The aim of this study was to estimate the incidence of COVID-19 disease in the French national population of dialysis patients, their course of illness and to identify the risk factors associated with mortality. Our study included all patients on dialysis recorded in the French REIN Registry in April 2020. Clinical characteristics at last follow-up and the evolution of COVID-19 illness severity over time were recorded for diagnosed cases (either suspicious clinical symptoms, characteristic signs on the chest scan or a positive reverse transcription polymerase chain reaction) for SARS-CoV-2. A total of 1,621 infected patients were reported on the REIN registry from March 16th, 2020 to May 4th, 2020. Of these, 344 died. The prevalence of COVID-19 patients varied from less than 1% to 10% between regions. The probability of being a case was higher in males, patients with diabetes, those in need of assistance for transfer or treated at a self-care unit. Dialysis at home was associated with a lower probability of being infected as was being a smoker, a former smoker, having an active malignancy, or peripheral vascular disease. Mortality in diagnosed cases (21%) was associated with the same causes as in the general population. Higher age, hypoalbuminemia and the presence of an ischemic heart disease were statistically independently associated with a higher risk of death. Being treated at a selfcare unit was associated with a lower risk. Thus, our study showed a relatively low frequency of COVID-19 among dialysis patients contrary to what might have been assumed.

The acute effects of both acetate and bicarbonate hemodialysis on erythrocyte transmembrane sodium fluxes were investigated in 15 patients with chronic uremia. We observed a significant (p < 0.0l) stimulation of the Na⁺, K⁺ pump in both procedures, with a significant correlation to the amount of fluid removed during hemodialysis (r = 0.56, p < 0.03). Outward Na⁺ cotransport fluxes significantly rose (p < 0.05) after acetate hemodialysis and decreased (p < 0.05) after bicarbonate hemodialysis. Minor and not significant pre- and posthemodialysis bidirectional changes were observed as regards the intraerythrocyte Na⁺ and K⁺ concentration, passive Na⁺ and K⁺ permeability, and Na⁺, Li⁺ countertransport. Hemodialysis may acutely affect the erythrocyte sodium pump and cotransport fluxes, possibly through the modulation of hormonal factors triggered by the extracellular volume changes.

D-Lysine, the non-physiological isomer of L-lysine, can competitively reduce protein non-enzymatic glycation in vitro. To study the effect of D-lysine in vivo, 6-8-week old Sprague-Dawley rats with streptozotocin-induced diabetes mellitus were treated from diagnosis for 45 days with two daily subcutaneous injections of D-lysine (0.5 g.ml-1.day-1). Another group of diabetic rats was only injected with equal volumes of physiological saline (0.9% NaCl). Glycated haemoglobin was measured by ion exchange chromatography, and glycated serum and lens proteins by boronate affinity gel chromatography. Serum and urinary creatinine concentrations were evaluated by the alkaline-picrate reaction. Urinary lysine concentrations at mid- and end-study were evaluated by cation exchange chromatography. Blood glucose concentrations, serum creatinine levels and creatinine clearances, measured at the end of the study, were similar in both diabetic groups (> 22.0 mmol/l, < or = 106 mumol/l and approximately 0.02 ml/s, respectively). Urinary lysine concentration in D-lysine-treated diabetic animals was more than 50-fold higher than in placebo-treated diabetic rats. In D-lysine-treated vs placebo-treated diabetic animals, a statistically significant reduction was found in the levels of glycated haemoglobin (stable HbA1; mean +/- SD = 3.00 +/- 0.74% vs 4.02 +/- 0.46%, p < 0.05; labile HbA1 = 3.92 +/- 0.89% vs 5.84 +/- 0.61%, p < 0.005), glycated serum proteins (1.40 +/- 0.47% vs 2.52 +/- 1.15%, p < 0.05) and glycated lens proteins (4.90 +/- 0.96% vs 5.98 +/- 0.65%, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

SUMMARY Rat erythrocytes with five different amounts of Na+ content have been prepared by using a new, nondetrimental Na+-loading method (net NaHPO 4 " influx through the anion carrier). This method allowed the determination of 1) maximal translocation rates and apparent dissociation constants for internal Na+ of the Na+-K+ pump, outward Na+-K+ cotransport, and Na+-Li+ countertransport and 2) rate constants of Na+ leak in erythrocytes from spontaneously hypertensive rats of the Okamoto strain and Wistar-Kyoto normotensive controls aged 2 to 26 weeks. Two major abnormalities were found in erythrocytes from spontaneously hypertensive rats: 1) a decreased cotransport affinity for internal Na +, which was constantly observed from 2 to 26 weeks of age (mean intracellular Na+ content for half-maximal stimulation of outward Na+-K+ cotransport = 33.1 ± 7.0 [SD] mmol/L cells in spontaneously hypertensive rats vs 16.7 ± 4.7 mmol/L cells in Wistar-Kyoto rats; p<0.001), and 2) a decreased maximal pump rate in adult (15-to 26-week-old) spontaneously hypertensive as compared with that for age-matched Wistar-Kyoto rats (9-37 vs 34-70 mmol/L cells/hr). Therefore, the low cotransport affinity for internal Na+ appears to be a stable, possibly genetic defect of spontaneously hypertensive rats. Conversely, the decreased maximal pump rate may be a secondary event, possibly reflecting the appearance of endogenous pump inhibitors in the plasma of adult spontaneously hypertensive rats. (Hypertension 11: 41-48, 1988) KEY WORDS • ion transport • sodium transport • hypertension • membranes erythrocyte • rats • spontaneously hypertensive rats E PIDEMIOLOGICAL, clinical, and experimental studies have suggested that an inborn error of Na + metabolism is involved in the pathogenesis of primary hypertension.1 This hypothesis has been extensively investigated by measuring Na + content and Na + flux in circulating cells from rats and humans with primary hypertension (for a review, see Reference 2). The results were very difficult to interpret in both animals and humans. In the former, abnormal cell Na + handling was frequently observed, but the nature of the transport alteration differed markedly among different strains (see, for instance, Reference 3). In the latter, marked discrepancies characterized the results of various clinical investigations.2 Much of this variability in the data can be accounted for by methodological problems. The flux studies were performed by measuring transport activity under a fixed

No abstract