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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Serotonin syndrome (SS) is a potentially life-threatening condition caused by drugs that act on serotonergic receptors or alter serotonin metabolism. We present a case of SS in a middle-aged female who was taking trazodone and sertraline as her home medications and developed SS after being started on quetiapine during her hospital course. A 54-year-old female with a past medical history of dementia and bipolar disorder was brought to the emergency department from a nursing home for altered mental status. Delirium was ruled out. Initial blood work was significant for an elevated creatine phosphokinase (CPK) level of 753 U/L. She was started on Quetiapine 100 mg bis in die (BID) after admission as she had a history of bipolar disorder and she was having acute mood symptoms (impulsive, irritable, confrontational, belligerent, and unable to be redirected). On the second day of admission, the patient started having diaphoresis, tremors, hyperreflexia, myoclonus, and ocular clonus. A diagnosis of SS was made using Hunter's criteria. All serotonergic medications were discontinued after which the patient started improving. She was also started on supportive therapy including IV fluids, lorazepam, and cyproheptadine. The patient was discharged on the fourth day of admission.