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Background Coronavirus disease 2019 (COVID-19)-related short-term mortality is high in dialysis patients, but longer-term outcomes are largely unknown. We therefore assessed patient recovery in a large cohort of dialysis patients 3 months after their COVID-19 diagnosis. Methods We analyzed data on dialysis patients diagnosed with COVID-19 from 1 February 2020 to 31 March 2021 from the European Renal Association COVID-19 Database (ERACODA). The outcomes studied were patient survival, residence and functional and mental health status (estimated by their treating physician) 3 months after COVID-19 diagnosis. Complete follow-up data were available for 854 surviving patients. Patient characteristics associated with recovery were analyzed using logistic regression. Results In 2449 hemodialysis patients (mean ± SD age 67.5 ± 14.4 years, 62% male), survival probabilities at 3 months after COVID-19 diagnosis were 90% for nonhospitalized patients (n = 1087), 73% for patients admitted to the hospital but not to an intensive care unit (ICU) (n = 1165) and 40% for those admitted to an ICU (n = 197). Patient survival hardly decreased between 28 days and 3 months after COVID-19 diagnosis. At 3 months, 87% functioned at their pre-existent functional and 94% at their pre-existent mental level. Only few of the surviving patients were still admitted to the hospital (0.8–6.3%) or a nursing home (∼5%). A higher age and frailty score at presentation and ICU admission were associated with worse functional outcome. Conclusions Mortality between 28 days and 3 months after COVID-19 diagnosis was low and the majority of patients who survived COVID-19 recovered to their pre-existent functional and mental health level at 3 months after diagnosis.

Background Patients on kidney replacement therapy (KRT) are at very high risk of coronavirus disease 2019 (COVID-19). The triage pathway for KRT patients presenting to hospitals with varying severity of COVID-19 illness remains ill-defined. We studied the clinical characteristics of patients at initial and subsequent hospital presentations and the impact on patient outcomes. Methods The European Renal Association COVID-19 Database (ERACODA) was analysed for clinical and laboratory features of 1423 KRT patients with COVID-19 either hospitalized or non-hospitalized at initial triage and those re-presenting a second time. Predictors of outcomes (hospitalization, 28-day mortality) were then determined for all those not hospitalized at initial triage. Results Among 1423 KRT patients with COVID-19 [haemodialysis (HD), n = 1017; transplant, n = 406), 25% (n = 355) were not hospitalized at first presentation due to mild illness (30% HD, 13% transplant). Of the non-hospitalized patients, only 10% (n = 36) re-presented a second time, with a 5-day median interval between the two presentations (interquartile range 2–7 days). Patients who re-presented had worsening respiratory symptoms, a decrease in oxygen saturation (97% versus 90%) and an increase in C-reactive protein (26 versus 73 mg/L) and were older (72 vs 63 years) compared with those who did not return a second time. The 28-day mortality between early admission (at first presentation) and deferred admission (at second presentation) was not significantly different (29% versus 25%; P = 0.6). Older age, prior smoking history, higher clinical frailty score and self-reported shortness of breath at first presentation were identified as risk predictors of mortality when re-presenting after discharge at initial triage. Conclusions This study provides evidence that KRT patients with COVID-19 and mild illness can be managed effectively with supported outpatient care and with vigilance of respiratory symptoms, especially in those with risk factors for poor outcomes. Our findings support a risk-stratified clinical approach to admissions and discharges of KRT patients presenting with COVID-19 to aid clinical triage and optimize resource utilization during the ongoing pandemic.

Background: The CKD-associated decline in soluble α-Klotho (α-Klotho) levels is considered detrimental. Some studies suggest a direct induction of α-Klotho concentrations by growth hormone (GH). In the present study, the effect of exogenous GH administration on α-Klotho concentrations in a clinical cohort with mild chronic kidney disease (CKD) and healthy subjects was studied. Methods: A prospective, single-center open case-control pilot study was performed involving 8 patients with mild CKD and 8 healthy controls matched for age and sex. All participants received subcutaneous GH injections (Genotropin®, 20 mcg/kg/day) for 7 consecutive days. α-Klotho concentrations were measured at baseline, after 7 days of therapy and 1 week after the intervention was stopped. Results: α-Klotho concentrations were not different between CKD-patients and healthy controls at baseline (554 (388-659) vs. 547 (421-711) pg/mL, P = 0.38). Overall, GH therapy increased α-Klotho concentrations from 554 (405-659) to 645 (516-754) pg/mL, P < 0.05). This was accompanied by an increase of IGF-1 concentrations from 26.8 ± 5.0 nmol/L to 61.7 ± 17.7 nmol/L (P < 0.05). GH therapy induced a trend toward increased α-Klotho concentrations both in the CKD group (554 (388-659) to 591 (358-742) pg/mL (P = 0.19)) and the healthy controls (547 (421-711) pg/mL to 654 (538-754) pg/mL (P = 0.13)). The change in α-Klotho concentration was not different for both groups (P for interaction = 0.71). α-Klotho concentrations returned to baseline levels within one week after the treatment (P < 0.05). Conclusions: GH therapy increases α-Klotho concentrations in subjects with normal renal function or stage 3 CKD. A larger follow-up study is needed to determine whether the effect size is different between both groups or in patients with more severe CKD. Trial registration: This trial is registered in EudraCT (2013-003354-24).

WOS: 000398117600023, PubMed ID: 28025382, Background. From an individual participant data (IPD) meta-analysis from four randomized controlled trials comparing haemodialysis (HD) with post-dilution online-haemodiafiltration (ol-HDF), previously it appeared that HDF decreases all-cause mortality by 14% (95% confidence interval 25; 1) and fatal cardiovascular disease (CVD) by 23% (39; 3). Significant differences were not found for fatal infections and sudden death. So far, it is unclear, however, whether the reduced mortality risk of HDF is only due to a decrease in CVD events and if so, which CVD in particular is prevented, if compared with HD. Methods. The IPD base was used for the present study. Hazard ratios and 95% confidence intervals for cause-specific mortality overall and in thirds of the convection volume were calculated using the Cox proportional hazard regression models. Annualized mortality and numbers needed to treat (NNT) were calculated as well. Results. Besides 554 patients dying from CVD, fatal infections and sudden death, 215 participants died from 'other causes', such as withdrawal from treatment and malignancies. In this group, the mortality risk was comparable between HD and ol-HDF patients, both overall and in thirds of the convection volume. Subdivision of CVD mortality in fatal cardiac, non-cardiac and unclassified CVD showed that ol-HDF was only associated with a lower risk of cardiac casualties [0.64 (0.61; 0.90)]. Annual mortality rates also suggest that the reduction in CVD death is mainly due to a decrease in cardiac fatalities, including both ischaemic heart disease and congestion. Overall, 32 and 75 patients, respectively, need to be treated by high-volume HDF (HV-HDF) to prevent one all-cause and one CVD death, respectively, per year. Conclusion. The beneficial effect of ol-HDF on all-cause and CVD mortality appears to be mainly due to a reduction in fatal cardiac events, including ischaemic heart disease as well as congestion. In HV-HDF, the NNT to prevent one CVD death is 75 per year., EuDial working group; European Nephrology and Dialysis Institute; Catalan Society of Nephrology; Fresenius Medical Care; Dutch Kidney Foundation [C02.2019]; Fresenius Medical Care, Netherlands; Gambro Lundia AB, Sweden; Dr E.E. Twiss Fund; International Society of Nephrology/Baxter Extramural Grant Program; Netherlands Organization for Health Research and DevelopmentNetherlands Organization for Health Research and Development [170882802]; national grant from the Health Ministry (Programme Hospitalier de Recherche Clinique, PHRC); Gambro through the Catalan Society of Nephrology; Roche Netherlands, The HDF Pooling project was designed, conducted and analysed independently of the financial contributors of the individual studies as listed below. Study data were collected and retained by the investigators and were not available for the financial contributors of the individual studies. S.A.E.P. and the meetings of the representatives of the combined authors of the four studies were financially supported by the EuDial working group. EuDial is an official working group of the European Renal Association-European Dialysis Transplant Association (ERA-EDTA, http://era-edta.org/eudial/European_Dialysis_Working_Group.html). No industry funding was received for any part of or activity related to the present analysis.; The Turkish HDF study was supported by European Nephrology and Dialysis Institute with an unrestricted grant. The study was performed in Fresenius Medical Care haemodialysis clinics in Turkey. ESHOL was supported by The Catalan Society of Nephrology and by grants from Fresenius Medical Care and Gambro through the Catalan Society of Nephrology. The CONTRAST study was supported by a grant from the Dutch Kidney Foundation (Nierstichting Nederland Grant C02.2019), and unrestricted grants from Fresenius Medical Care, Netherlands, and Gambro Lundia AB, Sweden. Additional support was received from the Dr E.E. Twiss Fund, Roche Netherlands, the International Society of Nephrology/Baxter Extramural Grant Program, and the Netherlands Organization for Health Research and Development (ZONMw Grant 170882802). The French HDF study was supported by a national grant from the Health Ministry (Programme Hospitalier de Recherche Clinique, PHRC) as a means to improve care and outcome of elderly chronic disease patients.

Symposium on Bone in Chronic Kidney Disease (CKD), CKD 2016, Amsterdam, Netherlands, 13 Sep 2016 - 13 Sep 2016; Journal of nephrology 30(5), 663-670 (2017). doi:10.1007/s40620-017-0408-8 special issue: "Special issue on “Bone in Chronic Kidney Disease” an activity of the ERA-EDTA WG on CKD-MBD", Published by Springer, Milano

Chronic haemodialysis patients have a disproportionately high risk for developing cardiovascular disease, which can only in part be explained by known risk factors such as dyslipidaemia, hypertension, hyperhomocysteinemia, diabetes mellitus and chronic volume expansion. A possible cause is that the haemodialysis treatment itself contributes to the accelerated atherosclerosis, observed in these patients. Nowadays, atherosclerosis is considered an inflammatory process, mediated by a dysfunction of the vascular endothelium. As a result, blood cells adhere to the vascular surface and release a variety of vasoactive mediators, cytokines, growth factors and free radicals. Due to the contact between blood and dialyzer, humoral systems and cellular elements are stimulated, and this may be viewed as an inflammatory reaction. As a consequence of this, the vascular surface of haemodialysis patients is repeatedly exposed to the influences of cytokines, coagulation products, vasoactive mediators, stimulated leukocytes and thrombocytes, and oxidative stress. It is therefore conceivable that the haemodialysis treatment itself enhances the greatly increased cardiovascular risk in chronic haemodialysis patients.

Objective: To evaluate in vitro the value of antacids as an alternative to H2 blockers to raise gastric juice pH for reliable PCO2 tonometry in the human stomach. Design and setting: Laboratory study in a university hospital. Interventions: A bath was filled with 0.1 M hydrochloric acid at pH 1.3 and CO2 was gassed through the acid to simulate an intragastric environment. Experiments were performed in duplicate. Both the manual saline technique and the new semi-continuous, semi-automated air technique of PCO2 tonometry were used to evaluate the effects of adding i) aluminium oxide/magnesium hydroxide (Antagel®) and ii) sodium bicarbonate on the PCO2. The latter technique was done to simulate intragastric CO2 production following buffering of gastric acid by bicarbonate in the mucosa, or in the saliva or pancreatic/duodenal juice entering the stomach, an effect that can be prevented in vivo by prior administration of H2 blockers. Endpoints: Changes in tonometrically determined PCO2 after the addition of alkali. A secondary endpoint was the difference between the manual saline and the semicontinuous air tonometry techniques. Measurements and main results: The mean pH increased from 1.3 to 4.0 after adding 40 ml aluminium oxide/magnesium hydroxide. The subsequent addition of sodium bicarbonate, dosed to increase pH above 6.5, caused a steep rise in PCO2 from 34 and 39 mmHg to 134 and 99 mmHg, for each experiment respectively, as measured by conventional tonometry, and from 37 and 38 mmHg to 116 and 115 mmHg, respectively, for the air technique. These changes were transient. Air tonometry detected changes in PCO2 more rapidly than the manual technique. Conclusions: Adding antacids elevates the PCO2 in hydrochloric acid and does not prevent CO2 generation after the addition of sodium bicarbonate, even though the pH is raised from about 1 to 4. The clinical use of antacids instead of H2 blockers to prevent spurious PCO2 elevations following buffering of acid by bicarbonate, and thereby increase the reliability of gastric tonometry, should be discouraged.