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Background and Aims There is an increased risk of thrombotic complications in patients with COVID-19. Hemodialysis patients are already at an increased risk for thromboembolic events such as stroke and pulmonary embolism. The aim of our study was to determine the incidence of late thrombotic complications (deep vein thrombosis, pulmonary embolism, stroke, new-onset vascular access thrombosis) in maintenance hemodialysis patients after recovery from COVID-19. Method We performed a retrospective cohort study of 200 prevalent hemodialysis patients in our center at the start of the pandemic. We excluded incident patients after the cohort entry date and those who required hemodialysis for acute kidney injury, and excluded patients with less than 1 month follow-up due to kidney transplantation or death from non-thrombotic causes. Results 185 prevalent hemodialysis patients finally met the inclusion criteria; 37 patients (17.6%) had SARS-CoV-2 infection, out of which 10 (27%) died during the acute phase of disease without evidence of thrombotic events. There was an increased risk of thrombotic events in COVID-19 survivors compared to the non-infected cohort (18.5% vs 1.9%, p=0.002) after a median follow-up of 7 months. Stroke incidence was 38.9 episodes/1000 patient-years in patients infected with SARS-CoV-2, compared to an incidence of 2.8 episodes/1000 patient-years in non-infected patients during the follow-up period. The median time from diagnosis of SARS-CoV-2 to the first thrombotic event was 62 days (interquartile range 5-118 days). Survival analysis with Kaplan-Meier curves revealed an increase in the rate of thrombotic events after SARS-CoV-2 compared to non-infected patients (see Figure 1). Mean survival from thrombotic event was 6.1±0.4 months in the COVID-infected group, compared to 6.97±0.04 months in the non-infected group (p Conclusion There is an increased risk of late thrombotic complications in hemodialysis patients after infection with COVID-19. Further studies should evaluate the benefit of prolonged prophylactic anticoagulation in hemodialysis patients after recovery from COVID-19.

Background and Aims Thirst mechanism is essential to maintain an adequate osmolarity and homeostasis. During summer heat waves, there is an increased morbidity and mortality in elderly patients that has led to generally recommend an increase in fluid intake in all elderly patients beyond thirst stimulation, even in those independent patients with free access to water. The aim of this study was to observe the differences in calculated serum osmolarity (cOsm) between young, elderly and very elderly patients who were neither institutionalized nor hospitalized, in different seasons throughout the year. Method We conducted a retrospective cross-sectional study in outpatients between 18-104 years old that had undergone a blood test between July 2019 and January 2020, in which serum osmolarity could be calculated. Patients with serum creatinine above 1.5 mg/dl were excluded. Results The study included 45236 blood samples from 41132 patients, 56.1% were female. 50% of patients were between 18 and 65 years old, 45.4% were between 65 and 85 years old and 4.6% were >85 years old. The mean cOsm in patients between 18-65 years was 288.3 mOsm/kg, compared to 289.8 mOsm/kg in those between 65- 85 years old (p85 years, mean cOsm was 289.4 mOsm/kg. When comparing cOsm between different seasons of the year, cOsm in summer months was about 1 mOsm/kg higher than in autumn-winter (288.9 mOsm/kg vs 287.8 mOsm/kg in young patients, p=0.0001; 290.5 mOsm/kg vs 289.4 mOsm/kg in elderly patients, p=0.0001). In the very elderly (>85 years) the difference was smaller and non-significant (289.6mOsm/kg vs 289.1mOsm/kg). Conclusion Under physiologic conditions, patients >65 years have a slightly higher calculated serum osmolarity than younger patients, nevertheless staying within normal range. These differences only increase in 1 mOsm/kg during the summer months. Therefore, it is not indicated to force an increase in fluid intake in the elderly or very elderly population under physiologic conditions.

Background Several studies have demonstrated that levels of circulating inflammatory markers such as tumour necrosis factorα (TNFα), are associated with early progression of diabetic nephropathy (DN). The aim of this study was to investigate whether there is an association between circulating TNFα receptor and disease progression in patients with advanced type 2 DN and severe proteinuria. Methods Between 2006 and 2011, we measured levels of circulating soluble TNFα receptor 1 (TNFR1) and soluble TNFα receptor 2 (TNFR2) at baseline and 4 and 12 months in 101 patients included in a multicenter randomized controlled trial to compare the effect of optimal doses of renin-angiotensin system blockers in monotherapy or in combination (dual blockade) to slow progression of established type 2 DN. The primary composite endpoint was a >50% increase in baseline serum creatinine, end-stage renal disease, or death. Results The median follow-up was 32 months (IQR, 18-48), during which time 28 patients (22.7%) achieved the primary endpoint. The TNFR1 level, but not the TNFR2 level, was correlated with other inflammatory markers. Cox regression analysis showed that the highest TNFR1 levels (HR, 2.60; 95%CI, 1.11–86.34) and baseline proteinuria (HR 1.32; 95%CI 1.15–1.52) were associated with the primary endpoint. The mixed model analysis revealed that TNFR1 and the TNFR2 levels did not change after starting treatment with renin-angiotensin system blockers. Conclusions Our results show that the highest levels of TNFR1 are independently associated with progression of renal disease and death in type 2 DN. The renin angiotensin blockers have no effect on these inflammatory markers.

Focal segmental glomerulosclerosis (FSGS) is a histological pattern of glomerular injury, rather than a single disease, that is caused by diverse clinicopathological entities with different mechanisms of injury with the podocyte as the principal target of lesion, leading to the characteristic sclerotic lesions in parts (i.e., focal) of some (i.e., segmental) glomeruli. The lesion of FSGS has shown an increasing prevalence over the past few decades and is considered the most common glomerular cause leading to ESKD. Primary FSGS, which usually presents with nephrotic syndrome, is thought to be caused by circulating permeability factors that have a main role in podocyte foot process effacement. Secondary forms of FSGS include maladaptive FSGS secondary to glomerular hyperfiltration such as in obesity or in cases of loss in nephron mass, virus-associated FSGS, and drug-associated FSGS that can result in direct podocyte injury. Genetic FSGS is increasingly been recognized and a careful evaluation of patients with atypical primary or secondary FSGS should be performed to exclude genetic causes. Unlike primary FSGS, secondary and genetic forms of FSGS do not respond to immunosuppression and tend not to recur after kidney transplantation. Distinguishing primary FSGS from secondary and genetic causes has a prognostic significance and is crucial for an appropriate management. In this review, we examine the pathogenesis, clinical approach to distinguish between the different causes, and current recommendations in the management of FSGS.