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Nat Rev Urol ; 19(6): 344-356, 2022 Jun.
Article in English | MEDLINE | ID: covidwho-1795727


On 11 March 2020, the WHO declared the coronavirus disease 2019 (COVID-19) outbreak a pandemic and COVID-19 emerged as one of the biggest challenges in public health and economy in the twenty-first century. The respiratory tract has been the centre of attention, but COVID-19-associated complications affecting the genitourinary tract are reported frequently, raising concerns about possible long-term damage in these organs. The angiotensin-converting enzyme 2 (ACE2) receptor, which has a central role in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) invasion, is highly expressed in the genitourinary tract, indicating that these organs could be at a high risk of cell damage. The detection of SARS-CoV-2 in urine and semen is very rare; however, COVID-19 can manifest through urological symptoms and complications, including acute kidney injury (AKI), which is associated with poor survival, severe structural changes in testes and impairment of spermatogenesis, and hormonal imbalances (mostly secondary hypogonadism). The effect of altered total testosterone levels or androgen deprivation therapy on survival of patients with COVID-19 was intensively debated at the beginning of the pandemic; however, androgen inhibition did not show any effect in preventing or treating COVID-19 in a clinical study. Thus, urologists have a crucial role in detecting and managing damage of the genitourinary tract caused by COVID-19.

COVID-19 , Prostatic Neoplasms , Androgen Antagonists , Androgens , Humans , Male , Pandemics , Prostatic Neoplasms/epidemiology , SARS-CoV-2 , Urologists
Infection ; 2021 Oct 30.
Article in English | MEDLINE | ID: covidwho-1491465


PURPOSE: To investigate the expression of the receptor protein ACE-2 alongside the urinary tract, urinary shedding and urinary stability of SARS-CoV-2 RNA. METHODS: Immunohistochemical staining was performed on tissue from urological surgery of 10 patients. Further, patients treated for coronavirus disease (COVID-19) at specialized care-units of a university hospital were assessed for detection of SARS-CoV-2 RNA in urinary samples via PCR, disease severity (WHO score), inflammatory response of patients. Finally, the stability of SARS-CoV-2 RNA in urine was analyzed. RESULTS: High ACE-2 expression (3/3) was observed in the tubules of the kidney and prostate glands, moderate expression in urothelial cells of the bladder (0-2/3) and no expression in kidney glomeruli, muscularis of the bladder and stroma of the prostate (0/3). SARS-CoV-2 RNA was detected in 5/199 urine samples from 64 patients. Viral RNA was detected in the first urinary sample of sequential samples. Viral RNA load from other specimen as nasopharyngeal swabs (NPS) or endotracheal aspirates revealed higher levels than from urine. Detection of SARS-CoV-2 RNA in urine was not associated with impaired WHO score (median 5, range 3-8 vs median 4, range 1-8, p = 0.314), peak white blood cell count (median 24.1 × 1000/ml, range 5.19-48.1 versus median 11.9 × 1000/ml, range 2.9-60.3, p = 0.307), peak CRP (median 20.7 mg/dl, 4.2-40.2 versus median 11.9 mg/dl, range 0.1-51.9, p = 0.316) or peak IL-6 levels (median: 1442 ng/ml, range 26.7-3918 versus median 140 ng/ml, range 3.0-11,041, p = 0.099). SARS-CoV-2 RNA was stable under different storage conditions and after freeze-thaw cycles. CONCLUSIONS: SARS-CoV-2 RNA in the urine of COVID-19 patients occurs infrequently. The viral RNA load and dynamics of SARS-CoV-2 RNA shedding suggest no relevant route of transmission through the urinary tract.