Background Novel coronavirus disease 2019 (COVID-19) emerged in Wuhan and rapidly spread, affecting >10 million cases worldwide. Caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and primarily manifesting as an acute respiratory failure with interstitial and alveolar pneumonia, it can also affect multiple organs. Kidney involvement was underestimated in early reports and its role remains controversial. The aim of this study was to analyse the role of kidney damage in COVID-19 outcome. Methods This is a prospective cohort study of 1603 consecutive patients admitted in a University Reference Hospital in the heart of the European outbreak. Results Median age was 64 years, 40.4% were female, 15.2% presented diabetes mellitus, 35.7% hypertension and 20.3% obesity. On admission, the prevalence of elevated serum creatinine (sCr), proteinuria, leucocyturia and haematuria were 21.0, 37.8, 31.8 and 45.6%, respectively. In total, 43.5% of those with an elevated sCr had previous chronic kidney disease (CKD) and 11.4% of those with normal sCr developed an in-hospital acute kidney injury (AKI); 17 patients needed acute haemodialysis; and 197 patients died during hospitalization. Cox proportional hazard regression confirmed that elevated baseline sCr [hazard ratio (95% confidence interval) 2.40 (1.79–3.22)], previous CKD [1.59 (1.06-2.37)], haematuria [1 + 1.68 (0.92–3.06), 2–3 + 2.69 (1.49–4.87)] and in-hospital AKI [1.50 (0.92–2.44)] were independent risk factors for in-hospital death after adjusting for age, sex and comorbidity. Conclusion The prevalence of acute and chronic kidney disease on admission and in-hospital AKI is higher than previously reported in Wuhan, and is associated with high in-hospital mortality. We should increase our awareness towards kidney involvement and design specific strategies for management of COVID-19 in these patients.

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Background COVID-19 patients on hemodialysis (HD) have high mortality. We investigated the value of RT-PCR and the dynamic changes of antibodies (ELISA IgM+IgA and IgG) in a large HD cohort. Methods Prospective observational study in ten Madrid HD centers. Infection rate, anti- SARS-CoV-2 body dynamics and the incidence of asymptomatic SARS-CoV-2 infection (defined by positive RT-PCR, IgM-IgA or IgG) were assessed. Results From March 1 to April 15, 2020, 136 (16.8%) of 808 HD patients were diagnosed of symptomatic COVID-19 by nasopharyngeal RT-PCR and 42/136 (31%) died. In the second fortnight of April, RT-PCR and anti-SARS-CoV-2 antibodies were assessed on 763 of the surviving patients. At this point, 69/91 (75,8%) symptomatic COVID-19 patients had anti-SARS-CoV-2 antibodies. Four weeks later, 15.4% (10/65) of initially antibody positive patients had become negative. Among patients without prior symptomatic COVID-19, 9/672 (1.3%) were RT-PCR positive and 101/672 patients (15.0%) were antibody positive. Four weeks later, 6224/86 (72.1%) of initially antibody positive patients had become negative. Considering only IgG tittles, serology remained positive after four weeks in 90% (54/60) of patients with symptomatic COVID-19 and in 52.5% (21/40) of asymptomatic patients. The probability of an adequate serologic response (defined as the development of anti-SARS-CoV2 antibodies that persisted at 4 weeks) was higher in patients who had symptomatic COVID-19 than in asymptomatic SARS-CoV2 infection (OR 4.04 [2.04-7.99] corrected for age, Charlson score and time on HD. Living in a nursing home (5.9 [2.3-15.1]) was the main risk factors for SARS-CoV2 infection Conclusion The anti-SARS-CoV-2 antibody immune response in HD patients depends on clinical presentation and the antibody titers decay earlier than previously reported for the general population. This inadequate immune response raises questions about the efficacy of future vaccines.

Objective To study the prognostic factors for mortality and hospital admission for patients on peritoneal dialysis (PD). Method Biannual data on individual characteristics, clinical and analytical progress, treatment, and events were studied for a cohort of incident patients undergoing PD (2003-2006) in a reference area of 8.8 million people. Results 489 patients (age 53.58 years, 61.6% male) with 3-year follow-up were included. They presented at inclusion with Charlson Comorbidity Index (CCI) of 5.25; previous cardiovascular (CV) event, 23.7%; diabetes mellitus (DM), 19.1%; and hypertension (HT), 89.9%. Annual hospitalization rate per patient-year at risk was 0.6. The variables that predicted admission were CCI [odds ratio (OR) 1.14 per point], DM (OR 1.66), and previous CV event (OR 1.90). Anemia maintained significance when corrected for CCI: hemoglobin, 0.79 per 1 g/dL Hb; CCI, 1.15 per point. Annual mortality rate was 5.4%. Those that died were older (67.47 vs 52.78 years) and had a higher CCI (8.35 vs 5.0), a lower initial Hb (11.5 vs 12.2 g/dL), a higher hospital admission rate, a higher annual rate of peritonitis, more previous CV events (50.0% vs 22.1%), and higher prevalence of DM (38.5% vs 17.9%). Survival analysis identified the following prognostic factors: CCI [hazard ratio (HR) 1.51 per point], CV event (HR 2.85), DM (HR 2.52), age (HR 1.06 per year), and mandatory referral to PD (HR 6.54). The effect of CV events and DM persisted after correction for age, and that of choice of technique after correcting for CCI and/or age. Conclusions The CCI is useful for risk estimation in PD patients. Previous CV event, DM, and age are the most relevant risk factors. Control of anemia has prognostic value for hospital admissions. Mandatory referral to PD is associated with higher mortality. The prognosis in PD depends on predialysis patient management.

An outstanding question of genome evolution is what stops the invasion of a host genome by transposable elements (TEs). The human genome, harboring the remnants of many extinct TE families, offers an extraordinary opportunity to investigate this problem. ERV9 is an endogenous retrovirus repeatedly mobilized during primate evolution, 15 to 6 million years ago (MYA), which left a trace of over a hundred provirus-like copies and at least 4,000 solitary long terminal repeats (LTRs) in the human genome. Then, its proliferation ceased for unknown reasons, and the family went extinct. We have made a detailed reconstruction of its last active subfamily, ERV9_XII, by examining 115 solitary LTRs from it. These insertions were grouped into 11 sets according to shared nucleotide variants, which could be placed in a sequential order of 10 to 6 MYA. At least 75% of the subfamily was produced 8 to 6 MYA, during a stage of intense proliferation. With new analytical tools, we show that the youngest and most prolific sets may have been produced by effectively instantaneous expansions of corresponding single-sequence variants. The extinction of this family apparently was not a consequence of its slow gradual degeneration, but the outcome of the fixation of specific restrictive alleles in the human-chimpanzee ancestral population. Three species-specific insertions (two in humans and one in chimpanzees) were identified, further supporting that extinction took place when these two species were beginning to diverge. These are the only fixed differences of this kind so far observed between humans and chimpanzees, apart from those belonging to the human endogenous retrovirus K family.

Background Spain has dramatically increased the number of controlled circulatory death donors (cDCD). The initial selection criteria for considering cDCD for kidney transplantation (KT) have been expanded progressively, with practically no limits in donor age during the last years. We aimed to analyze the early clinical outcomes using expanded (> 65 years) cDCD in comparison with standard ones. Methods Observational multicenter study including 19 transplant centers in Spain. We performed a systematic inclusion in a central database of every KT from expanded cDCD at each participant unit from January-2012 to January-2017. Surgical procedures and immunosuppressive protocols were based on local practices. Data was analyzed in the central office using logistic and Cox regression or competitive-risk models for multivariate analysis. Median time of follow-up was 18.1 months. Results 561 KT were performed with kidneys from cDCD, 135 from donors older than 65 years. As expected, recipients from older cDCD were also older (65.8 (SD 8.8) vs 53.7 (SD 11.4) years; p < 0.001) and with higher comorbidity. At 1 year, no differences were found amongst older and younger cDCD KT recipients in terms of serum creatinine (1.6 (SD 0.7) vs 1.5 (SD 0.8) mg/dl; p = 0.29). Non-death censored graft survival was inferior, but death-censored graft survival was not different (95.5 vs 98.2% respectively; p = 0.481). They also presented a trend towards higher delayed graft function (55.4 vs 46.7%; p = 0.09) but a similar rate of primary non-function (3.7 vs 3.1%; p = 0.71), and acute rejection (3.0 vs 6.3%; p = 0.135). In the multivariate analysis, in short follow-up, donor age was not related with worse survival or poor kidney function (eGFR < 30 ml/min). Conclusions The use of kidneys from expanded cDCD is increasing for older and comorbid patients. Short-term graft outcomes are similar for expanded and standard cDCD, so they constitute a good-enough source of kidneys to improve the options of KT wait-listed patients.

main study limitations were the small size of the study cohort and the lack of a control group. CONCLUSIONSCinacalcet is well tolerated and may improve biochemical control of SHPT in PD patients.

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