scholarly journals Pericyte-mediated constriction of renal capillaries evokes no-reflow and kidney injury following ischemia

2021 ◽  
Author(s):  
Felipe Freitas ◽  
David Attwell
Keyword(s):  
Acute Kidney Injury ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Rho Kinase ◽  
Kidney Injury ◽  
No Reflow ◽  
Vasa Recta ◽  
Sustained Reduction ◽  
Peritubular Capillaries ◽  
Severe Hemorrhage

Acute kidney injury is common, with ~13 million cases and 1.7 million deaths/year worldwide. A major cause is renal ischemia, typically following cardiac surgery, renal transplant or severe hemorrhage. We examined the cause of the sustained reduction in renal blood flow (no-reflow), which exacerbates kidney injury even after an initial cause of compromised blood supply is removed. After 60 min kidney ischemia and 30-60 min reperfusion, renal blood flow remained reduced, especially in the medulla, and kidney tubule damage was detected as Kim-1 expression. Constriction of the medullary descending vasa recta and cortical peritubular capillaries occurred near pericyte somata, and led to capillary blockages, yet glomerular arterioles and perfusion were unaffected, implying that the long-lasting decrease of renal blood flow contributing to kidney damage was generated by pericytes. Blocking Rho kinase to decrease pericyte contractility from the start of reperfusion increased the post-ischemic diameter of the descending vasa recta capillaries at pericytes, reduced the percentage of capillaries that remained blocked, increased medullary blood flow and reduced kidney injury. Thus, post-ischemic renal no-reflow, contributing to acute kidney injury, reflects pericytes constricting the descending vasa recta and peritubular capillaries. Pericytes are therefore an important therapeutic target for treating acute kidney injury.

scholarly journals P0544INHIBITION OF 15-HYDROXYPROSTAGLANDIN DEHYDROGENASE (15-PGDH) PROTECTS MICE AGAINST CONTRAST-INDUCED ACUTE KIDNEY INJURY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Byeong Woo KIm ◽  
Sun hee Kim ◽  
Ki beom Bae
Keyword(s):  
Acute Kidney Injury ◽  
Blood Flow ◽  
Protective Effect ◽  
Renal Blood Flow ◽  
Smooth Muscle Actin ◽  
Kidney Injury ◽  
Plasma Creatinine ◽  
Histological Evaluation ◽  
Vehicle Group ◽  
Before And After

Abstract Background and Aims Although the mechanism of contrast-induced acute kidney injury (CI-AKI) is not fully known, the imbalance of vasoconstrictive and vasodilative mediators plays a major role. Prostaglandin E2 (PGE2) is one of the vasodilators involved in this process. Inhibition of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) causes elevation of PGE2 level in tissue by delaying the rapid degradation of PGE2 by the enzyme. We tested the hypothesis that the 15-PGE2 inhibitor would protect against CI-AKI in a mouse model and attempted to elucidate the mechanism involved. Method 10-week aged male C57/BL6 Mice were injected with 10gI/kg of iodixanol by tail vein. Renal blood flow measurement, right nephrectomy, and blood sampling were taken at 48 hours after iodixanol injection. The 15-PGDH inhibitor was injected before and after iodixanol administration. Plasma creatinine, NGAL, KIM-1 were measured as biomarkers for renal function. Histological evaluation was analyzed by the necrosis scoring system and TUNEL assay. Arteriolar area of outer medulla was analyzed by α-smooth muscle actin stain. Renal blood flow was measured by the non-invasive laser doppler. Results Plasma creatinine (1.94±0.75 vs 1.11±0.44 mg/dL, p=0.005), NGAL (299.7±115.87 vs 140.4±76.56 ng/mL, p=0.004), and KIM-1 (2.09±2.34 vs 0.43±0.89 ng/mL, p=0.024) levels were significantly lower when the 15-PGDH inhibitor was injected before and after iodixanol administration than the vehicle group. But no significant renal protective effect was shown when the 15-PGDH inhibitor was injected before or after iodixanol administration. The 15-PGDH inhibitor administration before and after iodixanol injection showed a significantly wider renal arteriolar area (683.63±248.46 vs 1132.97±357.46 μm2, p=0.039) and larger renal blood flow (360.0±49.72 vs 635.1±27.20, p=0.011) than vehicle administration. Conclusion The 15-PGDH inhibitor has a renal protective effect against CI-AKI in mice by increasing renal blood flow when injected intravenously before and after iodine contrast media administration.

scholarly journals Renal blood flow and acute kidney injury in septic shock: an arduous conflict that smolders intrarenally?

2016 ◽  
Vol 90 (1) ◽  
pp. 22-24 ◽  
Author(s):  
Patrick M. Honore ◽  
Rita Jacobs ◽  
Elisabeth De Waele ◽  
Marc Diltoer ◽  
Herbert D. Spapen
Keyword(s):  
Septic Shock ◽  
Acute Kidney Injury ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Kidney Injury

Acute kidney injury in sepsis: Is renal blood flow more than just an innocent bystander?

2007 ◽  
Vol 33 (9) ◽  
pp. 1498-1500 ◽  
Author(s):  
Martin Matejovic ◽  
Peter Radermacher ◽  
Michael Joannidis
Keyword(s):  
Acute Kidney Injury ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Kidney Injury ◽  
Innocent Bystander

Renal Blood Flow Redistribution During Acute Kidney Injury

2010 ◽  
Vol 56 (4) ◽  
pp. 785-787 ◽  
Author(s):  
Filippo Mangione ◽  
Valeria Calcaterra ◽  
Ciro Esposito ◽  
Antonio Dal Canton
Keyword(s):  
Acute Kidney Injury ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Kidney Injury ◽  
Blood Flow Redistribution

Measuring renal blood flow in acute kidney injury

2012 ◽  
Vol 40 (6) ◽  
pp. 1972-1973
Author(s):  
Jean-Sebastien Rachoin
Keyword(s):  
Acute Kidney Injury ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Kidney Injury

Contrast-induced acute kidney injury

2015 ◽  
Author(s):  
Douglas Stewart ◽  
Gaurav Shah ◽  
Jeremiah R. Brown ◽  
Peter A. McCullough
Keyword(s):  
Acute Kidney Injury ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Kidney Injury ◽  
Cell Dysfunction ◽  
Transient Rise ◽  
The Hours ◽  
Proximal Tubular ◽  
Contrast Exposure ◽  
Considerable Damage

Contrast-induced acute kidney injury (CI-AKI) occurs because all forms of intravascular contrast contain iodine and their biochemical structures induce immediate changes in systemic and renal vasoreactivity. In the kidneys, contrast induces a transient decrease in renal blood flow. This is more pronounced in patients with chronic kidney disease and diabetes mellitus. The reduction in blood flow allows slowed transit of contrast and reabsorption by the proximal tubular cells where contrast is directly toxic resulting in tubular cell dysfunction and death. When there is considerable damage, a transient rise in serum creatinine and reduction in urine output will be observed in the hours to days after contrast exposure. Principles to reduce CI-AKI include limiting the amount of contrast used, intravascular volume expansion to maximize renal blood flow and speed transit of contrast, and possibly agents to reduce the oxidative damage caused by the contrast agents themselves.

Renal blood flow and function during recovery from experimental septic acute kidney injury

2007 ◽  
Vol 33 (9) ◽  
pp. 1614-1618 ◽  
Author(s):  
Christoph Langenberg ◽  
Li Wan ◽  
Moritoki Egi ◽  
Clive N. May ◽  
Rinaldo Bellomo
Keyword(s):  
Acute Kidney Injury ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Kidney Injury ◽  
Septic Acute Kidney Injury ◽  
And Function

scholarly journals Relevant Role of Von Willebrand Factor in Ischemia-Reperfusion Model of Acute Kidney Injury in Mice

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 2243-2243
Author(s):  
Shiro Ono ◽  
Hideto Matsui ◽  
Masashi Noda ◽  
Shogo Kasuda ◽  
Yasunori Matsunari ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Relevant Role ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract Acute kidney injury (AKI), an abrupt loss of renal function, is often seen in clinical settings and its mortality remains high even in the developed countries. An adhesive protein von Willebrand factor (VWF) plays a pivotal role in platelet thrombus formation and is recently understood as a key protein in a cross-talk between inflammation and thrombosis. Recent mouse model studies demonstrated that VWF-mediated thrombotic and inflammatory responses could play a role in the disease progression of myocardial infarction or brain stroke. Thus, we assumed that VWF may also be involved in the pathophysiology of AKI, the major cause of which could be an insufficient renal circulation and/or inflammatory cell infiltration in the kidney. To test this hypothesis, we studied the relevant role of VWF in AKI in mouse model of acute ischemia-reperfusion (I/R) kidney injury. All mice used were male, 8-12 weeks of age, healthy and whose right kidney was surgically removed by the standard mouse nephrectomy procedure 1 week prior to the kidney I/R experiment. The preliminary experiments confirmed that surgical removal of mouse right kidney did not affect their general conditions including renal functions. Mice were anesthetized with inhaled isoflurane and then placed in an abdominal position on a heating pad. Surgical incision was given on the left side of back and the left kidney was brought out and kept outside during the operation. Both renal artery and vein were clamped at the renal hilus by a clamping clip for 30 min ischemia. Then a clip was taken off to provoke the reperfusion of renal blood flow, which was monitored by Laser Doppler flowmetry (ALF21, Advance Co, Tokyo, Japan). The kidney was then put back in a body and skin incision was closed. The renal blood flow was measured again 30 h after reperfusion and mice were then sacrificed for blood collection. We compared 15 wild-type (WT) and 16 VWF-gene deleted (knock-out; KO) mice (from The Jackson Laboratory, Bar Harbor, ME). Excess blood loss was not observed in all mice (WT or KO) during whole surgical process. Although no difference was seen immediately after reperfusion, significantly (p < 0.05) higher renal blood flow at 30 h after reperfusion was confirmed in VWF-KO mice, as compared to WT (KO; 24.0±2.3 vs. WT; 15.1±1.46 ml/min/100g of kidney weight, and the reperfusion/base flow ratio: KO; 1.0±0.07 vs. WT; 0.6 ±0.07). Consistent with the renal blood flow data, the serum creatinine value at 30 h after reperfusion were significantly (p < 0.05) lower in VWF-KO mice than WT (KO; 2.77±0.11 vs. WT; 3.15±0.11 mg/dl). Our results suggest that VWF does play a role in the pathogenesis of AKI, in which VWF-dependent thrombotic or inflammatory responses may trigger thrombotic ischemia or endothelial damages of vascular bed in the kidney. Thus, proper functional regulation of VWF would be beneficial for better microcirculation and vessel functions in the kidney, suggesting a novel therapeutic potential against AKI. Disclosures No relevant conflicts of interest to declare.

scholarly journals Monitorization of NGAL, Creatinine and Renal Blood Flow in the Follow-up of Acute Kidney Injury in Intensive Care

2021 ◽  
Author(s):  
Mehmet Süleyman Sabaz ◽  
Halil Çetingök ◽  
Gökhan Sertcakacılar ◽  
Yusuf Ziya Yener ◽  
Erdal Atiç ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Failure ◽  
Blood Flow ◽  
Intensive Care ◽  
Renal Blood Flow ◽  
Early Stage ◽  
Kidney Injury ◽  
Serial Measurement ◽  
Neutrophil Gelatinase Associated Lipocalin

Objectıve: Acute Kidney Injury (AKI) and subsequent renal failure are the leading causes of morbidity and mortality in the intensive care unit (ICU). In this study, it was planned to compare Neutrophil Gelatinase-associated Lipocalin (NGAL) and creatinine values in patients diagnosed with AKI and to determine the effect of renal dose dopamine use on renal blood flow, development of chronic renal failure (CRF) and mortality. Materıals and methods: This prospective study was planned with 35 patients developed AKI in the ICU of Bakırköy Dr. Sadi Konuk Training and Research Hospital. The patients were randomized into 2 groups as 18 patients who received dopamine treatment with the recommendation of the cardiology clinic and 17 patients who did not receive dopamine treatment. Urea, creatinine and NGAL plasma levels were compared between groups. Results: There was no difference between the groups in terms of age, gender and AKI stage. The 0th, 24th hour results and 24-hour changes of urea, creatinine and NGAL values of dopamine patient, who took dopamine, were found to be similar to those of patients who did not take dopamine. A significant positive correlation was found between the 24-hour change in creatinine value and the 24-hour change in NGAL (r=0.374; p<0.05). There was no significant change in the diameter and flow of renal arteries between measurements in patients who received dopamine. The rates of patients who regain normal kidney functions, develop CRF or develop mortality between the two groups were found to be similar. Conclusıon: Treatment results of AKI developing in ICU are not satisfactory. Low-dose dopamine treatment has no effect on patient outcomes in these patients. NGAL is a biomarker that has the ability to show renal damage at an early stage. Serial measurement of NGAL concentration during ICU stay may benefit the clinician in early diagnosis and follow-up of AKI.

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