Background: Due to the unpredictable nature of COVID-19, there is a need to identify patients at high risk of severe course of the disease and a higher mortality rate. Objective: This study aims to find the correlation between frailty and mortality in adult, hospitalized patients with COVID-19. Methods: Clinical records of 201 patients who suffered from COVID-19 and were hospitalized between October 2020 and February 2021 were retrospectively analyzed. Demographic, clinical, and biochemical data were collected. Patients were assessed using Clinical Frailty Scale (CFS) and were divided into three groups: CFS 1–3 fit; CFS 4–6 vulnerable and with mild to moderate frailty; CSF 7–9, severe frailty. The association between frailty and in-hospital mortality was the primary outcome. Results: Severe frailty or terminal illness was observed in 26 patients (12.94%) from a cohort of 201 patients. Those patients were older (median age 80.73, p < 0.001) and had more comorbidities. Frailty was also associated with higher requirement for oxygen supplementation, greater risk of in-hospital complications and worse biochemical laboratory results. An increase in CFS score also correlated with higher mortality (OR = 1.89, p < 0.001). The Conclusions: Clinical Frailty Scale (CFS) can be used as a potentially useful tool in predicting mortality in patients with COVID-19.

The cardiovascular events are frequent complications in chronic kidney disease (CKD). In the general population the risk factors of CV disease are well established and divided into two groups: non-modifiable, and modifiable. The best-known modifiable risk factors leading to the atherosclerotic plaque formation are lipid disorders. In comparison, an association between serum lipid profile in haemodialyzed patients and cardiovascular mortality is more complex and still unclear. Furthermore, it is important to note that recent studies suggest an inverse relationship between lipid disorders and CV mortality in a haemodialyzed population called ‘reverse epidemiology’. The disparity between the general and haemodialyzed populations may be supported by the fact that the haemodialysis process itself contributes to the development of dyslipidaemia. Moreover, the chronic kidney disease is associated with metabolic abnormalities which can increase the risk of CVD occurrence. It is estimated that one-third of the patients on haemodialysis have lipid profile abnormalities, the most common one is hypertriglyceridemia. The assessment of the lipid profile has so far been performed in a fasting and non-fasting (postprandial) state, but both of these methods have some limitations. This review evaluates the current knowledge about lipid profile abnormalities in haemodialyzed patients and discusses a potential role of the Oral Fat Tolerance Test (OFTT) as a new tool in clinical practice that may improve the diagnosis of postprandial hypertriglyceridemia.

The treatment of chronic kidney disease is based mainly on haemodialysis. During this procedure, cardiovascular haemodynamic parameters change, which can lead to complications in the circulatory system and shorten patient survival. Currently, new biomarkers are being sought that could predict survival in haemodialysis patients. The aim of this study was to evaluate whether Gal-3, GDF-15, sST2, and CysC could be useful biomarkers in patients with end-stage renal failure undergoing haemodialysis in predicting the patient survival. This study included 76 patients with end-stage kidney disease treated with haemodialysis. We assessed the variability in the plasma concentrations of these proteins; evaluated correlations between Gal-3, GDF-15, and sST2 concentrations and selected haemodialysis parameters; and determined the relationship between the risk of death and Gal-3, GDF-15, sST2, and CysC concentrations. There was a decrease in the Gal-3 plasma concentrations and an increase in the GDF-15 and sST2 plasma concentrations during haemodialysis. Among the studied proteins, only the sST2 concentrations differed significantly between the patients who survived and died. The logarithm of the sST2 concentrations, both before and after haemodialysis, was an independent mortality risk factor in univariate analysis (respectively: hazard ratio [HR] 3.179, 95% confidence interval [CI] 1.492–6.777, p = 0.0027, and HR 3.011, 95% CI 1.447–6.264, p = 0.0032) and multivariate analysis, which also included age, male gender, and body mass index (respectively: HR 2.776, 95% CI 1.306–5.903, p = 0.0080, and HR 2.496, 95% CI 1.224–5.090, p = 0.012). These results suggest the use of sST2 in clinical practice to identify patients at higher risk of death.

Gitelman syndrome (GS) is a rare, autosomal recessive salt-losing tubulopathy caused by mutations in the SLC12A3 gene. It involves dysfunction of the sodium-chloride cotransporter positioned on the apical membranes of the distal convoluted tubule cells, causing sodium shortage and mimicking the use of thiazide diuretics. Hyperaldosteronism secondary to sodium depletion and hypovolemia causes hypokalaemia and metabolic alkalosis. This is associated with inhibition of the Transient Receptor Potential Cation Channel, Subfamily M, Member 6 –TRPM6 channel, which leads to urinary magnesium leakage and hypomagnesemia, subsequently stopping PTH secretion and resulting in hypocalcemia and hypocalciuria. Gitelman syndrome frequently presents later in life, as the symptoms are usually not very threatening. However, early identification, diagnosis, and urgent intervention are essential to improve patient prognosis and quality of life. Importantly, both hypomagnesemia and hypokalaemia can impair insulin secretion and sensitivity. Furthermore, hyperaldosteronism caused by the secondary activation of the R-A-A system can also lead to these disorders. Glucose metabolism problems have been shown to prevail amongst GS patients and manifest more frequently in comparison to the general population. When it comes to the treatment used to reduce hyperglycemia in GS-related T2DM, we consider which of the available drugs are the best for those patients. The article analyses the association of Gitelman syndrome with diabetes mellitus based on the available medical literature—as there are no clinical trials or meta-analyses available for this group, it is presented as a narrative review.