scholarly journals Patients at risk for contrast-induced acute kidney injury

2013 ◽  
pp. 223-229
Author(s):  
Michele Meschi ◽  
Simona Detrenis ◽  
Marcella Saccò ◽  
Marcello Bertorelli ◽  
Enrico Fiaccadori ◽  
...  

Subjects with hypovolemia and/or dehydration and pre-existing renal failure are considered at highest risk for radiocontrast-medium-induced acute kidney injury (RCI-AKI), and this risk increases in the presence of glomerular filtration rate or creatinine clearance rates lower than 60 mL/min (stage 3-5 chronic kidney disease according to the National Kidney Foundation). The authors critically review the evidence-based literature on RCI-AKI, its diagnosis, epidemiological aspects, predisposing conditions, and markers of risk, including advanced age. Procedures requiring the use of iodinated contrast media are increasingly performed in patients over 70 years of age, and there is no definitive consensus regarding the role of advanced age as a marker of risk for RCI-AKI.

2020 ◽  
Vol 66 (10) ◽  
pp. 1335-1337
Author(s):  
Pastora Maria de Araújo Duarte ◽  
Francisco André Gomes Bastos Filho ◽  
João Vitor Araujo Duarte ◽  
Beatrice Araújo Duarte ◽  
Isabella Araujo Duarte ◽  
...  

SUMMARY The COVID-19 (SARS-CoV-2) infection started in China, Wuhan City, Hubei Province, in December 2019, and it was declared a pandemic in mid-March 2020, caused by a new coronavirus strain called SARS-CoV-2. The pathogenesis of kidney injury attributed to SARS- CoV-2 is not well defined yet. Observations show that the kidney damage caused by the new virus mutation is mainly tubular, with impairment of glomerular filtration and high levels of urea and creatinine. A study with seriously ill patients with COVID-19 showed that acute kidney injury was present in 29%. In the face of this evidence, based on recent studies, we can see the great renal contribution as an impact factor in the evolution of COVID-19, not just as a complicator of severity, but maybe part of the initial cascade of the process, requiring a deeper analysis using conventional biomarkers of kidney injury and more aggressive clinical intervention in patients at risk, in an attempt to reduce mortality.


2018 ◽  
Vol 315 (2) ◽  
pp. F291-F299 ◽  
Author(s):  
Xiaoyan Wen ◽  
Liyan Cui ◽  
Seth Morrisroe ◽  
Donald Maberry ◽  
David Emlet ◽  
...  

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.


2010 ◽  
Vol 43 (1) ◽  
pp. 237-240 ◽  
Author(s):  
Suhail Al-Salam ◽  
Ahmad Shaaban ◽  
Maha Alketbi ◽  
Naveed U. Haq ◽  
Samra Abouchacra

Sign in / Sign up

Export Citation Format

Share Document