Déséquilibre de potassium par la COVID ?

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Persistent Hypokalemia post SARS-coV-2 infection, is it a life-long complication? Case report
Annals of Medicine and Surgery Volume 62, February 2021, Pages 358-361 Mohammed Obaid Alnafiey

Highlights
• COVID-19 is a new disease and its complications are not fully understood.
• The alteration of the ACE2 receptors and RAS system dysregulation lasted for 5 months.
• Presistent electrolytes disturbance after COVID-19 infection is a burden on both patients and their treating physicians.

Introduction and importance
SARS-CoV-2 is a novel infection that has affected millions of people around the world. Complications of the infection may affect multiple systems including cardiovascular, neurological, gastrointestinal, urinary, and pulmonary systems. Hypokalemia, which is a life-threatening condition that may lead to arrhythmia and possibly death, has been noticed in more than half of the COVID-19 patients. Further understanding of the disease process and its complications is necessary to guide in preventing the complications from happening in the first place and finding treatment for patients with an already established complications.

Case presentation
A 34-year old male from Philippines who lives in Saudi Arabia – Riyadh and works as health care provider with no previous history of any medical illness. Presented by himself to the emergency department (ED) with dry cough, shortness of breath, fever, malaise, and fatigability for five days. On examination (RR 25), (T 38.6 °C) and (O2 89% Room air), on auscultation there was a decrease on air entry bilaterally with scattered crepitations, no wheezing or stridor. Covid-19 swab was positive, (Day 1) potassium 2.91 (mmol/L) magnesium (mmol/L) with normal baseline before getting infected.

Clinical discussion
Patient while in the hospital was on daily potassium oral and IV replacement with IV magnesium replacement. Investigation showed 24Hr urine potassium 47.3 (mmol/L), 24Hr urine magnesium 5.52 (mmol/L), 24Hr urine Creatinine 9.25 (mmol/L), (TTKG) Transtubular Potassium Gradient 18 and (VBG) PH:7.38, Pco2:44 (mmHg) Po2:55 (mmHg) HCO3:25 (mEq/L). Patient has an increased renal potassium loss with normal VBG on separate days and normal Blood pressure that excludes diseases with associated acidemia or alkalemia. Our patient didn't want to go for any invasive diagnostic procedures and favored to wait for spontaneous recovery.

Conclusion
We followed up the potassium level of our patient for more than 5 months since he was diagnosed with COVID-19 to find out that he is still having hypokalemia, as well as, hypomagnesemia. Long term complications of COVID-19 infection such as hypokalemia and hypomagnesemia need to be observed and followed up closely to avoid life-threatening arrythmias and seizures. The attention of the scientific community to possible long term or permanent complications is needed to help find preventive measures and treatment for patients with complications.

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Hypokalemia as a sensitive biomarker of disease severity and the requirement for invasive mechanical ventilation requirement in COVID-19 pneumonia: A case series of 306 Mediterranean patients
Oscar Moreno-Pérez International Journal of Infectious Diseases VOLUME 100, P449-454, NOVEMBER 01, 2020

Highlights
• There is a high prevalence of hypokalemia among patients with COVID-19 pneumonia.
• This suggests the presence of a disorder in renin–angiotensin system activity.
• Hypokalemia is associated with the requirement for invasive mechanical ventilation.
• Hypokalemia appears to be a sensitive biomarker for the progression of severity in COVID-19.
• Serum levels of potassium should be monitored closely in these patients.

Objectives
Serum levels of potassium (K+) appear to be significantly lower in severe cases of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the clinical significance of this is unknown. The objective was to investigate whether hypokalemia acts as a biomarker of severity in coronavirus disease 2019 (COVID-19) pneumonia and is associated with major clinical outcomes.
Methods
A retrospective cohort study of inpatients with COVID-19 pneumonia (March 3 to May 2, 2020) was performed. Patients were categorized according to nadir levels of K+ in the first 72 h of admission: hypokalemia (K+ ≤3.5 mmol/l) and normokalemia (K+ >3.5 mmol/l). The main outcomes were all-cause mortality and the need for invasive mechanical ventilation (IMV); these were analyzed by multiple logistic regression (odds ratio (OR), 95% confidence interval (CI)).
Results
Three hundred and six patients were enrolled. Ninety-four patients (30.7%) had hypokalemia and these patients showed significantly higher comorbidity (Charlson comorbidity index ≥3, 30.0% vs 16.3%; p =  0.02) and CURB65 scores (median (interquartile range): 1.5 (0.0–3.0) vs 1.0 (0.0–2.0); p =  0.04), as well as higher levels of some inflammatory parameters at baseline. After adjustment for confounders, hypokalemia was independently associated with requiring IMV during the admission (OR 8.98, 95% CI 2.54–31.74). Mortality was 15.0% (n = 46) and was not influenced by low K+. Hypokalemia was associated with longer hospital and ICU stays.
Conclusions
Hypokalemia is prevalent in patients with COVID-19 pneumonia. Hypokalemia is an independent predictor of IMV requirement and seems to be a sensitive biomarker of severe progression of COVID-19.

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Hypokalemia in Patients with COVID-19
Gaetano Alfano Clin Exp Nephrol . 2021 Apr;25(4):401-409.

Abstract
Background: Patients with COVID-19 experience multiple clinical conditions that may cause electrolyte imbalances. Hypokalemia is a concerning electrolyte disorder closely associated with severe complications. This study aimed to estimate prevalence, risk factors and outcome of hypokalemia in a cohort of patients with confirmed COVID-19.

Methods: A retrospective analysis was conducted on 290 non-ICU admitted patients with COVID-19 at the tertiary teaching hospital of Modena, Italy, from February 16 to April 14, 2020.

Results: Hypokalemia was detected in 119 out of 290 patients (41%) during hospitalization. Mean serum potassium was 3.1 ± 0.1 meq/L. The majority of patients (90.7%) patients experienced only a mild decrease in serum potassium level (3-3.4 mEq/L). Hypokalemia was associated with hypocalcemia, which was detected in 50% of subjects. Urine potassium-to-creatinine ratio, measured in a small number of patients (n = 45; 36.1%), revealed an increase of urinary potassium excretion in most cases (95.5%). Risk factors for hypokalemia were female sex (odds ratio (OR) 2.44; 95% CI 1.36-4.37; P 0.003) and diuretic therapy (OR 1.94, 95% CI 1.08-3.48; P 0.027). Hypokalemia, adjusted for sex, age and SOFA score, was not associated with ICU transfer (OR 0.52; 95% CI 0.228-1.212; P = 0.131), in-hospital mortality (OR, 0.47; 95% CI 0.170-1.324; P = 0.154) and composite outcome of ICU transfer or in-hospital mortality (OR 0.48; 95% CI 0.222-1.047; P = 0.065) in our cohort of patients.

Conclusions: Hypokalemia was a frequent disorder in subjects with COVID-19. Female sex and diuretic therapy were identified as risk factors for low serum potassium levels. Hypokalemia was unrelated to ICU transfer and death in this cohort of patients.

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How SARS-CoV-2 might affect potassium balance via impairing epithelial sodium channels?
Maryam Noori Mol Biol Rep . 2021 Aug 15;1-7.

Severe acute respiratory syndrome coronaviruses 2 (SARS-CoV-2) is the causative agent of current coronavirus disease 2019 (COVID-19) pandemic. Electrolyte disorders particularly potassium abnormalities have been repeatedly reported as common clinical manifestations of COVID-19. Here, we discuss how SARS-CoV-2 may affect potassium balance by impairing the activity of epithelial sodium channels (ENaC).

The first hypothesis could justify the incidence of hypokalemia. SARS-CoV-2 cell entry through angiotensin-converting enzyme 2 (ACE2) may enhance the activity of renin-angiotensin-aldosterone system (RAAS) classical axis and further leading to over production of aldosterone. Aldosterone is capable of enhancing the activity of ENaC and resulting in potassium loss from epithelial cells. However, type II transmembrane serine protease (TMPRSS2) is able to inhibit the ENaC, but it is utilized in the case of SARS-CoV-2 cell entry, therefore the ENaC remains activated. The second hypothesis describe the incidence of hyperkalemia based on the key role of furin. Furin is necessary for cleaving both SARS-CoV-2 spike protein and ENaC subunits. While the furin is hijacked by the virus, the decreased activity of ENaC would be expected, which causes retention of potassium ions and hyperkalemia.

Given that the occurrence of hypokalemia is higher than hyperkalemia in COVID-19 patients, the first hypothesis may have greater impact on potassium levels. Further investigations are warranted to determine the exact role of ENaC in SARS-CoV-2 pathogenesis.

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Gastrointestinal Symptoms in Association With Hypokalemia Can Be a Predictor of Inferior Outcomes in COVID-19
Nicholas Wong Wai Cheong Cureus. 2021 Apr 13;13(4):e14466.

The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus disease-2 (SARS-C0V-2), has affected many lives globally. In Singapore, majority of the infected individuals are foreign workers residing in dormitories. A retrospective review conducted over two weeks (April 13 to April 26, 2020) of migrant workers admitted to a public hospital in Singapore revealed that a significant number of them developed hypokalemia. The purpose of this study was to examine any association that might exist between COVID-19 and hypokalemia. Fifty patients in this study had hypokalemia, translating to a prevalence of 28.4% (95% CI: 21.9-35.7). Gastrointestinal (GI) loss was a significant cause of hypokalemia with a prevalence of GI symptoms in the study group (diarrhea, vomiting, poor oral intake) of 5.7% (95% CI: 2.8-10.2). Clinicians should consider screening for hypokalemia in COVID-19 patients and initiate potassium replacement to mitigate any potential arrhythmias.

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Traduction de l'étude

Les symptômes gastro-intestinaux associés à l'hypokaliémie peuvent être un prédicteur de résultats inférieurs dans COVID-19
Nicholas Wong Wai Cheong Cureus. 13 avril 2021;13(4):e14466.

La pandémie de la maladie à coronavirus 2019 (COVID-19), causée par la maladie à coronavirus 2 du syndrome respiratoire aigu sévère (SRAS-C0V-2), a affecté de nombreuses vies dans le monde. À Singapour, la majorité des personnes infectées sont des travailleurs étrangers résidant dans des dortoirs. Une étude rétrospective menée sur deux semaines (13 avril au 26 avril 2020) sur des travailleurs migrants admis dans un hôpital public de Singapour a révélé qu'un nombre important d'entre eux ont développé une hypokaliémie. Le but de cette étude était d'examiner toute association qui pourrait exister entre COVID-19 et l'hypokaliémie. Cinquante patients dans cette étude avaient une hypokaliémie, se traduisant par une prévalence de 28,4 % (IC à 95 % : 21,9-35,7). La perte gastro-intestinale (GI) était une cause significative d'hypokaliémie avec une prévalence de symptômes gastro-intestinaux dans le groupe d'étude (diarrhée, vomissements, mauvaise prise orale) de 5,7 % (IC à 95 % : 2,8-10,2). Les cliniciens doivent envisager de dépister l'hypokaliémie chez les patients COVID-19 et initier un remplacement du potassium pour atténuer toute arythmie potentielle.