Bergsimpson4933
Complement activation may play a pathogenic role in patients with severe coronavirus disease 2019 (COVID-19) by contributing to tissue inflammation and microvascular thrombosis.
Serial samples were collected from patients receiving maintenance haemodialysis (HD). Thirty-nine patients had confirmed COVID-19 and 10 patients had no evidence of COVID-19. Plasma C5a and C3a levels were measured using enzyme-linked immunosorbent assay.
We identified elevated levels of plasma C3a and C5a in HD patients with severe COVID-19 compared with controls. Serial sampling identified that C5a levels were elevated prior to clinical deterioration in patients who developed severe disease. C3a more closely mirrored both clinical and biochemical disease severity.
Our findings suggest that activation of complement plays a role in the pathogenesis of COVID-19, leading to endothelial injury and lung damage. C5a may be an earlier biomarker of disease severity than conventional parameters such as C-reactive protein and this warrants further investigation in dedicated biomarker studies. Our data support the testing of complement inhibition as a therapeutic strategy for patients with severe COVID-19.
Our findings suggest that activation of complement plays a role in the pathogenesis of COVID-19, leading to endothelial injury and lung damage. C5a may be an earlier biomarker of disease severity than conventional parameters such as C-reactive protein and this warrants further investigation in dedicated biomarker studies. Our data support the testing of complement inhibition as a therapeutic strategy for patients with severe COVID-19.
The antidiuretic hormone (ADH) or arginine vasopressin (AVP) regulates the body's water balance. Recently, modifications in AVP levels have been related to osteoporosis during ageing and microgravity/bed rest. #link# Therefore the present study was devised to assess whether the absence of AVP, as in patients with central diabetes insipidus (CDI), modulates renal calcium excretion.
We retrospectively analysed data from 12 patients with CDI with measured 24-h urinary excretion levels of calcium. Data were available at the moment of the diagnosis when patients were drug-free and after therapy with dDAVP, an analog of AVP. Hypercalciuria was defined as 24-h urinary Ca
>275 mg/day in males and >250 mg/day in females and a urinary calcium (Ca)creatinine (Cr) ratio >0.20 mg/mg.
Untreated CDI patients had a daily urinary Ca
excretion of 383 ± 47 mg/day and a urinary CaCr ratio of 0.26 ± 0.38 mg/mg. The urine osmolarity significantly increased after the administration of dDAVP by 210% and the urinary flow decreased by 72%. Furthermore, the estimated glomerular filtration rate (eGFR) increased by 7%, which did not reach statistical significance. dDAVP treatment did not significantly modify the urinary Ca
concentration; however, the daily calcium excretion and the urinary CaCr ratio were significantly decreased (160 ± 27 mg/day and 0.11 ± 0.02 mg/mg, respectively).
Patients with CDI show hypercalciuria even though urine is more diluted than normal controls, and dDAVP reverses this effect. These data support the intriguing relationship between AVP and osteoporosis in ageing and microgravity/bed rest.
Patients with CDI show hypercalciuria even though urine is more diluted than normal controls, and dDAVP reverses this effect. These data support the intriguing relationship between AVP and osteoporosis in ageing and microgravity/bed rest.
selleck products (CKD) after lung transplantation (LT) is underestimated. The aim of the present study was to measure the loss of glomerular filtration rate (GFR) 1 year after LT and to identify the risk factors for developing Stage ≥3 CKD.
LT patients in the University Hospital of Lyon had a pre- and post-transplantation measurement of their GFR (mGFR), and GFR was also estimated using the Chronic Kidney Disease Epidemiology Collaboration equation.
During the study period, 111 patients were lung transplant candidates, of which 91 had a pre-transplantation mGFR, and 29 had a mGFR at 1 year after LT. Six patients underwent maintenance haemodialysis after transplantation. Mean mGFR was 106 mL/min/1.73 m
before LT and 58 mL/min/1.73 m
1 year after LT (P < 0.05) with a mean loss of 48 mL/min/1.73 m
per patient. The risk of developing Stage ≥3 CKD after LT was higher in patients with lower pre-LT mGFR (odds ratio for each 1 mL/min/1.73 m
increase 0.94, 95% confidence interval 0.88-0.99). Receiver operator characteristics curves for the sensitivity and specificity of eGFR and mGFR for the prediction of CKD Stage ≥3 after LT found that pre-LT mGFR of 101 mL/min/1.73 m
and pre-LT eGFR of 124 mL/min/1.73 m
were the optimal thresholds for predicting Stage ≥3 CKD after LT.
The present study underlines the value of mGFR in the pre-LT stage and found major renal function loss after LT, and consequently two-thirds of patients have Stage ≥3 CKD at 1 year. All patients with a pre-LT mGFR <90 mL/min/1.73 m
warrant particular attention.
The present study underlines the value of mGFR in the pre-LT stage and found major renal function loss after LT, and consequently two-thirds of patients have Stage ≥3 CKD at 1 year. All patients with a pre-LT mGFR less then 90 mL/min/1.73 m2 warrant particular attention.
Optimal management of chronic kidney disease (CKD) anaemia remains controversial and few studies have evaluated real-world management of anaemia in advanced CKD in the context of guideline recommendations.
We performed an observational study from the Swedish Renal Registry evaluating the epidemiology and treatment patterns of anaemia across Stages 3b-5 in non-dialysis (ND) and dialysis-dependent (DD) CKD patients during 2015. Logistic regression and Cox models explored the associations between anaemia treatments, inflammation, erythropoietin resistance index (ERI) and subsequent 1-year risk of major adverse cardiovascular events (MACEs).
Data from 14 415 (ND, 11 370; DD, 3045) patients were included. Anaemia occurred in 60% of ND and 93% of DD patients. DD patients used more erythropoiesis-stimulating agents (ESAs; 82% versus 24%) and iron (62% versus 21%) than ND patients. All weekly ESA doses were converted to a weight-adjusted weekly epoetin equivalent dose. The prescribed ESA doses were low to moderate [median 48.
