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Patients with COVID-19 may experience multiple conditions (e.g., fever, hyperventilation, anorexia, gastroenteritis, acid-base disorder) that may cause electrolyte imbalances. Hypokalemia is a concerning electrolyte disorder that may increase the susceptibility to various kinds of arrhythmia. This study aimed to estimate prevalence, risk factors and outcome of hypokalemia in a cohort of non-critically ill patients. A retrospective analysis was conducted on 290 hospitalized patients with confirmed COVID-19 infection at the tertiary teaching hospital of Modena, Italy. Hypokalemia (<3.5 mEq/L) was detected in 119 patients (41%). The decrease of serum potassium level was of mild entity (3-3.4 mEq/L) and occurred in association with hypocalcemia (P=0.001) and lower level of serum magnesium (P=0.028) compared to normokaliemic patients. Urine K: creatinine ratio, measured in a small subset of patients (n=45; 36.1%), showed an increase of urinary potassium excretion in the majority of the cases (95.5%). Causes of kaliuria were diuretic therapy (53.4%) and corticosteroids (23.3%). In the remaining patients, urinary potassium loss was associated with normal serum magnesium, low sodium excretion (FENa< 1%) and metabolic alkalosis. Risk factors for hypokalemia were female gender (P=0.002; HR 0.41, 95%CI 0.23-0.73) and diuretic therapy (P=0.027; HR 1.94, 95%CI 1.08-3.48). Hypokalemia, adjusted for sex, age and SOFA score, resulted not associated with ICU admission (P=0.131, 95% CI 0.228-1.212) and in-hospital mortality (P=0.474; 95% CI 0,170-1,324) in our cohort of patients. Hypokalemia is a frequent disorder in COVID-19 patients and urinary potassium loss may be the main cause of hypokalemia. The disorder was mild in the majority of the patients and was unrelated to poor outcomes. Nevertheless, hypokalemic patients required potassium supplements to dampen the risk of arrhythmias.

<i>Staphylococcus aureus</i> is a Gram-positive bacterium commonly associated with severe infections in hospitalized patients. <i>S. aureus</i> produces many virulence factors leading to local and distant pathological processes. Invasiveness of <i>S. aureus</i> generally induces metastatic infections such as bacteremia, infective endocarditis, osteomyelitis, arthritis, and endophthalmitis. Peritoneal localization from extra-abdominal infection can be a potential consequence of <i>S. aureus</i> infection. Two cases of metastatic peritonitis have been described in patients on peritoneal dialysis with concomitant peripheral vascular catheter-related bloodstream infection. We reported a case of peritoneal metastatic infection caused by methicillin-resistant <i>Staphylococcus aureus</i> (MRSA) in a patient on maintenance hemodialysis. A 37-year-old man was admitted with fever and chill due to jugular central vascular catheter (CVC)-related bloodstream infection caused by MRSA<i>.</i> CVC was placed after switching the patient from peritoneal dialysis to hemodialysis for scarce adherence to fluid restriction. Detection of MRSA on the peritoneal effluent combined with a total white blood cell count of 554 cells/mm³ prompted the diagnosis of satellite MRSA peritonitis. Antibiotic treatment with daptomycin and simultaneous CVC and peritoneal catheter removal resolved the infectious process. No further metastatic localizations were detected elsewhere. In conclusion, <i>S. aureus</i> can induce metastatic infections far from the site of primary infection. As reported in this case, peritonitis can be secondary to the hematogenous dissemination of <i>S. aureus</i> especially in hospitalized patients having a central line.

Background and Aims Hemophagocytic lymphohistiocytosis (HLH) is a severe hyperinflammatory syndrome induced by aberrantly activated macrophages and cytotoxic T cells. The primary (genetic) form, caused by mutations affecting lymphocyte cytotoxicity and immune regulation, is most common in children, whereas the secondary (acquired) form is most frequent in adults. Secondary HLH is commonly triggered by infections or malignancies but may also be induced by autoinflammatory/autoimmune disorders, in which case it is called macrophage activation syndrome. The diagnosis of HLH in adults should be based on the HLH-2004 diagnostic criteria in conjunction with clinical judgment and the patient’s history. Renal involvement has previously been reported in 24 adult cases, mostly as acute renal failure. Collapsing glomerulopathy is extremely rare with only six previous cases reported in the literature. Case presentation We report the case of an African man, 31 years old, presented with fever, acute kidney injury: serum creatinine 10.3 mg/dl; urine protein 600 mg/dl, macrohematuria, ANA/ANCA were negative, low serum C3, organomegaly, anemia, thrombocytopenia, hypertriglyceridemia, hypofibrinogenemia, hyperferritinemia, direct and indirect antiglobulin (Coombs) tests were negative, low haptoglobin; elevated LDH; normal partial thromboplatin time. Peripheral blood smear examination reveal few schistocytes. ADAMTS13 activity was found to be 25%. HBV-DNA and HIV were negative. Anticardiolipin antibodies were negative. Lab exam suggested the relapse of an EBV infection and primary mycoplasma infection. Because of uremic symptoms and persisting oliguria we started replacement therapy by hemodialysis. Plasmapheresis was started because of suspected thrombotic microangiopathy. Suprisingly the kidney biopsy was consistent with collapsing glomerulopathy with evidence of tubular injury while the bone marrow biopsy diagnosed an EBV NK/T-Cell lymphoma. During the course of his hospitalization, the patient suffered high fever. C-reactive protein, WBC and procalcitonin levels were elevated. Antimicrobial agents were initiated, starting with ceftriaxone then upgraded to piperacillin/tazobactam and then the shifted to teicoplanin and meropenem. Blood, urine and stool cultures were negative.VRE positive, IgM Mycoplasma pneumoniae were positive; EBV PCR on bone marrow blood was positive. Malaria screening was negative. The antibiotic therapy was finally switched to doxycycline as unique agent. Steroid therapy (dexamethasone daily 40 mg) and IVIG (daily 35g) were initiated then these drug were stopped. CHOP-like regimen ( Etoposide 75 mg/m2, twice a week for two weeks then once a week until the seventh week) and Rituximab (375 mg/m2, once a week for 4 weeks) were initiated and continued for two weeks. Later on the patient died because of sepsis and multi-organ failure. Conclusions The multidisciplinary approach is very important. Physicians should be aware of HLH, because early recognition may prevent irreversible organ damage and subsequent death.4,5 In adults, HLH-associated mortality remains high, especially in patients with underlying malignancies. Collapsing glomerulopathy is the most commonly reported finding on renal biopsy. Renal prognosis appears to be poor with most patients remaining dialysis-dependent. The increased awareness of HLH, together with a more rapid diagnostic workup and new therapeutic approaches, will improve the prognosis of HLH in adults.