[COVID-19 recurrence due to reinfection with SARS-CoV-2 in a hemodialysis patient: there and back again].

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.

[Severe hyperkalemia in patients referred to an emergency departement: the role of antialdosterone drugs and of renin-angiotensin system blockers]. / Iperpotassiemia severa in pazienti afferenti ad un pronto soccorso: ruolo degli antagonisti dell'aldosterone e dei modulatori del sistema renina-angiotensina.

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.

Salt intake and kidney disease.

We have reviewed the role of salt intake in kidney diseases, particularly in relation to renal hemodynamics, renal excretion of proteins, renal morphological changes and progression of chronic renal failure. High salt intake may have detrimental effects on glomerular hemodynamics, inducing hyperfiltration and increasing the filtration fraction and glomerular pressure. This may be particularly important in elderly, obese, diabetic or black patients, who have a high prevalence of salt-sensitivity. Changes in salt intake may influence urinary excretion of proteins in patients with essential hypertension, or diabetic and non diabetic nephropathies. Moreover, high sodium intake may blunt the antiproteinuric effect of various drugs, including angiotensin-converting-enzyme inhibitors and calcium antagonists. Experimental studies show a direct tissue effect of salt on the kidney, independent of its ability to increase blood pressure, inducing hypertrophy, fibrosis and a decrease in glomerular basement membrane anionic sites. However, no firm conclusion can be drawn about the relationship between salt consumption and progression of chronic renal failure, because most information comes from conflicting, small, retrospective, observational studies. In conclusion, it would appear that restriction of sodium intake is an important preventive and therapeutic measure in patients with chronic renal diseases of various origin, or at risk of renal damage, such as hypertensive or diabetic patients.