External validation of the KFRE and Grams prediction models for kidney failure and death in a Spanish cohort of patients with advanced chronic kidney disease.

BACKGROUND: The Kidney Failure Risk Equation (KFRE) is a 2- and 5-year kidney failure prediction model that is applied in chronic kidney disease (CKD) G3 + . The Grams model predicts kidney failure and death at 2 and 4 years in CKD G4 + . There are limited external validations of the Grams model, especially for predicting mortality before kidney failure. METHODS: We performed an external validation of the Grams and Kidney Failure Risk Equation prediction models in incident patients with CKD G4 + at Hospital Universitario Fundación Alcorcón, Spain, between 1/1/2014 and 31/12/2018, ending follow-up on 30/09/2023. Discrimination was performed calculating the area under the receiver-operating characteristic curve. Calibration was assessed using the Hosmer-Lemeshow test and the Brier score. RESULTS: The study included 339 patients (mean age 72.2 ± 12.7 years and baseline estimated glomerular filtration rate 20.6 ± 5.0 ml/min). Both models showed excellent discrimination. The area under the curve (AUC) for Kidney Failure Risk Equation-2 and Grams-2 were 0.894 (95% CI 0.857-0.931) and 0.897 (95%CI 0.859-0.935), respectively. For Grams-4 the AUC was 0.841 (95%CI 0.798-0.883), and for Kidney Failure Risk Equation-5 it was 0.823 (95% CI 0.779-0.867). For death before kidney failure, the Grams model showed acceptable discrimination (AUC 0.708 (95% CI 0.626-0.790) and 0.744 (95% CI 0.683-0.804) for Grams-2 and Grams-4, respectively). Both models presented excellent calibration for predicting kidney failure. Grams model calibration to estimate mortality before kidney failure was also excellent. In all cases, Hosmer-Lemeshow test resulted in a p-value greater than 0.05, and the Brier score was less than 0.20. CONCLUSIONS: In a cohort of patients with CKD G4 + from southern Europe, both the Grams and Kidney Failure Risk Equation models are accurate in estimating the risk of kidney failure. Additionally, the Grams model provides a reliable estimate of the risk of mortality before kidney failure.

Late thrombotic complications after SARS-CoV-2 infection in hemodialysis patients.

INTRODUCTION: 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. METHODS: 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. FINDINGS: One-hundred and eighty five 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. Multivariate regression analysis showed that COVID-19 infection increased risk for late thrombotic events adjusted for age, sex, hypertension, diabetes, antithrombotic treatment, and previous thrombotic events (Odds Ratio (OR) 26.4, 95% confidence interval 2.5-280.6, p = 0.01). Clinical and laboratory markers did not predict thrombotic events. CONCLUSIONS: 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.

Focal Segmental Glomerulosclerosis: State-of-the-Art and Clinical Perspective.

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.

Nuevos retos en las nefritis tubulointersticiales inducidas por fármacos / New challenges in tubulointerstitial nephritis induced by drugs

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High levels of circulating TNFR1 increase the risk of all-cause mortality and progression of renal disease in type 2 diabetic nephropathy.

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.