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.

Background: Acute kidney injury (AKI) is a recently recognized complication of coronavirus disease-2019 (COVID-19). This study aims to evaluate the incidence, risk factors and case-fatality rate of AKI in patients with documented COVID-19. Methods: We reviewed the health medical records of 307 consecutive patients hospitalized for symptoms of COVID-19 at the University Hospital of Modena, Italy. Results: AKI was diagnosed in 69 out of 307 (22.4%) patients. The stages of AKI were stage 1 in 57.9%, stage 2 in 24.6% and stage 3 in 17.3%. Hemodialysis was performed in 7.2% of the subjects. AKI patients had a mean age of 74.7±9.9 years and higher serum levels of the main marker of inflammation and organ involvement (lung, liver, hearth and liver) than non-AKI patients. AKI events were more frequent in subjects with severe lung comprise. Two peaks of AKI events coincided with in-hospital admission and death of the patients. Kidney injury was associate with a higher rate of urinary abnormalities including proteinuria (0.448±0.85 vs 0.18±0.29; P=<0.0001) and hematuria (P=0.032) compared to non-AKI patients. At the end of follow-up, 65.2% of the patients did not recover their renal function after AKI. Risk factors for kidney injury were age, male sex, CKD and non-renal SOFA. Adjusted Cox regression analysis revealed that AKI was independently associated with in-hospital death (hazard ratio [HR]=3.74; CI 95%, 1.34-10.46) compared to non-AKI patients. Groups of patients with AKI stage 2-3 and failure to recover kidney function were associated with the highest risk of in-hospital mortality. Lastly, long-hospitalization was positively associated with a decrease of serum creatinine, likely due to muscle depletion occurred with prolonged bed rest. Conclusions: AKI was a dire consequence of patients with COVID-19. Identification of patients at high-risk for AKI and prevention of kidney injury by avoiding dehydration and nephrotoxic agents is imperative in this vulnerable cohort of patients.

Monoclonal gammopathies have been associated with kidney injury. Nephrotoxicity of the secreted monoclonal (M)-protein relies on a complex interplay between biological characteristics and serum concentration. Little is known about the epidemiology and clinical manifestations of the different types of monoclonal gammopathies in patients with kidney disease. We enrolled all patients with monoclonal gammopathy who underwent kidney biopsy between January 2000 and March 2017. Data about demographics, clinical manifestations and histological lesions were collected retrospectively. Monoclonal gammopathy was detected in 174 (13%) patients with a mean age of 66.4±13.1 years. M-protein was secreted by monoclonal gammopathy of undetermined significate (MGUS) (52,8%), myeloma multiple (MM) (25.2%), primary amyloidosis (AL) (9,1%), smoldering MM (7 %), non-Hodgkin lymphoma (NHL) (6.8%) and HL (1.7%). Monoclonal gammopathy of renal significance (MGRS) accounted for 6.5% in patients with MGUS and 14.2% in patients with smoldering MM. Evaluation of kidney biopsy revealed that M-protein was directed involved in causing kidney injury in MM (93.1%) and NHL (8,3%). MM was the only gammopathy significantly associated with an increased risk of kidney injury (odds ratio [OR]=47.5, CI95%, 13.7-164.9; P=<0.001). While there were no significant differences in the progression toward end-stage renal disease or dialysis (P=0.776), these disorders were associated with a different risk of death (P=0.047) at the end of the follow-up. Monoclonal gammopathy was a frequent finding in patients with kidney disease. Kidney biopsy had a key role in identifying the underlying monoclonal gammopathy and recognizing the causal relationship between M-protein and kidney injury.

Cardiovascular assessment before kidney transplantation (KT) remains uncertain despite contemporary guidelines. Historically, many transplant centers have adopted intensive screening strategies to detect obstructive coronary artery disease (CAD), often resulting in stress testing, coronary angiography, revascularization, dual antiplatelet therapy, and potentially delayed transplantation. However, evidence that systematic detection and prophylactic treatment of stable CAD improve outcomes in asymptomatic KT candidates remains limited. Recent American, British, and European guidance increasingly supports more selective, risk-adapted assessment, yet the low level of supporting evidence leaves substantial discretion in patient and test selection, as well as wait-list surveillance. This implementation gap is particularly relevant for historically high-testing centers seeking to revise established protocols. Moreover, the cardiovascular phenotype of advanced chronic kidney disease extends beyond obstructive epicardial CAD and includes myocardial, microvascular, structural, and systemic abnormalities that may be better captured by physiological vulnerability and functional reserve. Exercise-based assessment may therefore provide prognostic information beyond ischemia detection. In this Viewpoint, we examine the evidence challenging intensive CAD-centered screening, discuss the evolving role of functional testing and risk-adapted surveillance, and illustrate how these principles were translated into a multidisciplinary local protocol revision. The emerging challenge is not simply to perform fewer tests but to identify who truly benefits from additional testing and to select the right test for the right patient at the right time.