Objectives Effective treatments for coronavirus disease 2019 (COVID-19) are urgently needed. We hypothesized that colchicine, by counteracting proinflammatory pathways implicated in the uncontrolled inflammatory response of COVID-19 patients, reduces pulmonary complications, and improves survival. Methods This retrospective study included 71 consecutive COVID-19 patients (hospitalized with pneumonia on CT scan or outpatients) who received colchicine and compared with 70 control patients who did not receive colchicine in two serial time periods at the same institution. We used inverse probability of treatment propensity-score weighting to examine differences in mortality, clinical improvement (using a 7-point ordinary scale), and inflammatory markers between the two groups. Results Amongst the 141 COVID-19 patients (118 [83.7%] hospitalized), 70 (50%) received colchicine. The 21-day crude cumulative mortality was 7.5% in the colchicine group and 28.5% in the control group (P = 0.006; adjusted hazard ratio: 0.24 [95%CI: 0.09 to 0.67]); 21-day clinical improvement occurred in 40.0% of the patients on colchicine and in 26.6% of control patients (adjusted relative improvement rate: 1.80 [95%CI: 1.00 to 3.22]). The strong association between the use of colchicine and reduced mortality was further supported by the diverging linear trends of percent daily change in lymphocyte count (P = 0.018), neutrophil-to-lymphocyte ratio (P = 0.003), and in C-reactive protein levels (P = 0.009). Colchicine was stopped because of transient side effects (diarrhea or skin rashes) in 7% of patients. Conclusion In this retrospective cohort study colchicine was associated with reduced mortality and accelerated recovery in COVID-19 patients. This support the rationale for current larger randomized controlled trials testing the safety/efficacy profile of colchicine in COVID-19 patients.
Background Polycystic kidney diseases (PKD) are an important cause of chronic kidney disease (CKD). ADPKD due to PKD1 or PKD2 mutations is the most common form, but other genes can be responsible for ADPKD or its phenocopies. Among them, a form of atypical ADPKD caused by DNAJB11 mutations (DNAJB11-PKD) has been recently described. Methods We retrospectively recruited a cohort of 27 patients from 6 different families sharing common ancestries and harboring the same DNAJB11 mutation (c.100C > T, p.Arg34*), and we compared it with a cohort of 42 typical ADPKD patients. Results DNAJB11-PKD patients show small/normal sized kidneys, with significantly smaller cysts and a slower progression to end-stage kidney disease (ESKD) than ADPKD patients. In the DNAJB11-PKD cohort the cystic phenotype could not be detected by ultrasound in about half of the patients, but all cases with available CT/MR displayed cysts. Clinically, DNAJB11-PKD patients displayed proteinuria (mostly albuminuria). Compared to ADPKD, DNAJB11-PKD patients were older and had higher prevalence of type 2 diabetes mellitus (19 vs 0%; P = 0.007) and nephrolithiasis (62 vs 29%; P = 0.01), while the prevalence of cardiac valvular defects was lower (4 vs 51%; P < 0.001). Conclusions Overall, clinical features of DNAJB11-PKD were more subtle compared to those of ADPKD. DNAJB11-PKD shows a unique renal and extra-renal phenotype, clinical presentation, and natural history. Therefore, our data support that this genetic disease is classified separately from ADPKD.
IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide and it is characterized by mesangial IgA deposition. Asymptomatic hematuria with various degrees of proteinuria is the most common clinical presentation and up to 20-40% of patients develop end-stage kidney disease (ESKD) within 20 years after disease onset. The pathogenesis of IgAN involves four sequential processes known as the “four-hit hypothesis” that starts with the production of a galactose-deficient IgA1 (gd-IgA1), followed by the formation of anti-gd-IgA1 IgG or IgA1 autoantibodies and immune complexes that ultimately deposit in the glomerular mesangium, leading to inflammation and injury. Although several key questions about the production of gd-IgA1 and the formation of anti-gd-IgA1 antibodies remain unanswered, a growing body of evidence is shedding light on the innate and adaptive immune mechanisms involved in this complex pathogenic process. Herein, we will focus on these mechanisms that, along with genetic and environmental factors, are thought to play a key role in disease pathogenesis.
Background and aims: Critically ill patients with acute kidney injury (AKI) undergo major muscle wasting in the first few days of ICU stay. An important concern in this clinical setting is the lack of adequate tools for routine bedside evaluation of the skeletal muscle mass, both for the determination of nutritional status at admission, and for monitoring. In this regard, the present study aims to ascertain if ultrasound (US) is able to detect changes in quadriceps muscle thickness of critically ill patients with acute kidney injury (AKI) over short periods of time.Methods: This is a prospective observational study with a follow-up at 5 days. All adult patients with AKI hospitalized at the Renal ICU of the Parma University Hospital over 12 months, with a hospital stay before ICU admission no longer than 72 h, and with a planned ICU stay of at least 5 days, were eligible for the study. An experienced investigator assessed quadriceps rectus femoris and vastus intermedius thickness (QRFT and QVIT) at baseline and after 5 days of ICU stay.Results: We enrolled 30 patients with 74 ± 11 years of age and APACHE II score of 22 ± 5. Muscle thickness decreased by 15 ± 13% within the first 5 days of ICU stay (P < 0.001 for all sites as compared to ICU admission). Patients with more severe muscle loss had lower probability of being discharged home (OR: 0.04, 95%CI: 0.00–0.74; P = 0.031).Conclusions: In critically ill patients with AKI, bedside muscle US identifies patients with accelerated muscle wasting.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.