Acute pyelonephritis(APN)is a bacterial infection resulting in kidney inflammation,typically arising as a complication of an ascending urinary tract infection that ascends from the bladder to the kidneys.Clinical diag...Acute pyelonephritis(APN)is a bacterial infection resulting in kidney inflammation,typically arising as a complication of an ascending urinary tract infection that ascends from the bladder to the kidneys.Clinical diagnosis is generally based on clinical and laboratory findings.Recent guidelines recommend not performing diagnostic imaging unless a complicated APN is suspected or the infection affects high-risk patients such as the elderly,immunocompromised individuals,or diabetics.Contrast-enhanced ultrasound(CEUS)is a valuable tool in both the diagnosis and follow-up of APN.It aids in distinguishing small simple nephritic involvement from abscess complications and monitoring their evolution over time during antibiotic therapy.Given its lack of ionizing radiation and nephrotoxicity,CEUS is a valid diagnostic modality for approaching and monitoring pyelonephritis,improving early identification and characterization of inflammatory lesions.This review aims to summarize the main evidence on the use of ultrasound and CEUS in the diagnosis of APN and its follow-up.展开更多
Coronavirus disease 2019(COVID-19)is,at present,one of the most relevant global health problems.In the literature hepatic alterations have been described in COVID-19 patients,and they are mainly represented by worseni...Coronavirus disease 2019(COVID-19)is,at present,one of the most relevant global health problems.In the literature hepatic alterations have been described in COVID-19 patients,and they are mainly represented by worsening of underlying chronic liver disease leading to hepatic decompensation and liver failure with higher mortality.Several potential mechanisms used by severe acute respiratory syndrome coronavirus 2(SARS-Co V-2)to cause liver damage have been hypothesized.COVID-19 primary liver injury is less common than secondary liver injury.Most of the available data demonstrate how liver damage in SARSCo V-2 infection is likely due to systemic inflammation,and it is less likely mediated by a cytopathic effect directed on liver cells.Moreover,liver alterations could be caused by hypoxic injury and drugs(antibiotics and non-steroidal antiinflammatory drugs,remdesivir,tocilizumab,tofacitinib and dexamethasone).SARS-Co V-2 infection can induce multiple vascular district atherothrombosis by affecting simultaneously cerebral,coronary and peripheral vascular beds.Data in the literature highlight how the virus triggers an exaggerated immune response,which added to the cytopathic effect of the virus can induce endothelial damage and a prothrombotic dysregulation of hemostasis.This leads to a higher incidence of symptomatic and confirmed venous thrombosis and of pulmonary embolisms,especially in central,lobar or segmental pulmonary arteries,in COVID-19.There are currently fewer data for arterial thrombosis,while myocardial injury was identified in 7%-17%of patients hospitalized with SARS-Co V-2 infection and 22%-31%in the intensive care unit setting.Available data also revealed a higher occurrence of stroke and more serious forms of peripheral arterial disease in COVID-19 patients.Hemostasis dysregulation is observed during the COVID-19 course.Lower platelet count,mildly increased prothrombin time and increased Ddimer are typical laboratory features of patients with severe SARS-Co V-2 infection,described as“COVID-19 associated coagulopathy.”These alterations are correlated to poor outcomes.Moreover,patients with severe SARS-Co V-2 infection are characterized by high levels of von Willebrand factor with subsequent ADAMTS13 deficiency and impaired fibrinolysis.Platelet hyperreactivity,hypercoagulability and hypofibrinolysis during SARS-Co V-2 infection induce a pathological state named as“immuno-thromboinflammation.”Finally,liver dysfunction and coagulopathy are often observed at the same time in patients with COVID-19.The hypothesis that liver dysfunction could be mediated by microvascular thrombosis has been supported by postmortem findings and extensive vascular portal and sinusoidal thrombosis observation.Other evidence has shown a correlation between coagulation and liver damage in COVID-19,underlined by the transaminase association with coagulopathy,identified through laboratory markers such as prothrombin time,international normalized ratio,fibrinogen,D-dimer,fibrin/fibrinogen degradation products and platelet count.Other possible mechanisms like immunogenesis of COVID-19 damage or massive pericyte activation with consequent vessel wall fibrosis have been suggested.展开更多
文摘Acute pyelonephritis(APN)is a bacterial infection resulting in kidney inflammation,typically arising as a complication of an ascending urinary tract infection that ascends from the bladder to the kidneys.Clinical diagnosis is generally based on clinical and laboratory findings.Recent guidelines recommend not performing diagnostic imaging unless a complicated APN is suspected or the infection affects high-risk patients such as the elderly,immunocompromised individuals,or diabetics.Contrast-enhanced ultrasound(CEUS)is a valuable tool in both the diagnosis and follow-up of APN.It aids in distinguishing small simple nephritic involvement from abscess complications and monitoring their evolution over time during antibiotic therapy.Given its lack of ionizing radiation and nephrotoxicity,CEUS is a valid diagnostic modality for approaching and monitoring pyelonephritis,improving early identification and characterization of inflammatory lesions.This review aims to summarize the main evidence on the use of ultrasound and CEUS in the diagnosis of APN and its follow-up.
文摘Coronavirus disease 2019(COVID-19)is,at present,one of the most relevant global health problems.In the literature hepatic alterations have been described in COVID-19 patients,and they are mainly represented by worsening of underlying chronic liver disease leading to hepatic decompensation and liver failure with higher mortality.Several potential mechanisms used by severe acute respiratory syndrome coronavirus 2(SARS-Co V-2)to cause liver damage have been hypothesized.COVID-19 primary liver injury is less common than secondary liver injury.Most of the available data demonstrate how liver damage in SARSCo V-2 infection is likely due to systemic inflammation,and it is less likely mediated by a cytopathic effect directed on liver cells.Moreover,liver alterations could be caused by hypoxic injury and drugs(antibiotics and non-steroidal antiinflammatory drugs,remdesivir,tocilizumab,tofacitinib and dexamethasone).SARS-Co V-2 infection can induce multiple vascular district atherothrombosis by affecting simultaneously cerebral,coronary and peripheral vascular beds.Data in the literature highlight how the virus triggers an exaggerated immune response,which added to the cytopathic effect of the virus can induce endothelial damage and a prothrombotic dysregulation of hemostasis.This leads to a higher incidence of symptomatic and confirmed venous thrombosis and of pulmonary embolisms,especially in central,lobar or segmental pulmonary arteries,in COVID-19.There are currently fewer data for arterial thrombosis,while myocardial injury was identified in 7%-17%of patients hospitalized with SARS-Co V-2 infection and 22%-31%in the intensive care unit setting.Available data also revealed a higher occurrence of stroke and more serious forms of peripheral arterial disease in COVID-19 patients.Hemostasis dysregulation is observed during the COVID-19 course.Lower platelet count,mildly increased prothrombin time and increased Ddimer are typical laboratory features of patients with severe SARS-Co V-2 infection,described as“COVID-19 associated coagulopathy.”These alterations are correlated to poor outcomes.Moreover,patients with severe SARS-Co V-2 infection are characterized by high levels of von Willebrand factor with subsequent ADAMTS13 deficiency and impaired fibrinolysis.Platelet hyperreactivity,hypercoagulability and hypofibrinolysis during SARS-Co V-2 infection induce a pathological state named as“immuno-thromboinflammation.”Finally,liver dysfunction and coagulopathy are often observed at the same time in patients with COVID-19.The hypothesis that liver dysfunction could be mediated by microvascular thrombosis has been supported by postmortem findings and extensive vascular portal and sinusoidal thrombosis observation.Other evidence has shown a correlation between coagulation and liver damage in COVID-19,underlined by the transaminase association with coagulopathy,identified through laboratory markers such as prothrombin time,international normalized ratio,fibrinogen,D-dimer,fibrin/fibrinogen degradation products and platelet count.Other possible mechanisms like immunogenesis of COVID-19 damage or massive pericyte activation with consequent vessel wall fibrosis have been suggested.
