Since December 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused an outbreak of coronavirus disease 2019 (COVID-19) in the city Wuhan of China.¹ The virus invades human cells by binding angiotensin-converting enzyme 2 (ACE2) on a cell membrane² that is widely distributed in many human vital organs, such as heart, liver, kidney, and lungs.³ Angiotensin-converting enzyme 2 is the principal counter-regulatory mechanism for the main axis of the rennin-angiotensin system (RAS), which is critical in the control of blood pressure and electrolyte balance.⁴ SARS-CoV-2 binds ACE2 and enhances the degradation of ACE2 and, thus, decreases the counteraction of ACE2 on RAS. This leads to increased reabsorption of sodium and water, thereby increasing blood pressure and excretion of potassium (K⁺).⁵ In addition, patients with COVID-19 often have gastrointestinal symptoms, such as diarrhea and vomiting.⁶ Collectively, the effects of COVID-19 on RAS and the gastrointestinal system probably lead to disruptions of homeostasis of electrolytes and pH.

Aim: To investigate whether the Staphylococcus argenteus is present in Eastern China and to verify the utility of a new screening process. Materials & methods: Phenotype observation, PCR assay targeting a hypothetical nonribosomal peptide synthetase (NRPS) gene, phylogenetic analysis of rpoB and multilocus sequence typing were used to screen and identify strains of S. argenteus from 839 presumptive S. aureus isolates. Results: Eighty-nine (89/839, 10.6%) of the presumptive S. aureus isolates produced white colonies on tryptone soya agar plates. Of the white-colony isolates, six (6/89, 7%) were S. argenteus, 75 (75/89, 84%) were S. aureus and eight (8/89, 9%) were other bacteria. Conclusion: The PCR-based method targeting the NRPS gene can simultaneously identify and distinguish S. argenteus and S. aureus. All representative sequences of rpoB generated in this study were deposited in GenBank under accession numbers SJTU F20002, KT767581; SJTU F20269, KT767582; SJTU F20419, KT767583; SJTU F20420, KT767584; ...

BACKGROUND: SARS-CoV-2 has caused a series of COVID-19 globally. SARS-CoV-2 binds angiotensin I converting enzyme 2 (ACE2) of renin–angiotensin system (RAS) and causes prevalent hypokalemia METHODS: The patients with COVID-19 were classified into severe hypokalemia, hypokalemia, and normokalemia group. The study aimed to determine the relationship between hypokalemia and clinical features, the underlying causes and clinical implications of hypokalemia. RESULTS: By Feb 15, 2020, 175 patients with COVID-19 (92 women and 83 men; median age, 46 [IQR, 34–54] years) were admitted to hospital in Wenzhou, China, consisting 39 severe hypokalemia-, 69 hypokalemia-, and 67 normokalemia patients. Gastrointestinal symptoms were not associated with hypokalemia among 108 hypokalemia patients ( P > 0.05). Body temperature, CK, CK-MB, LDH, and CRP were significantly associated with the severity of hypokalemia ( P <0.01). 93% of severe and critically ill patients had hypokalemia which was most common among elevated CK, CK-MB, LDH, and CRP. Urine K ⁺ loss was the primary cause of hypokalemia. 1 severe hypokalemia patients was given 3 g/day, adding up to an average of 34 (SD=4) g potassium during hospital stay. The exciting finding was that patients responded well to K ⁺ supplements when they were inclined to recovery. CONCLUSIONS: Hypokalemia is prevailing in patients with COVID-19. The correction of hypokalemia is challenging because of continuous renal K ⁺ loss resulting from the degradation of ACE2. The end of urine K ⁺ loss indicates a good prognosis and may be a reliable, in-time, and sensitive biomarker directly reflecting the end of adverse effect on RAS system.