervention, and the factors predicting renal recovery are not well delineated and remain controversial. We present a case of acute type B thoracic aortic dissection with left kidney ischemia. Evaluation of renal function was performed by the means of internationally accepted Risk, Injury, Failure, Loss of kidney function, End stage kidney disease and Acute Kidney Injury Network classifications for acute kidney injury, renal duplex sonography, and intravascular ultrasound that demonstrated left renal artery dissection with a flap completely compressing the true lumen. The patient underwent thoracic endovascular aortic repair and left renal artery stent and recovered well. Six months later, at the follow-up visit, retrograde type A aortic dissection was found, which was successfully repaired. Reversal of renal ischemia after aortic dissection depends on the precise assessment of renal function and prompt intervention.

scholarly journals Acute Kidney Injury in COVID-19

2021 ◽  
Vol 22 (15) ◽  
pp. 8081
Author(s):  
Marta Głowacka ◽  
Sara Lipka ◽  
Ewelina Młynarska ◽  
Beata Franczyk ◽  
Jacek Rysz
Keyword(s):  
Acute Kidney Injury ◽  
Strong Association ◽  
Kidney Injury ◽  
Respiratory Illness ◽  
Angiotensin Converting Enzyme 2 ◽  
Tubular Cells ◽  
Collapsing Glomerulopathy ◽  
Proximal Tubular ◽  
Insight Into

COVID-19 is mainly considered a respiratory illness, but since SARS-CoV-2 uses the angiotensin converting enzyme 2 receptor (ACE2) to enter human cells, the kidney is also a target of the viral infection. Acute kidney injury (AKI) is the most alarming condition in COVID-19 patients. Recent studies have confirmed the direct entry of SARS-CoV-2 into the renal cells, namely podocytes and proximal tubular cells, but this is not the only pathomechanism of kidney damage. Hypovolemia, cytokine storm and collapsing glomerulopathy also play an important role. An increasing number of papers suggest a strong association between AKI development and higher mortality in COVID-19 patients, hence our interest in the matter. Although knowledge about the role of kidneys in SARS-CoV-2 infection is changing dynamically and is yet to be fully investigated, we present an insight into the possible pathomechanisms of AKI in COVID-19, its clinical features, risk factors, impact on hospitalization and possible ways for its management via renal replacement therapy.

scholarly journals Sepsis-associated acute kidney injury

2021 ◽  
Vol 17 (6) ◽  
pp. 44-50
Author(s):  
L.A. Maltseva ◽  
L.V. Novytska-Usenko ◽  
V.V. Nykonov ◽  
T.V. Kanchura
Keyword(s):  
Acute Kidney Injury ◽  
Intensive Care ◽  
Renal Replacement Therapy ◽  
Replacement Therapy ◽  
Creatinine Level ◽  
Kidney Injury ◽  
Plasma Creatinine ◽  
Advantages And Disadvantages ◽  
Plasma Creatinine Level

Acute kidney injury (AKI) is a condition that develops as a result of a rapid decrease in the glomerular filtration rate, which leads to the accumulation of nitrogenous, including urea and creatinine, and non-nitrogenous metabolic products with electrolytic disorders, impairment of the acid-base balance, and the volume of fluid excreted by the kidneys. Objective: to provide a review of the literature concerning sepsis-associated acute kidney injury. We presented the problems of diagnosis, risk factors, the pathogenesis of sepsis-associated acute kidney injury, as well as to outline terminologically the clinical form of sepsis-associated acute kidney injury: the paradigm shifts from ischemia and vasoconstriction to hyperemia and vasodilation, from acute tubular necrosis to acute tubular apoptosis. Sepsis contributes significantly to the development of AKI: in sepsis, it occurs in 19 % of patients; nevertheless, it is much more frequent in septic shock (45 % of cases), the mortality of individuals with AKI is especially high in non-septic and septic conditions (45 and 73 %, respectively). To effectively diagnose the functional state of the kidneys and conduct nephroprotective therapy, stratification scales for assessing the severity of acute kidney damage are applied, which are based on the determination of plasma creatinine level and urine output: RIFLE (risk, injury, failure, loss of kidney function, and end-stage renal failure), AKIN (Acute Kidney Injury Network), KDIGO (Kidney Disease Improving Global Outcomes); the experts considered KDIGO scale more modern and perfect. It has been found that plasma creatinine is not an early biomarker of AKI that indicates the advisability of using other integral indicators. AKI biomarkers are substances that either participate in the pathological process or witness it allowing diagnose AKI even before an increase in plasma creatinine level. The characteristics of the structure, role of functions of such biomarkers as neutrophil gelatinase-associated lipocalin, cystatin C, interleukin-18, kidney injury molecule-1 and others are given. Intensive care for sepsis-associated acute kidney injury includes the standard therapy corresponding to 2016 Surviving Sepsis Campaign and KDIGO guidelines. Also, the paper focuses on renal replacement therapy (RRT): renal and extrarenal indications for the initiation, factors affecting the initiation of RRT, the timing of initiation, ways of optimization, the timing of RRT discontinuation, recommendations for the dose of RRT, the dose of renal replacement therapy in sepsis-associated AKI, choice of method, advantages and disadvantages of continuous RRT and intermittent hemodialysis, medication support for continuous therapy, the role of hemodialysis machine in the intensive care unit.

Abstract 055: Benefit of Mineralocorticoid Receptor Antagonism in Acute Kidney Injury: Role of Smooth Muscle Rac1

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Jonatan Barrera-Chimal ◽  
Gwennan André-Grégoire ◽  
Sonia Prince ◽  
Peter Kolkhof ◽  
Vincent Sauzeau ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Smooth Muscle ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Fold Increase ◽  
Renal Ischemia ◽  
Rac1 Activity ◽  
Mineralocorticoid Receptor Antagonism

Introduction: Renal ischemia/reperfusion (IR) is a major cause of acute kidney injury (AKI). The benefit of novel non-steroidal MR antagonists such as finerenone in the IR context has not been evaluated and the mechanisms underlying the benefit of MR antagonism remain unclear. Objectives: To test the efficacy of finerenone in ischemic AKI and to evaluate the specific contribution of the MR expressed in endothelial or smooth muscle cell (SMC) in renal IR injury. Methods: We included 18 male C57/B6 mice that were divided in: sham, renal ischemia for 20 min and IR plus treatment with finerenone (10 mg/kg) by gavage once a day at -48, -24 and -1 h before IR. Alternatively, MR inactivation in endothelial cells (MR endoKO mice /Vecadh-cre) or in smooth muscle cells (MR SMCKO mice/SMA-cre) was induced in 3-month-old mice. Sham surgery or bilateral renal IR for 20 min was performed and mice were studied 24 h after reperfusion. Primary rat SMC cultures were used to assess the signaling pathways modulated by MR. Results: In C57/B6 WT, MR fl/fl and MR endoKO mice, IR induced kidney dysfunction and tubular injury. After IR, Finerenone-treated mice and the MR SMCKO mice presented normal renal function and a significant reduction of histological alterations, while MR endoKO mice were not protected. The benefit of finerenone and MR KO in SMC was associated with reduced oxidative stress-mediated lipid peroxidation as compared to MR fl/fl or WT mice. In aldosterone-stimulated rat SMC, we observed a 100% increase in hydrogen peroxide production and a 2-fold increase in Rac1 activity; MR and Rac1 antagonism blunted these effects. Moreover, mice deficient of Rac1 in SMC were also protected against ischemic AKI. Conclusion: Finerenone limits renal injury induced by IR. Moreover, genetic deletion of MR in SMC only has similar effects. This benefit was associated with reduced oxidative stress, by affecting oxidative stress production via SMC Rac1.

MiR-182 Promotes Ischemia/Reperfusion-Induced Acute Kidney Injury in Rat by Targeting FoxO3

2021 ◽  
pp. 1-10
Author(s):  
Yang Du ◽  
Jin-zhuo Ning
Keyword(s):  
Acute Kidney Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Renal Ischemia ◽  
Downstream Target ◽  
Tubular Necrosis ◽  
Renal Histology ◽  
Cell Hypoxia ◽  
Gain Loss

<b><i>Background:</i></b> Renal ischemia/reperfusion (I/R) injury (RIRI) is the main cause of acute kidney injury (AKI) in patients. We investigated the role of miR-182 after renal ischemia/reperfusion (I/R) in rat to characterize the microRNA (miRNA) network activated during development and recovery from RIRI. <b><i>Methods and Results:</i></b> 12 h after lethal (45 min) renal ischemia, AKI was verified by renal histology (tubular necrosis and regeneration), blood urea nitrogen level, and renal mRNA expression in Wistar rats. We found that miR-182 markedly increased after renal I/R. In cell hypoxia/reoxygenation model, we found similar upregulation of miR-182. In function gain/loss assay, we confirmed an impaired effect of miR-182 and identified Forkhead box O3 (FoxO3) as a direct downstream target of it. By using miR-182 antagomir, the I/R injury was markedly ameliorated. <b><i>Conclusions:</i></b> Our results demonstrate that miR-182 promotes cell apoptosis and I/R injury through directly binding to FoxO3. The present study will provide potential therapeutic targets for renal I/R-induced AKI, and open a new avenue for AKI treatment by manipulating miRNAs levels.

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