scholarly journals Cardiorenal syndrome: acute kidney injury secondary to cardiovascular disease and role of protein-bound uraemic toxins

2014 ◽  
Vol 592 (18) ◽  
pp. 3969-3983 ◽  
Author(s):  
Suree Lekawanvijit ◽  
Henry Krum
Keyword(s):  
Cardiovascular Disease ◽  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Cardiorenal Syndrome

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.

[PP.17.32] THE ROLE OF BIOMARKERS IN EARLY DIAGNOSTIC OF ACUTE KIDNEY INJURY IN PATIENTS WITH ACUTE CARDIORENAL SYNDROME

2017 ◽  
Vol 35 ◽  
pp. e231
Author(s):  
M. Kurmanov ◽  
M. Efremovtseva ◽  
S. Avdoshina ◽  
S. Villevalde ◽  
Z. Kobalava
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Early Diagnostic

scholarly journals The acute kidney injury to chronic kidney disease transition in a mouse model of acute cardiorenal syndrome emphasizes the role of inflammation

2020 ◽  
Vol 97 (1) ◽  
pp. 95-105 ◽  
Author(s):  
Katsuyuki Matsushita ◽  
Turgay Saritas ◽  
Mahaba B. Eiwaz ◽  
Nicholas McClellan ◽  
Ian Coe ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Mouse Model ◽  
Kidney Injury ◽  
Cardiorenal Syndrome

scholarly journals A zebrafish model of infection-associated acute kidney injury

2018 ◽  
Vol 315 (2) ◽  
pp. F291-F299 ◽  
Author(s):  
Xiaoyan Wen ◽  
Liyan Cui ◽  
Seth Morrisroe ◽  
Donald Maberry ◽  
David Emlet ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Unmet Need ◽  
Kidney Injury ◽  
Edwardsiella Tarda ◽  
Adult Zebrafish ◽  
Zebrafish Model ◽  
Pericardial Edema ◽  
Kidney Injury Molecule 1 ◽  
Dose Dependent

Sepsis-associated acute kidney injury (S-AKI) independently predicts mortality among critically ill patients. The role of innate immunity in this process is unclear, and there is an unmet need for S-AKI models to delineate the pathophysiological response. Mammals and zebrafish ( Danio rerio) share a conserved nephron structure and homologous innate immune systems, making the latter suitable for S-AKI research. We introduced Edwardsiella tarda to the zebrafish. Systemic E. tarda bacteremia resulted in sustained bacterial infection and dose-dependent mortality. A systemic immune reaction was characterized by increased mRNA expressions of il1b, tnfa, tgfb1a, and cxcl8-l1 ( P < 0.0001, P < 0.001, P < 0.001, and P < 0.01, respectively). Increase of host stress response genes ccnd1 and tp53 was observed at 24 h postinjection ( P < 0.0001 and P < 0.05, respectively). Moderate E. tarda infection induced zebrafish mortality of over 50% in larvae and 20% in adults, accompanied by pericardial edema in larvae and renal dysfunction in both larval and adult zebrafish. Expression of AKI markers insulin-like growth factor-binding protein-7 (IGFBP7), tissue inhibitor of metalloproteinases 2 (TIMP-2), and kidney injury molecule-1 (KIM-1) was found to be significantly increased in the septic animals at the transcription level ( P < 0.01, P < 0.05, and P < 0.05) and in nephric tubules compared with noninfected animals. In conclusion, we established a zebrafish model of S-AKI induced by E. tarda injection, with both larval and adult zebrafish showing nephron injury in the setting of infection.

Acute kidney injury secondary to renal large B-cell lymphoma: role of early renal biopsy

2010 ◽  
Vol 43 (1) ◽  
pp. 237-240 ◽  
Author(s):  
Suhail Al-Salam ◽  
Ahmad Shaaban ◽  
Maha Alketbi ◽  
Naveed U. Haq ◽  
Samra Abouchacra
Keyword(s):  
Acute Kidney Injury ◽  
B Cell ◽  
Renal Biopsy ◽  
Cell Lymphoma ◽  
Kidney Injury ◽  
B Cell Lymphoma ◽  
Large B Cell Lymphoma ◽  
Large B Cell
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