Background: Lung ultrasound (LUS) is a useful imaging method for identifying COVID-19 pneumonia. The aim of this study was to explore the role of LUS in predicting the severity of the disease and fatality in patients with COVID-19. Methods: This was a single-center, follow-up study, conducted from 1 November 2020, to 22 March 2021. The LUS protocol was based on the assessment of 14 lung zones with a total score up to 42, which was compared to the disease severity and fatality. Results: A total of 133 patients with COVID-19 pneumonia confirmed by RT-PCR were enrolled, with a median time from hospital admission to lung ultrasound of one day. The LUS score was correlated with clinical severity at hospital admission (Spearman’s rho 0.40, 95% CI 0.24 to 0.53, p < 0.001). Patients with higher LUS scores were experiencing greater disease severity; a high flow nasal cannula had an odds ratio of 1.43 (5% CI 1.17–1.74) in patients with LUS score > 29; the same score also predicted the need for mechanical ventilation (1.25, [1.07–1.48]). An LUS score > 30 (1.41 [1.18–1.68]) and age over 68 (1.26 [1.11–1.43]) were significant predictors of fatality. Conclusions: LUS at hospital admission is shown to have a high predictive power of the severity and fatality of COVID-19 pneumonia.

Autophagy is the primary intracellular degradation system, and it plays an important role in many biological and pathological processes. Studies of autophagy involvement in developmental processes are important for understanding various processes. Among them are fibrosis, degenerative diseases, cancer development, and metastasis formation. Diabetic kidney disease is one of the main causes of chronic kidney disease and end-stage renal failure. The aim of this study was to investigate the immunohistochemical expression patterns of LC3B, LAMP2A, and GRP78 during different developmental stages of early-developing human kidneys and in samples from patients with type II diabetes mellitus. During the 7/8th DW, moderate expression of LC3B and LAMP2A and strong expression of GRP78 were found in the mesonephric glomeruli and tubules. In the 9/10th DW, the expression of LC3B and LAMP2A was even more pronounced in the mesonephric tubules. LC3B, LAMP2A, and GRP78 immunoreactivity was also found in the paramesonephric and mesonephric ducts and was stronger in the 9/10th DW compared with the 7/8th DW. In addition, the expression of LC3B, LAMP2A, and GRP78 also appeared in the mesenchyme surrounding the paramesonephric duct in the 9/10th DW. In the 15/16th DW, the expression of LC3B in the glomeruli was weak, that of LAMP2A was moderate, and that of GRP78 was strong. In the tubuli, the expression of LC3B was moderate, while the expression of LAMP2A and GRP78 was strong. The strongest expression of LC3B, LAMP2A, and GRP78 was observed in the renal medullary structures, including developing blood vessels. In postnatal human kidneys, the most extensive LC3B, LAMP2A, and GRP78 expression in the cortex was found in the epithelium of the proximal convoluted tubules, with weak to moderate expression in the glomeruli. The medullary expression of LC3B was weak, but the expression of LAMP2A and GRP78 was the strongest in the medullary tubular structures. Significantly lower expression of LC3B was found in the glomeruli of the diabetic patients in comparison with the nondiabetic patients, but there was no difference in the expression of LC3B in the tubule–interstitial compartment. The expression of LAMP2A was significantly higher in the tubule–interstitial compartments of the diabetic patients in comparison with the nondiabetic patients, while its expression did not differ in the glomeruli. Extensive expression of GRP78 was found in the glomeruli and the tubule–interstitial compartments, but there was no difference in the expression between the two groups of patients. These data give us new information about the expression of LC3B, LAMP2A, and GRP78 during embryonic, fetal, and early postnatal development. The spatiotemporal expression of LC3B, LAMP2A, and GRP78 indicates the important role of autophagy during the early stages of renal development. In addition, our data suggest a disturbance in autophagy processes in the glomeruli and tubuli of diabetic kidneys as an important factor in the pathogenesis of diabetic kidney disease.

Cilj: Prikazati bolesnika koji je u redovitom postupku hemodijalize, a kod kojeg je došlo do aktiviranja implantiranog supkutanog kardioverter-defibrilatora (S-ICD) zbog hiperkalijemije, kako bi se naglasila važnost ranog prepoznavanja ovog uzroka neodgovarajuće isporuke električnih šokova (EŠ). Prikaz slučaja: Muškarac u dobi od 65 godina pozvao je hitnu medicinsku službu (HMS) radi učestalih aktivacija uređaja S-ICD. Radi se o bolesniku s terminalnim zatajenjem bubrežne funkcije koji je u programu kronične hemodijalize, a koji ima postavljen S-ICD radi sekundarne prevencije nagle srčane smrti. Nakon dolaska tima HMS-a snimljen je 12- kanalni elektrokardiogram koji je pokazao pravilan ritam s patološki proširenim QRS kompleksima, frekvencije ventrikula oko 50/min. Bolesnik je zaprimljen u objedinjeni hitni bolnički prijam radi daljnjeg liječenja. Tijekom početne obrade učinjena je analiza krvi uz krevet bolesnika koja je pokazala izrazito povišene vrijednosti kalija (8,6 mmol/L). Primijenjena je odgovarajuća terapija (kalcijev glukonat, infuzija inzulina i glukoze, inhalacija salbutamola) te je bolesnik primljen u jedinicu intenzivne medicine radi žurne hemodijalize. Nakon što je postignuta korekcija elektrolitskog disbalansa, došlo je i do normalizacije EKG-a te nije bilo daljnjih aktivacija uređaja S-ICD. Ispitivanjem uređaja zaključeno je da je do aktivacije uređaja došlo zbog hiperkalijemije s posljedičnim patološkim promjenama QRS kompleksa (QRS 300 ms), što je pogrešno prepoznato kao maligna aritmija. Zaključak: Tijekom zbrinjavanja bolesnika s aktivacijama uređaja S-ICD potrebno je razmišljati i o mogućnosti neodgovarajuće isporuke električnih šokova. Neodgovarajuća isporuka električnih šokova najčešće je uzrokovana preosjetljivošću u očitanju T-vala, a hiperkalijemija je čest uzrok, upravo u skupini hemodijaliziranih bolesnika koji imaju implantiranu ovu vrstu kardioverter-defibrilatora.

Zatajivanje srca klinički je sindrom koji obuhvaća simptome i znakove nastale uslijed porasta intrakardijalnih tlakova ili smanjenog minutnog volumena, što je uzrokovano strukturnim i/ili funkcionalnim abnormalnostima srca. Akutno zatajivanje srca (AZS) životno je ugrožavajuće stanje koje zahtijeva žurno zbrinjavanje u hitnoj medicinskoj službi, odnosno neplaniranu hospitalizaciju. Očituje se kroz četiri glavne kliničke prezentacije koje se često preklapaju, a to su akutno dekompenzirano srčano popuštanje, akutni plućni edem, kardiogeni šok i izolirano desnostrano srčano zatajenje. Dijagnoza AZS-a postavlja se prvenstveno na osnovi kliničkih znakova i simptoma te se potvrđuje odgovarajućim dijagnostičkim pretragama. Zbrinjavanje u okviru hitne medicinske službe sastoji se od istovremene kliničke procjene, nužne dijagnostičke obrade i primjene ciljane terapije. Ovisno o stanju bolesnika liječenje uključuje oksigenoterapiju te najčešće primjenu neinvazivnih ventilacijskih modaliteta, dok osnovna farmakološka terapija najčešće obuhvaća primjenu intravenskih diuretika i vazodilatatora, ovisno o vrijednostima arterijskog tlaka i stupnju kongestije. Rana intravenska primjena diuretika Henleove petlje temelj je liječenja AZS-a. Inotropi se primjenjuju za hemodinamsku stabilizaciju bolesnika s niskim minutnim volumenom srca te hipotenzijom. Napredno liječenje AZS-a u slučajevima AZS-a refrakternog na konzervativnu terapiju najčešće uključuje primjenu modaliteta mehaničke cirkulatorne potpore.