Coronavirus Disease 2019 and Hypertension: How Anti-Hypertensive Drugs Affect COVID-19 Medications and Vice Versa.

BACKGROUND: As a medical problem, hypertension is one of the most common disorders in cardiovascular disease. High blood pressure has been identified as one of the most familiar risk factors for the ongoing COVID-19 pandemic. We planned to explore the possible interactions between anti-hypertensive agents and drugs targeting SARS-CoV-2 with broad investigations on these medications' mechanism of action and adverse effects. METHOD: Two co-authors searched the electronic databases (PubMed, Scopus, and Google Scholar) to collect papers relevant to the subject. The keywords searched were angiotensin-converting enzyme inhibitors (ACEI), angiotensin-II receptor blockers (ARBs), sympatholytic drugs (alpha-1 blockers, beta-blockers), vasodilators (calcium channel blockers, nitrates, and hydralazine), diuretics, chloroquine, hydroxychloroquine, lopinavir/ritonavir, remdesivir, favipiravir, interferons, azithromycin, anti-cytokine agents, glucocorticoids, anticoagulant agents, nitric oxide and epoprostenol. RESULTS: QT prolongation, hypokalemia, arrhythmia, and increasing the serum level of drugs are the most dangerous adverse effects in the patients on COVID-19 medications and anti-hypertensive drugs. CONCLUSION: This review emphasized the importance of the potential interaction between drugs used against COVID-19 and anti-hypertensive agents and caution must be exercised when these medications are being used simultaneously.

Potential Mechanisms of the SARS-CoV-2-induced AKI Progression to CKD: A Forward-Looking Perspective

Coronavirus disease 2019 (COVID‑19) was identified in December 2019 and is still expanding in most parts of the world. The wide variety of affected organs is likely based upon the shared expression of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) important entry-receptor angiotensin-converting enzyme 2 (ACE2). For this reason, the broad distribution of ACE2 receptors in different tissues plays a crucial role in the multi-organ dysfunction and fatality due to COVID-19. Because of the high prevalence of acute kidney injury (AKI) in patients with COVID-19, we review the molecular understanding into viral infection mechanisms and implications for AKI. Furthermore, mechanisms of the AKI to chronic kidney disease (CKD) progression, such as the relative contribution of immune cell reaction, fibroblasts activation, endothelial dysfunction, and subsequent hypoxia may contribute to the association of AKI with worse outcomes during this virus pandemic. We highlight the state of the knowledge on SARS-CoV-2-dependent mechanisms for AKI and list the potential management choices for the prevention of AKI aggravation and the impending possibility of CKD. Finally, we intend to provide a much better understanding of why Coronavirus induces AKI and its subsequent progression to CKD in the coming years and further discuss the acute and long-term renal consequences. DOI: 10.52547/ijkd.6311

Is COVID-19 a risk factor for progression of benign prostatic hyperplasia and exacerbation of its related symptoms?: a systematic review.

BACKGROUND: To explore the potential mechanisms of SARS-CoV-2 in targeting the prostate gland, leading to exacerbation of benign prostatic hyperplasia (BPH) symptoms and greater risks of BPH complications such as acute urinary retention. METHODS: A categorized and comprehensive search in the literature has been conducted by 10 April 2021 using international databases including PubMed, Embase, Web of Science, Scopus, and Cochrane Library in line with the PRISMA guidelines recommendations. PICO strategy was used to formulate the research question. The following terms were used: urology, COVID-19, coronavirus, BPH, inflammation, androgen receptors, LUTS, IPSS, PSA, and SARS-CoV-2 or a combination of them. Studies with irrelevant purposes and duplicates were excluded. The selected studies were performed on humans and published in English. RESULTS: The research revealed 89 articles. After title screening and considering exclusion criteria, 52 papers were included for the systematic review. BPH is a common condition affecting older men. SARS-CoV-2 infects the host cell by binding to angiotensin converting enzyme 2 (ACE2). A hyperactivated RAS system during infection with SARS-CoV-2 may lead to activation of pro-inflammatory pathways and increased cytokine release. Thus, this virus can lead to exacerbation of lower urinary tract symptoms (LUTS) and trigger inflammatory processes in the prostate gland. Since androgen receptors (AR) play an important role in the BPH pathophysiology and infection with SARS-CoV-2 may be androgen-mediated, BPH progression and its related symptoms can be a complication of COVID-19 through AR involvement and metabolic disturbances. CONCLUSIONS: Based on the current findings, SARS-CoV-2 can possibly damage the prostate and worsen BPH and its related LUTS through ACE2 signaling, AR-related mechanisms, inflammation, and metabolic derangement. We encourage future studies to investigate the possible role of COVID-19 in the progression of BPH-related LUTS and examine the prostatic status in susceptible patients with relevant available questionnaires (e.g., IPSS) and serum biomarkers (e.g., PSA).

Potential mechanisms of SARS-CoV-2 action on male gonadal function and fertility: Current status and future prospects.

The novel coronavirus was recognised in December 2019 and caught humanity off guard. The virus employs the angiotensin-converting enzyme 2 (ACE2) receptor for entry into human cells. ACE2 is expressed on different organs, which is raising concern as to whether these organs can be infected by the virus or not. The testis appears to be an organ enriched with levels of ACE2, while the possible mechanisms of involvement of the male reproductive system by SARS-CoV-2 are not fully elucidated. The major focus of the present studies is on the short-term complications of the coronavirus and gains importance on studying the long-term effects, including the possible effects of the virus on the male reproductive system. The aim of this review was to provide new insights into different possible mechanisms of involvement of male gonads with SARS-CoV-2 including investigating the ACE2 axis in testis, hormonal alterations in patients with COVID-19, possible formation of anti-sperm antibodies (ASA) and subsequently immunological infertility as a complication of SARS-CoV-2 infection. Finally, we suggest measuring the sperm DNA fragmentation index (DFI) as a determiner of male fertility impairment in patients with COVID-19 along with other options such as sex-related hormones and semen analysis. Invasion of SARS-CoV-2 to the spermatogonia, Leydig cells and Sertoli cells can lead to sex hormonal alteration and impaired gonadal function. Once infected, changes in ACE2 signalling pathways followed by oxidative stress and inflammation could cause spermatogenesis failure, abnormal sperm motility, DNA fragmentation and male infertility.