Chronic kidney disease (CKD) is a debilitating progressive illness that affects more than 10% of the world's population. In this literature review, we discussed the roles of nutritional interventions, lifestyle modifications, hypertension (HTN) and diabetes mellitus (DM) control, and medications in delaying the progression of CKD. Walking, weight loss, low-protein diet (LPD), adherence to the alternate Mediterranean (aMed) diet, and Alternative Healthy Eating Index (AHEI)-2010 slow the progression of CKD. However, smoking and binge alcohol drinking increase the risk of CKD progression. In addition, hyperglycemia, altered lipid metabolism, low-grade inflammation, over-activation of the renin-angiotensin-aldosterone system (RAAS), and overhydration (OH) increase diabetic CKD progression. The Kidney Disease: Improving Global Outcomes (KDIGO) guidelines recommend blood pressure (BP) control of <140/90 mmHg in patients without albuminuria and <130/80 mmHg in patients with albuminuria to prevent CKD progression. Medical therapies aim to target epigenetic alterations, fibrosis, and inflammation. Currently, RAAS blockade, sodium-glucose cotransporter-2 (SGLT2) inhibitors, pentoxifylline, and finerenone are approved for managing CKD. In addition, according to the completed Study of Diabetic Nephropathy with Atrasentan (SONAR), atrasentan, an endothelin receptor antagonist (ERA), decreased the risk of renal events in diabetic CKD patients. However, ongoing trials are studying the role of other agents in slowing the progression of CKD.

Introduction/Objective BTEX (benzene, toluene, ethylbenzene, and xylene) is well know for its toxicity via through environmental, occupational and recreational exposures. However, there is limited literature about the carcinogenic effect of BTEX. Hence, we aim to study the prevalence and association of cancer amongst individuals with exposure of BTEX. Methods/Case Report A retrospective cross-sectional study was performed between 2013 and 2018 utilizing the NHANES database. Adult individuals having data on socio-demographic questionnaires and lab findings on exposure to BTEX were included. Prevalence of cancer was identified amongst exposure to BTEX (vs no-BTEX). Univariate (chi-squre test and Mann–Whitney U test) and Multivariate (survey logistic regression) analysis was performed to evaluate the epidemiologic characteristics of individuals exposred to BTEX and association of cancer with BTEX exposure in comparison to no BTEX exposure.The p value of &lt;0.05 considered statistically significant. Results (if a Case Study enter NA) 124,162 participants were identified with BTEX exposure. Individuals with BTEX exposure were young (40 vs 51 year old), male (91% vs female: 87%), and Mexican American (92% vs Non-Hispanic Black: 89% vs Non-Hispanic White: 89% vs other Hispanic: 87%). Univariate analysis showed higher total prevalence of cancer in BTEX (9.3% vs. 1.3%; p&lt;0.0001) compared to no BTEX. Individuals with BTEX exposure had higher prevalnece of blood cancer (0.47% vs 0.00; p&lt;0.0001), leukemia (0.56% vs 0.00; p&lt;0.001), and lymphoma (1.72% vs 0.39%; p&lt;0.0001) in comparison with no exposure. Multivaritate analysis showed participants with BTEX exposure had 10% higher risk of cancer (aOR: 1.10; 95%CI: 1.10-1.10; p&lt;0.0001) compared to no BTEX exposure. Additionally, exposure to individual components of benzene (aOR: 1.24; 95%CI: 1.24; p&lt;0.0001), ethylbenzene (aOR: 1.08; 95%CI: 1.08-1.08; p&lt;0.0001), and o-xylene (aOR: 1.19; 95%CI: 1.19-1.19; p&lt;0.0001) had higher risk of cancer compared to no exposure participants. Conclusion Our study conclude higher risk of cancer among participants with exposure to benzene, ethylbenzene and o-xylene. Future studies are warranted to evaluate the association of various types of cancers in BTEX exposure.

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e16543 Background: The clear cell renal cell carcinoma (ccRCC) is the most prevalent genitourinary cancer, and carries a poor prognosis. Information regarding whole genome sequencing, a prognostic prediction system, and overall survival in ccRCC is limited. While loss of VHL is commonly implicated in ccRCC, two genes indicated in other cancers, SDHD and ARID1A, have limited literature on their correlation to ccRCC. Hence, we aimed to analyze the genomic profile, epidemiological characteristics and overall survival of ccRCC. Methods: We utilized cBioPortal cancer genomics [The Cancer Genome Atlas (TCGA) PanCancer Atlas, TCGA Firehose Legacy, and TCGA Nature 2013] to study the genetic mutations associated with ccRCC. Epidemiological characteristics and genetic profiles were evaluated, and a query was generated to calculate 5 year and 10 year survival rate with the most common mutations. Log-rank test and Kaplan–Meier estimator were used in analyzing the survival function. Patients with two or more overlapping mutations (72) were excluded. Results: We identified 761 patients with ccRCC, out of which 442 had primary ccRCC with all demographic details available. 65.8% were males, 58.1% were Caucasian, and 7.2% were African American. Majority of patients (199) were between the ages of 50-65 years. 286 (64.7%) were alive and 156 (35.3%) were deceased. The common mutations associated with reduced survival were VHL, BAP1, SDHA, SDHD, and ARID1A. Median survival of patients with VHL, BAP1, SDHA, SDHD, ARID1A mutations was 118.85, 93.04, 40.70, 2.04, and 6.02 months respectively in comparison with unaltered mutation group (78.44 months) (p < 0.0001). (Table 1) Survival was lowest amongst SDHD [2.04 months] and ARID1A [6.02 months]. (p = 3.26e-10). In survival analysis, SDHD and ARID1A were associated with lowest survival after initial diagnosis at 60 months (Figure 1) and 120 months (Figure 2). (p = 2.592e-3). Conclusions: Our study found that SDHD, ARID1A, and SDHA genes were associated with the worst prognosis in ccRCC with median survival of 2.04, 6.02, and 40.70 months. This study may provide insight for targeted therapies for ccRCC and improve the prognosis of these patients. [Table: see text]

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