scholarly journals Severity and Outcomes in Relationship to Known Exposures and Susceptibilities among Afro-Caribbean Patients with Hospital-acquired Acute Kidney Injury

Author(s):  
KK Hoe ◽  
EN Barton ◽  
TL Han ◽  
TH Hoe
2011 ◽  
Vol 12 (1) ◽  
Author(s):  
Qionghong Xie ◽  
Ying Zhou ◽  
Zhongye Xu ◽  
Yanjiao Yang ◽  
Dingwei Kuang ◽  
...  

2021 ◽  
Vol 23 (2) ◽  
pp. 137-140
Author(s):  
Zoltán H Endre ◽  

Acute kidney injury (AKI) is a major clinical problem in the community and in hospital, with hospital-acquired AKI reported in about 20% of adult and 30% of paediatric admissions.


2020 ◽  
Author(s):  
E. Gkekas ◽  
TYT. Tang ◽  
M. Brazell ◽  
M. Brennan ◽  
H. Ayub ◽  
...  

Abstract Background: Acute Kidney Injury (AKI) is a sudden decline in kidney function. Early detection and prompt treatment of AKI is vital in improving the outcome of patients. We introduced in-reach nephrology services at South Tyneside District Hospital (STDH) as part of a reconfiguration of local NHS services. Aims: The principal aim of this study is to analyse patient outcomes relating to service developments and to explore prognostic characteristics among a cohort of AKI-3 patients Design: This was a single centre retrospective impact evaluation study.Methods: We studied all patients (n=246) who either presented with or developed AKI-3 during their admission at South Tyneside District Hospital from 2016 to 2018. The inclusion criteria included age 18-95 years and a diagnosis of AKI-3 as per KDIGO classification. Exclusion include those on established dialysis regime or on palliative care. Results: A total of 246 patients were admitted with AKI-3. There were 64 deaths from AKI-3 over the three-year period. Mortality decreased from 29.5% to 20.7% from 2016 to 2018. In patients with Community Acquired (CA-AKI3) the overall mortality rate was 24.2% (n=182), whereas the overall mortality rate of those with Hospital Acquired (HA-AKI3) was 31.3% (n=64). The pre-AKI use of ACEi, A2RB or diuretics increased from 39.7% in 2016 (n=78), to 59.3% in 2017 (n=86) and 64.6% in 2018 (n=82). Conversely, mortality associated with the use of these medications reduced each consecutive year (32.3%, 25.5%, 18.9%).Conclusion: Development of nephrology in-reach services, staff education measures and a primary care pathway could reduce AKI-3 mortality among patients in inpatient and community settings.


2019 ◽  
Vol 317 (4) ◽  
pp. G447-G452
Author(s):  
Kavish R. Patidar ◽  
Pranav S. Garimella ◽  
Etienne Macedo ◽  
James E. Slaven ◽  
Marwan S. Ghabril ◽  
...  

Acute kidney injury (AKI) is a common complication in hospitalized patients with cirrhosis. Uromodulin, a protein uniquely produced by the kidney and released both in the urine and circulation, has been shown to regulate AKI and is linked to tubular reserve. Although low levels of urine uromodulin are associated with AKI after cardiac surgery, it is unclear whether circulating uromodulin can stratify the risk of AKI, particularly in a susceptible population such as hospitalized patients with cirrhosis. Thus, we investigated whether plasma uromodulin measured at the time of admission is associated with subsequent hospital-acquired AKI (defined by a rise in serum creatinine >0.3mg/dL within 48 h or ≥ 1.5 times baseline) in patients with cirrhosis. A total of 98 patients [mean age 54 yr, Model for Endstage Liver Disease Sodium (MELD-Na) score 19, and baseline creatinine of 0.95 mg/dL] were included, of which 13% ( n = 13) developed AKI. Median uromodulin levels were significantly lower in patients who developed AKI compared with patients who did not (9.30 vs. 13.35 ng/mL, P = 0.02). After adjusting for age, sex, diabetes, hypertension, albumin, and MELD-Na score as covariates on multivariable logistic regression, uromodulin was independently associated with AKI [odd ratios of 1.19 (95% confidence interval 1.02, 1.37; P = 0.02)]. Lower uromodulin levels on admission are associated with increased odds of subsequent AKI in hospitalized patients with cirrhosis. Further studies are needed to better understand the role of uromodulin in the pathogenesis and as a predictive biomarker of AKI in this population. NEW & NOTEWORTHY In this study, we found that admission plasma uromodulin levels are significantly lower in patients who developed subsequent acute kidney injury (AKI) during their hospital stay compared with patients who did not. Additionally, uromodulin is independently associated with AKI development after adjusting for clinically relevant parameters such as age, sex, diabetes, hypertension, severity of cirrhosis, and kidney function. To our knowledge, this is the first study linking plasma uromodulin with AKI development in patients with cirrhosis.


2018 ◽  
Vol 33 (suppl_1) ◽  
pp. i122-i122
Author(s):  
Nora Sarishvili ◽  
Irma Tchockonelidze ◽  
Nona Babutsidze ◽  
Tamar Tevdoradze ◽  
Tamar Kasradze ◽  
...  

2020 ◽  
Vol 8 (21) ◽  
pp. 1438-1438
Author(s):  
Yanqin Li ◽  
Mengqi Xiong ◽  
Minliang Yang ◽  
Long Wang ◽  
Sheng Nie ◽  
...  

2019 ◽  
Vol 317 (2) ◽  
pp. F264-F274 ◽  
Author(s):  
Satoshi Tanimura ◽  
Katsuyuki Tanabe ◽  
Hiromasa Miyake ◽  
Kana Masuda ◽  
Keigo Tsushida ◽  
...  

Acute kidney injury (AKI) is frequently encountered in clinical practice, particularly secondarily to cardiovascular surgery and administration of nephrotoxic agents, and is increasingly recognized for initiating a transition to chronic kidney disease. Clarifying the pathogenesis of AKI could facilitate the development of novel preventive strategies, because the occurrence of hospital-acquired AKI is often anticipated. Vasohibin-1 (VASH1) was initially identified as an antiangiogenic factor derived from endothelial cells. VASH1 expression in endothelial cells has subsequently been reported to enhance cellular stress tolerance. Considering the importance of maintaining peritubular capillaries in preventing the progression of AKI, the present study aimed to examine whether VASH1 deletion is involved in the pathogenesis of cisplatin-induced AKI. For this, we injected male C57BL/6J wild-type (WT) and VASH1 heterozygous knockout (VASH1+/−) mice intraperitoneally with either 20 mg/kg cisplatin or vehicle solution. Seventy-two hours after cisplatin injection, increased serum creatinine concentrations and renal tubular injury accompanied by apoptosis and oxidative stress were more prominent in VASH1+/− mice than in WT mice. Cisplatin-induced peritubular capillary loss was also accelerated by VASH1 deficiency. Moreover, the increased expression of ICAM-1 in the peritubular capillaries of cisplatin-treated VASH1+/− mice was associated with a more marked infiltration of macrophages into the kidney. Taken together, VASH1 expression could have protective effects on cisplatin-induced AKI probably by maintaining the number and function of peritubular capillaries.


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