Since the first emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), also known as novel coronavirus (2019-nCoV), in Wuhan, China, in December 2019 (Tan et al., 2020), the virus has spread rapidly worldwide and, therefore, has been officially declared a pandemic outbreak with more than 10 million confirmed cases and 499,000 deaths according to the WHO report (Situation Report, 2020). Pneumonia with fever seems to be the most common presentation of SARS-CoV-2 infection (Guan et al., 2020; Wang, Hu et al., 2020). SARS-CoV-2 was also detected in specimens of faeces and a small percentage of blood and urine

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).

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Background. Polycystic ovary syndrome (PCOS) is the most common reproductive disorder in premenopausal women. This syndrome is also associated with many metabolic and cardiovascular complications. These complications are major risk factors for renal injury and kidney disease. Therefore, this study aimed to investigate the types of functional and structural kidney injuries in a hyperandrogenic female rat model. Methods. Female Sprague-Dawley rats were randomly divided into three groups (n=10 each): control, sham, and dehydroepiandrosterone (DHEA). Plasma total testosterone and kidney functional indices were measured using enzyme-linked immunosorbent assay (ELISA) and colorimetric techniques. Ovarian and renal histological changes were also evaluated qualitatively and quantitatively by Hematoxylin-Eosin (H&E) staining. Results. Plasma total testosterone in the DHEA group increased about 9-fold compared to the control and sham groups. There was also a significant increase in Cr, BUN, and absolute excretion of sodium ion. Insignificant increases in glomerular filtration rate (GFR), urine flow rate (V0), and absolute excretion of potassium ion were observed in DHEA group compared to other groups. However, significant damages were observed in the glomerular and tubular parts of the kidneys and the follicular parts of the ovaries in DHEA-receiving rats. Conclusion. Hyperandrogenemia is likely to cause systemic abnormalities through a variety of mechanisms, followed by obvious destruction of kidney and ovarian tissues. Accordingly, DHEA administration provides a useful animal model for studying the mechanism of PCOS-mediated renal injury. Practical Implications. The present study Findings can be helpful in identifying the mechanism of PCOS-induced renal injury, especially in younger women.

Introduction:The underlying pathophysiology of pulmonary arterial hypertension (PAH) is multifactorial; however, the significance of chronic volume overload and its subsequent effects on cardiac function must be studied thoroughly. The main objective of this study was to determine the predictive parameters of PAH in patients undergoing continuous ambulatory peritoneal dialysis (CAPD) using transthoracic echocardiography (TTE) and bioimpedance analysis (BIA).Methods: In this cross-sectional study, 43 eligible CAPD patients were chosen. The patients were examined by TTE and BIA before the morning dialysis session, and baseline patient characteristics, echocardiography, and BIA parameters were recorded.Results: Sixteen (37.2%) patients were diagnosed with PAH. Patients with PAH had significantly greater left atrial diameter (LAD), left ventricular mass index (LVMI), and higher grades of diastolic dysfunction (DDF). Systolic pulmonary artery pressure (sPAP) correlated with LAD (p < 0.001, r = 0.566), interventricular septal diameter (IVSD) (p = 0.004, r = 0.425), LVMI (p = 0.030, r = 0.323), and extracellular water/total body water (ECW/TBW) ratio (p = 0.002, r = 0.458). Conclusion: Two volume status-related parameters including ECW/TBW ratio and inferior vena cava (IVC) expiratory diameter, and cardiac-related TTE findings such as LAD and DDF were predictors of sPAP in CAPD patients.

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Background Diabetic nephropathy occurs in about one-third of diabetic patients. This health problem is characterized by increased urinary albumin excretion, leading to decreased glomerular filtration rate and renal failure. In this regard, previous investigations have revealed the possibility of a relationship between vitamin D deficiency and diabetic nephropathy. The present study assessed the relationship between vitamin D deficiency and albuminuria in patients with type 2 diabetes. Methods This study was conducted with 200 participants with type 2 diabetes mellitus from December 2019 to January 2021. The patients’ 25-hydroxyvitamin D (25OHD) serum level and urinary albumin-to-creatinine ratio (UACR) were measured concurrently. Afterward, the subjects were divided into three groups based on their albuminuria level. Finally, 25OHD serum level and other clinical characteristics were compared among these albuminuria groups, and the relation between albuminuria level and 25OHD was analyzed. Results The prevalence of vitamin D deficiency in macroalbuminuric patients (UACR≥300 mg/g) was 61.8%, and in microalbuminuric (30 ≤ UACR< 300 mg/g) and normoalbuminuric groups (UACR< 30 mg/g) was 33.3% and 24%, respectively. Further analysis revealed a significant negative relationship between 25OHD and albuminuria(r = − 0.257, p-value< 0.001). According to ROC curve analysis, a 25OHD level ≤ 21 ng/ml was considered an optimal cut-off point value for having macroalbuminuria in diabetic patients. Conclusions The current study evaluates the relation between vitamin D deficiency and the prevalence of albuminuria in the setting of diabetes. Overall, the prevalence of macroalbuminuria increased when the 25OHD serum level was less than 20 ng/ml.