The COVID-19 pandemic has caused millions of infections and deaths so far. After recovery, the possibility of reinfection has been reported. Patients on hemodialysis are at high risk of contracting SARS-CoV-2 and developing serious complications. Furthermore, they are a relatively hypo-anergic population, in which the development and duration of the immune and antibody response is still partially unknown. This may play a role in the possible susceptibility to reinfection. To date, only 3 cases of SARS-CoV-2 reinfection from strains prior to the Omicron variant in patients on chronic hemodialysis have been reported in literature. In all of them, the first infection was detected by screening in the absence of symptoms, potentially indicating a poor immune response, and there are no data about the antibody titre developed. We report a case of recurrence of COVID-19 in 2020 - first infection likely from Wuhan strain; reinfection likely from English variant (Alpha) after 7 months - in a hemodialysis patient with clinical symptoms and pulmonary ultrasound abnormalities. Swabs were negative in the interval between episodes (therefore excluding any persistence of positivity) and the lack of antibody protection after the first infection was documented by the serological test. The role of the potential lack - or rapid loss - of immune protection following exposure to SARS-CoV-2 in hemodialysis patients needs to be better defined, also in consideration of the anti-COVID vaccination campaign and the arrival of the Omicron variant, which appears to elude the immunity induced by vaccines and by previous variants. For this purpose, prospective multicenter studies are in progress in several European countries. This case also highlights the need for a careful screening with nasopharyngeal swabs in dialysis rooms, even after patients overcome infection and/or are vaccinated.

Background People with reduced glomerular filtration rate (GFR) often have elevated cardiac troponin T (cTnT) levels. It remains unclear how cTnT levels develop over time in those with chronic kidney disease (CKD). The aim of this study was to prospectively study the association between cTnT and GFR over time in older advanced‐stage CKD patients not on dialysis. Methods and Results The EQUAL (European Quality Study) study is an observational prospective cohort study in stage 4 to 5 CKD patients aged ≥65 years not on dialysis (incident estimated GFR, <20 mL/min/1.73 m²). The EQUAL cohort used for the purpose of this study includes 171 patients followed in Sweden between April 2012 and December 2018. We used linear mixed models, adjusted for important groups of confounders, to investigate the effect of both measured GFR and estimated GFR on high‐sensitivity cTnT (hs‐cTnT) trajectory over 4 years. Almost all patients had at least 1 hs‐cTnT measurement elevated above the 99th percentile of the general reference population (≤14 ng/L). On average, hs‐cTnT increased by 16%/year (95% CI, 13–19; P <0.0001). Each 15 mL/min/1.73 m 2 lower mean estimated GFR was associated with a 23% (95% CI, 14–31; P <0.0001) higher baseline hs‐cTnT and 9% (95% CI, 5–13%; P <0.0001) steeper increase in hs‐cTnT. The effect of estimated GFR on hs‐cTnT trajectory was somewhat lower than a previous myocardial infarction (15%), but higher than presence of diabetes mellitus (4%) and male sex (5%). Conclusions In CKD patients, hs‐cTnT increases over time as renal function decreases. Lower CKD stage (each 15 mL/min/1.73 m 2 lower) is independently associated with a steeper hs‐cTnT increase over time in the same range as other established cardiovascular risk factors.

We analyzed the clinical features and the factors associated with the presence of hyperkalemia (serum potassium >5.3 mmol/L) in a cohort of patients presenting to an Emergency Department. A total of 168 cases were observed (89 males and 79 females), mean age 77.512 years. Fifty-six patients were diabetics (33.3%), 51 patients had chronic kidney disease (30%) and 36 patients with cardiac failure (21.4%). Sixty-nine patients (41%) were treated with RAS-blockers (ACE-I n = 50; ARBs, n = 19). 65 subjects were taking loop diuretics (39%), 17 (10%) thiazides. Thirty-one (18%) were assuming antialdosterone drugs; 16 (52%) out of these had a positive history of heart failure and 14 (41%) had a positive history of chronic kidney disease. In 85 cases (51%) patients were receiving an ACE/ARB or an antialdosterone drug. In 125 patients (74%) eGFR at presentation was <60 ml/min/1.73 m2. Serum potassium values were significantly higher in patients treated with both ACE/ARB and antialdosterone drugs. In 20 cases (12%) serum potassium was 6.5 mmol/L; these patients assumed antialdosterone drugs more frequently, alone and mostly in association with ACE-I/ARBs (65% vs 7%; p<0.0001). The simultaneous assumption of ACE-I/ARBs and antialdosterone drugs emerges as the major cause of severe hyperkalemia in our cases, thus confirming the warnings about this association in the presence of advanced age and reduced glomerular filtration rate.