Complete deficiency of alternative pathway (AP) complement factors, explained by homozygous mutations, is a well-known risk factor for invasive bacterial infections; however, this is less obvious for heterozygous mutations. We describe two siblings with a heterozygous NM_001928.3(CFD)c.125C>A p.(Ser42*) mutation in the complement factor D (fD) gene having a history of recurrent bacterial infections. We determined the effect of heterozygous fD deficiency on AP complement activity. We determined the effect of fD levels on complement activation as measured by AP activity, complement C3 binding to the bacterial surface of (Nm), (Sp) and non-typeable (NTHi), and complement-mediated killing of Nm and NTHi. In addition, we measured the effect of vaccination of complement C3 binding to the bacterial surface and killing of Nm. Reconstitution of fD-deficient serum with fD increased AP activity in a dose- and time-dependent way. Reconstitution of patient serum with fD to normal levels increased complement C3 binding to Sp, Nm and NTHi, as well as complement-mediated killing of Nm and NTHi. Vaccination increased complement C3 binding and resulted in complete killing of Nm without fD reconstitution. We conclude that low fD serum levels (<0.5μgmL ) lead to a reduced speed of complement activation, which results in diminished bacterial killing, consistent with recurrent bacterial infections observed in our index patients. Specific antibodies induced by vaccination are able to overcome the diminished bacterial killing capacity in patients with low fD levels.We conclude that low fD serum levels ( less then 0.5 μg mL-1) lead to a reduced speed of complement activation, which results in diminished bacterial killing, consistent with recurrent bacterial infections observed in our index patients. Specific antibodies induced by vaccination are able to overcome the diminished bacterial killing capacity in patients with low fD levels. Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-COV2) depends on RNA-dependent RNA polymerase (RdRp) enzyme complex for its genomic replications and thus can be inhibited by nucleoside analogues. An example is Remdesivir, which is a non-obligate chain terminator of RdRp. Therefore, we investigate the activities of Remdesivir against COVID-19. This is a systematic-review and meta-analysis of the literature on the through MEDLINE (from Jan 2019 to January 2021), EMBASE (from Jan 2019 to January 2021), Publics Ovidius Naso (Ovoid), Database of Abstracts of Reviews of Effects and the Cochrane Central Register of Controlled Trials in Issue 1 of 12, January 2021. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) checklist was applied and the questions generated in conformity with the participants, interventions, comparisons, outcomes, and study design (PICOS). Nintedanib Statistical analysis was performed in Stata v. 12.1 (StataCorp, Texas USA). The outcome of the reviewed relevant journals and the cross-references including clinical trials, systematic reviews and metanalysis were documented. Out of 569,000 articles, 11 roundly-suited the inclusion criteria. The comparative effects of Remdesivir on death (OR=0.79; 95% CI=0.57, 1.08) and recovery (OR=2.22; p5% CI=1.80, 2.73) were calculated. Remdesivir is useful in the treatment of COVID-19 especially the severe disease. However, it should be used with caution since all the adverse effects are not known. We recommend Remdesivir as an alternative/third-force in the treatment of severe and critical COVID-19.Remdesivir is useful in the treatment of COVID-19 especially the severe disease. However, it should be used with caution since all the adverse effects are not known. We recommend Remdesivir as an alternative/third-force in the treatment of severe and critical COVID-19.[This corrects the article DOI 10.1093/ckj/sfaa172.][This corrects the article DOI 10.1093/ckj/sfaa172.].[This corrects the article DOI 10.1093/ckj/sfaa029.][This corrects the article DOI 10.1093/ckj/sfaa029.].A 3-week-old boy with viral gastroenteritis was by error given 200 mL 1 mmol/mL hypertonic saline intravenously instead of isotonic saline. His plasma sodium concentration (PNa) increased from 136 to 206 mmol/L. Extreme brain shrinkage and universal hypoperfusion despite arterial hypertension resulted. Treatment with glucose infusion induced severe hyperglycaemia. Acute haemodialysis decreased the PNa to 160 mmol/L with an episode of hypoperfusion. The infant developed intractable seizures, severe brain injury on magnetic resonance imaging and died. The most important lesson is to avoid recurrence of this tragic error. The case is unique because a known amount of sodium was given intravenously to a well-monitored infant. Therefore the findings give us valuable data on the effect of fluid shifts on the PNa, the circulation and the brain's response to salt intoxication and the role of dialysis in managing it. The acute salt intoxication increased PNa to a level predicted by the Edelman equation with no evidence of osmotic inactivation of sodium. Treatment with glucose in water caused severe hypervolaemia and hyperglycaemia; the resulting increase in urine volume exacerbated hypernatraemia despite the high urine sodium concentration, because electrolyte-free water clearance was positive. When applying dialysis, caution regarding circulatory instability is imperative and a treatment algorithm is proposed.Whether C5 blocking may improve the outcomes of patients developing chemotherapy-induced thrombotic microangiopathy (TMA) remains elusive. Lung fibrosis is a well-known complication of bleomycin, whereas TMAs are very rare ( less then 20 cases described). Here, we report an exceptional case of a male patient that developed acute respiratory distress syndrome and TMA following administration of bleomycin, cisplatin and etoposide . Refractoriness to plasma exchanges prompted us to use eculizumab as salvage therapy. Eculizumab led to complete remission of the TMA before Day 2. However, the patient progressed towards refractory respiratory failure, suggesting that pathophysiological mechanisms of bleomycin-induced lung fibrosis and TMA differ.