scholarly journals Ethnicity-Stratified Analysis of the Association between TNF-α Genetic Polymorphisms and Acute Kidney Injury: A Systematic Review and Meta-Analysis

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Guanzhong Chen ◽  
Bowen Liu ◽  
Huanqiang Li ◽  
Ziling Mai ◽  
Liyao Zhang ◽  
...  

Background. Several studies have reported conflicting findings regarding the association between tumor necrosis factor-alpha (TNF-α) genetic polymorphisms and acute kidney injury (AKI). Therefore, we performed this meta-analysis to further investigate whether TNF-α variants are related to AKI susceptibility. Methods. A comprehensive search of observational studies on the association of TNF-α polymorphism with AKI susceptibility was conducted in the PubMed, Cochrane, and Embase databases through February 10, 2020. Pooled odds ratios (ORs) and 95% corresponding confidence intervals (95% CIs) were analyzed to evaluate the strength of the relationship. Results. A total of 8 studies involving 6694 patients (2559 cases and 4135 controls) were included. Pooled analysis showed a trend of increased risk between the TNF-α rs1800629 variant and AKI (A vs. G: OR   95 % CI = 1.33   0.98 ‐ 1.81 ) among the overall population. Ethnicity-stratified analysis indicated that the TNF-α rs1800629 variant was a risk factor for Asians ( OR   95 % CI = 1.93   1.59 ‐ 2.35 ) while it is not for Caucasians ( OR   95 % CI = 1.04   0.91 ‐ 1.20 ). Additionally, we also found that TNF-α rs1799964 polymorphism was observed to have a significant relationship with AKI risk in Asian patients (C vs. T, OR   95 % CI = 1.26   1.11 ‐ 1.43 ). Conclusions. The TNF rs1800629 polymorphism exhibited a trend toward AKI susceptibility with ethnic differences. The relationship was found to be significant among the Asian population, but not among those of Caucasian origin. Additionally, the TNF-α rs1799964 polymorphism was also related to a significantly increased risk of AKI in Asians.

2021 ◽  
pp. 1-23
Author(s):  
Zhubin Lun ◽  
Ziling Mai ◽  
Liwei Liu ◽  
Guanzhong Chen ◽  
Huanqiang Li ◽  
...  

<b><i>Objective:</i></b> Previous studies have shown that the relationship between hypertension (HT) and contrast-associated acute kidney injury (CA-AKI) is not clear. We apply a systematic review and meta-analysis to assess the association between HT and CA-AKI. <b><i>Methods:</i></b> We searched for articles on the study of risk factors for CA-AKI in the Embase, Medline, and Cochrane Database of Systematic Reviews (by March 25, 2021). Two authors independently performed quality assessment and extracted data such as the studies’ clinical setting, the definition of CA-AKI, and the number of patients. The CA-AKI was defined as a serum creatinine (SCr) increase ≥25% or ≥0.5 mg/dL from baseline within 72 h. We used fixed or random models to pool adjusted OR (aOR) by STATA. <b><i>Results:</i></b> A total of 45 studies (2,830,338 patients) were identified, and the average incidence of CA-AKI was 6.48%. There was an increased risk of CA-AKI associated with HT (aOR: 1.378, 95% CI: 1.211–1.567, <i>I</i><sup>2</sup> = 67.9%). In CA-AKI with a SCr increase ≥50% or ≥0.3 mg/dL from baseline within 72 h, an increased risk of CA-AKI was associated with HT (aOR: 1.414, 95% CI: 1.152–1.736, <i>I</i><sup><i>2</i></sup> = 0%). In CA-AKI with a Scr increase ≥50% or ≥0.3 mg/dL from baseline within 7 days, HT increases the risk of CA-AKI (aOR: 1.317, 95% CI: 1.049–1.654, <i>I</i><sup><i>2</i></sup> = 51.5%). <b><i>Conclusion:</i></b> Our meta-analysis confirmed that HT is an independent risk factor for CA-AKI and can be used to identify risk stratification. Physicians should pay more attention toward prevention and treatment of patients with HT in clinical practice.


2019 ◽  
Vol 8 (3) ◽  
pp. 372 ◽  
Author(s):  
Charat Thongprayoon ◽  
Wisit Kaewput ◽  
Natanong Thamcharoen ◽  
Tarun Bathini ◽  
Kanramon Watthanasuntorn ◽  
...  

Background: The study’s aim was to summarize the incidence and impacts of post-liver transplant (LTx) acute kidney injury (AKI) on outcomes after LTx. Methods: A literature search was performed using the MEDLINE, EMBASE and Cochrane Databases from inception until December 2018 to identify studies assessing the incidence of AKI (using a standard AKI definition) in adult patients undergoing LTx. Effect estimates from the individual studies were derived and consolidated utilizing random-effect, the generic inverse variance approach of DerSimonian and Laird. The protocol for this systematic review is registered with PROSPERO (no. CRD42018100664). Results: Thirty-eight cohort studies, with a total of 13,422 LTx patients, were enrolled. Overall, the pooled estimated incidence rates of post-LTx AKI and severe AKI requiring renal replacement therapy (RRT) were 40.7% (95% CI: 35.4%–46.2%) and 7.7% (95% CI: 5.1%–11.4%), respectively. Meta-regression showed that the year of study did not significantly affect the incidence of post-LTx AKI (p = 0.81). The pooled estimated in-hospital or 30-day mortality, and 1-year mortality rates of patients with post-LTx AKI were 16.5% (95% CI: 10.8%–24.3%) and 31.1% (95% CI: 22.4%–41.5%), respectively. Post-LTx AKI and severe AKI requiring RRT were associated with significantly higher mortality with pooled ORs of 2.96 (95% CI: 2.32–3.77) and 8.15 (95%CI: 4.52–14.69), respectively. Compared to those without post-LTx AKI, recipients with post-LTx AKI had significantly increased risk of liver graft failure and chronic kidney disease with pooled ORs of 3.76 (95% CI: 1.56–9.03) and 2.35 (95% CI: 1.53–3.61), respectively. Conclusion: The overall estimated incidence rates of post-LTx AKI and severe AKI requiring RRT are 40.8% and 7.0%, respectively. There are significant associations of post-LTx AKI with increased mortality and graft failure after transplantation. Furthermore, the incidence of post-LTx AKI has remained stable over the ten years of the study.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dong Wang ◽  
Liqun He ◽  
Xiaotian Zhang

AbstractMany studies tried to assess the relationship between -308G/A polymorphism of tumor necrosis factor alpha (TNF-α) gene and risk of metabolic syndrome (MS), but their results were contradictory. This meta-analysis aimed to precisely evaluate this association. A systematic literature search was performed in Pubmed database and WanFang Med Online, STATA software 14.0 was used for the meta-analysis. Eleven independent studies containing 3277 cases and 3312 controls were included in our meta-analysis. In overall analysis, significant association was found between -308G/A polymorphism of TNF-α and MS in both allele model (OR 1.47, 95% CI 1.09–1.98, P 0.013) and dominant model (OR 1.77, 95% CI 1.21–2.58, P 0.003). In the subgroup analysis, the A allele was associated with increased risk of MS in Asia group (allele model: OR 1.82 95% CI 1.31–2.53, P < 0.001; dominant model: OR 2.30, 95% CI 1.64–3.21 P < 0.001; homozygous model: OR 2.29, 95% CI 1.31–4.01, P 0.004), and decreased risk of MS in Europe group (dominant model: OR 0.83, 95% CI 0.70–0.99, P < 0.001; recessive model: OR 0.51, 95% CI 0.28–0.92, P 0.025; homozygous model: OR 0.49 95% CI 0.27–0.89, P 0.02). The A allele also appeared to linked to increased risk of MS in CDS group and IDF groups. No significant association was observed in NCEPATPIII group. Our results suggested that -308G/A of TNF-α gene was a risk factor for MS, but it may played different roles in different ethnics, further studies with larger sample size and more other ethnics should be performed to confirm our conclusions.


2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Raju K. Mandal ◽  
Munawwar Ali Khan ◽  
Arif Hussain ◽  
Naseem Akhter ◽  
Arshad Jawed ◽  
...  

Abstract Purpose: Tumor necrosis factor-α (TNF-α), secreted by the activated macrophages, may participate in the onset and progression of colorectal cancer (CRC). The association of TNF-α –308 G&gt;A (rs1800629) single-nucleotide polymorphism (SNP) with CRC risk has been investigated by many studies but the results are inconclusive. A trial sequential meta-analysis was performed for precise estimation of the relationship between TNF-α –308 G&gt;A gene polymorphism with CRC risk. Methods: Medline (PubMed), EMBASE (Excerpta-Medica) and Google Scholar were mined for relevant articles. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to estimate the significance of association. Results: The pooled analysis indicated no risk associated with TNF-α –308 G&gt;A SNP and overall CRC risk in five genetic comparison models, i.e. allelic (A vs. G: P = 0.524; OR = 1.074, 95% CI = 0.863–1.335), homozygous (AA vs. GG: P = 0.489; OR = 1.227, 95% CI = 0.688–2.188), heterozygous (AG vs. GG: P = 0.811; OR = 1.024, 95% CI = 0.843–1.244), dominant (AA+AG vs. GG: P = 0.630; OR = 1.055, 95% CI = 0.849–1.311) and recessive (AA vs. AG+GG: P = 0.549; OR = 1.181, 95% CI = 0.686–2.033). Subgroup analysis revealed that TNF-α –308 G&gt;A SNP is associated with reduced risk of CRC in Asian ethnicity. The study showed no publication bias. Conclusions: No association of TNF-α –308 G&gt;A SNP with overall CRC risk was found. This SNP is likely to be protective against CRC in Asian population when compared with Caucasian population. Larger prospective-epidemiological studies are warranted to elucidate the roles of TNF-α –308 G&gt;A SNP in the etiology of CRC and to endorse the present findings.


2019 ◽  
Vol 69 (11) ◽  
pp. 1881-1887 ◽  
Author(s):  
Doaa M Aljefri ◽  
Sean N Avedissian ◽  
Nathaniel J Rhodes ◽  
Michael J Postelnick ◽  
Kevin Nguyen ◽  
...  

Abstract Background This study analyzed the relationship between vancomycin area under the concentration-time curve (AUC) and acute kidney injury (AKI) reported across recent studies. Methods A systematic review of PubMed, Medline, Scopus, and compiled references was conducted. We included randomized cohort and case-control studies that reported vancomycin AUCs and risk of AKI (from 1990 to 2018). The primary outcome was AKI, defined as an increase in serum creatinine of ≥0.5 mg/L or a 50% increase from baseline on ≥2 consecutive measurements. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. Primary analyses compared the impact of AUC cutpoint (greater than ~650 mg × hour/L) and AKI. Additional analysis compared AUC vs trough-guided monitoring on AKI incidence. Results Eight observational studies met inclusion/exclusion criteria with data for 2491 patients. Five studies reported first-24-hour AUCs (AUC0-24) and AKI, 2 studies reported 24- to 48-hour AUCs (AUC24-48) and AKI, and 2 studies reported AKI associated with AUC- vs trough-guided monitoring. AUC less than approximately 650 mg × hour/L was associated with decreased AKI for AUC0-24 (OR, 0.36 [95% CI, .23–.56]) as well as AUC24-48 (OR, 0.45 [95% CI, .27–.75]). AKI associated with the AUC monitoring strategy was significantly lower than trough-guided monitoring (OR, 0.68 [95% CI, .46–.99]). Conclusions AUCs measured in the first or second 24 hours and lower than approximately 650 mg × hour/L may result in a decreased risk of AKI. Vancomycin AUC monitoring strategy may result in less vancomycin-associated AKI. Additional investigations are warranted.


2020 ◽  
Vol 10 (4) ◽  
pp. 250-256
Author(s):  
J. Tyler Haller ◽  
Keaton Smetana ◽  
Michael J. Erdman ◽  
Todd A. Miano ◽  
Heidi M. Riha ◽  
...  

Background and Purpose: While an association between hyperchloremia and worse outcomes, such as acute kidney injury and increased mortality, has been demonstrated in hemorrhagic stroke, it is unclear whether the same relationship exists after acute ischemic stroke. This study aims to determine the relationship between moderate hyperchloremia (serum chloride ≥115 mmol/L) and acute kidney injury in patients with ischemic stroke. Methods: This is a multicenter, retrospective, propensity-matched cohort study of adults admitted for acute ischemic stroke. The primary objective was to determine the relationship between moderate hyperchloremia and acute kidney injury, as defined by the Acute Kidney Injury Network criteria. Secondary objectives included mortality and hospital length of stay. Results: A total of 407 patients were included in the unmatched cohort (332 nonhyperchloremia and 75 hyperchloremia) and 114 patients (57 in each group) were matched based upon propensity scores. In the matched cohort, hyperchloremia was associated with an increased risk of acute kidney injury (relative risk 1.91 [95% confidence interval 1.01-3.59]) and a longer hospital length of stay (16 vs 12 days; P = .03). Mortality was higher in the hyperchloremia group (19.3% vs 10.5%, P = .19), but this did not reach statistical significance. Conclusions: In this study, hyperchloremia after ischemic stroke was associated with increased rates of acute kidney injury and longer hospital length of stay. Further research is needed to determine which interventions may increase chloride levels in patients with acute ischemic stroke and the association between hyperchloremia and clinical outcomes.


Genes ◽  
2019 ◽  
Vol 10 (5) ◽  
pp. 364 ◽  
Author(s):  
Zulfan Zazuli ◽  
Leila S. Otten ◽  
Britt I. Drögemöller ◽  
Mara Medeiros ◽  
Jose G. Monzon ◽  
...  

Although previous research identified candidate genetic polymorphisms associated with cisplatin nephrotoxicity, varying outcome definitions potentially contributed to the variability in the effect size and direction of this relationship. We selected genetic variants that have been significantly associated with cisplatin-induced nephrotoxicity in more than one published study (SLC22A2 rs316019; ERCC1 rs11615 and rs3212986; ERCC2 rs1799793 and rs13181) and performed a replication analysis to confirm associations between these genetic polymorphisms and cisplatin nephrotoxicity using various outcome definitions. We included 282 germ cell testicular cancer patients treated with cisplatin from 2009–2014, aged >17 years recruited by the Canadian Pharmacogenomics Network for Drug Safety. Nephrotoxicity was defined using four grading tools: (1) Common Terminology Criteria for Adverse Events (CTCAE) v4.03 for acute kidney injury (AKI) or CTCAE-AKI; (2) adjusted cisplatin-induced AKI; (3) elevation of serum creatinine; and (4) reduction in the estimated glomerular filtration rate (eGFR). Significant associations were only found when using the CTCAE v4.03 definition: genotype CA of the ERCC1 rs3212986 was associated with decreased risk of cisplatin nephrotoxicity (ORadj = 0.24; 95% CI: 0.08–0.70; p = 0.009) compared to genotype CC. In contrast, addition of allele A at SLC22A2 rs316019 was associated with increased risk (ORadj = 4.41; 95% CI: 1.96–9.88; p < 0.001) while genotype AC was associated with a higher risk of cisplatin nephrotoxicity (ORadj = 5.06; 95% CI: 1.69–15.16; p = 0.004) compared to genotype CC. Our study showed that different case definitions led to variability in the genetic risk ascertainment of cisplatin nephrotoxicity. Therefore, consensus on a set of clinically relevant outcome definitions that all such studies should follow is needed.


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