scholarly journals Angiotensin II Type 1 Receptor Antagonism Attenuates Abnormalities in Dynamic Renal Blood Flow Autoregulation in Rats with Endotoxin-Induced Acute Kidney Injury

2010 ◽  
Vol 33 (3) ◽  
pp. 200-208 ◽  
Author(s):  
Nicoletta Nitescu ◽  
Gerald F. DiBona ◽  
Elisabeth Grimberg ◽  
Gregor Guron
Keyword(s):  
Acute Kidney Injury ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Kidney Injury ◽  
Receptor Antagonism ◽  
Renal Blood Flow Autoregulation

scholarly journals Albumin infusion improves renal blood flow autoregulation in patients with acute decompensation of cirrhosis and acute kidney injury

2014 ◽  
Vol 35 (2) ◽  
pp. 335-343 ◽  
Author(s):  
Rita Garcia-Martinez ◽  
Lorette Noiret ◽  
Sambit Sen ◽  
Rajeshwar Mookerjee ◽  
Rajiv Jalan
Keyword(s):  
Acute Kidney Injury ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Kidney Injury ◽  
Albumin Infusion ◽  
Acute Decompensation ◽  
Renal Blood Flow Autoregulation

scholarly journals Hepatorenal Syndrome

2021 ◽  
Author(s):  
Arshpal Gill ◽  
Ra’ed Nassar ◽  
Ruby Sangha ◽  
Mohammed Abureesh ◽  
Dhineshreddy Gurala ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Failure ◽  
Blood Flow ◽  
Mortality Rate ◽  
Kidney Injury ◽  
Type I ◽  
Tubular Necrosis ◽  
Cirrhotic Patients

Hepatorenal Syndrome (HRS) is an important condition for clinicians to be aware of in the presence of cirrhosis. In simple terms, HRS is defined as a relative rise in creatinine and relative drop in serum glomerular filtration rate (GFR) alongside renal plasma flow (RPF) in the absence of other competing etiologies of acute kidney injury (AKI) in patients with hepatic cirrhosis. It represents the end stage complication of decompensated cirrhosis in the presence of severe portal hypertension, in the absence of prerenal azotemia, acute tubular necrosis or others. It is a diagnosis of exclusion. The recognition of HRS is of paramount importance for clinicians as it carries a high mortality rate and is an indication for transplantation. Recent advances in understanding the pathophysiology of the disease improved treatment approaches, but the overall prognosis remains poor, with Type I HRS having an average survival under 2 weeks. Generally speaking, AKI and renal failure in cirrhotic patients carry a very high mortality rate, with up to 60% mortality rate for patients with renal failure and cirrhosis and 86.6% of overall mortality rates of patients admitted to the intensive care unit. Of the various etiologies of renal failure in cirrhosis, HRS carries a poor prognosis among cirrhotic patients with acute kidney injury. HRS continues to pose a diagnostic challenge. AKI can be either pre-renal, intrarenal or postrenal. Prerenal causes include hypovolemia, infection, use of vasodilators and functional due to decreased blood flow to the kidney, intra-renal such as glomerulopathy, acute tubular necrosis and post-renal such as obstruction. Patients with cirrhosis are susceptible to developing renal impairment. HRS may be classified as Type 1 or rapidly progressive disease, and Type 2 or slowly progressive disease. There are other types of HRS, but this chapter will focus on Type 1 HRS and Type 2 HRS. HRS is considered a functional etiology of acute kidney injury as there is an apparent lack of nephrological parenchymal damage. It is one several possibilities for acute kidney injury in patients with both acute and chronic liver disease. Acute kidney injury (AKI) is one of the most severe complications that could occur with cirrhosis. Up to 50% of hospitalized patients with cirrhosis can suffer from acute kidney injury, and as mentioned earlier an AKI in the presence of cirrhosis in a hospitalized patient has been associated with nearly a 3.5-fold increase in mortality. The definition of HRS will be discussed in this chapter, but it is characterized specifically as a form of acute kidney injury that occurs in patients with advanced liver cirrhosis which results in a reduction in renal blood flow, unresponsive to fluids this occurs in the setting of portal hypertension and splanchnic vasodilation. This chapter will discuss the incidence of HRS, recognizing HRS, focusing mainly on HRS Type I and Type II, recognizing competing etiologies of renal impairment in cirrhotic patients, and the management HRS.

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
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