FGfor the Acute Dialysis Quality Initiative (ADQI) consensus group
for the Acute Dialysis Quality Initiative (ADQI) consensus group
+23
A consensus conference on cardio-renal syndromes (CRS) was held in Venice Italy, in September 2008 under the auspices of the Acute Dialysis Quality Initiative (ADQI). The following topics were matter of discussion after a systematic literature review and the appraisal of the best available evidence: definition/classification system; epidemiology; diagnostic criteria and biomarkers; prevention/protection strategies; management and therapy. The umbrella term CRS was used to identify a disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. Different syndromes were identified and classified into five subtypes. Acute CRS (type 1): acute worsening of heart function (AHF–ACS) leading to kidney injury and/or dysfunction. Chronic cardio-renal syndrome (type 2): chronic abnormalities in heart function (CHF-CHD) leading to kidney injury and/or dysfunction. Acute reno-cardiac syndrome (type 3): acute worsening of kidney function (AKI) leading to heart injury and/or dysfunction. Chronic reno-cardiac syndrome (type 4): chronic kidney disease leading to heart injury, disease, and/or dysfunction. Secondary CRS (type 5): systemic conditions leading to simultaneous injury and/or dysfunction of heart and kidney. Consensus statements concerning epidemiology, diagnosis, prevention, and management strategies are discussed in the paper for each of the syndromes.
1 September 2008 in European Journal of Heart Failure
Natriuretic peptide (NP) levels (B-type natriuretic peptide (BNP) and N-terminal proBNP) are now widely used in clinical practice and cardiovascular research throughout the world and have been incorporated into most national and international cardiovascular guidelines for heart failure. The role of NP levels in state-of-the-art clinical practice is evolving rapidly. This paper reviews and highlights ten key messages to clinicians: NP levels are quantitative plasma biomarkers of heart failure (HF).NP levels are accurate in the diagnosis of HF.NP levels may help risk stratify emergency department (ED) patients with regard to the need for hospital admission or direct ED discharge.NP levels help improve patient management and reduce total treatment costs in patients with acute dyspnoea.NP levels at the time of admission are powerful predictors of outcome in predicting death and re-hospitalisation in HF patients.NP levels at discharge aid in risk stratification of the HF patient.NP-guided therapy may improve morbidity and/or mortality in chronic HF.The combination of NP levels together with symptoms, signs and weight gain assists in the assessment of clinical decompensation in HF.NP levels can accelerate accurate diagnosis of heart failure presenting in primary care.NP levels may be helpful to screen for asymptomatic left ventricular dysfunction in high-risk patients. Published by Elsevier B.V. on behalf of European Society of Cardiology.
25 February 2010 in Nephrology Dialysis Transplantation
FGfor the Acute Dialysis Quality Initiative (ADQI) Consensus Group
for the Acute Dialysis Quality Initiative (ADQI) Consensus Group
+23
Observational and clinical trial data have accrued to show that acute/chronic heart disease can directly contribute to and/or accelerate acute/chronic worsening kidney function and vice versa. A description of the epidemiology of heart–kidney interaction, as defined by the proposed consensus cardio-renal syndrome (CRS) definitions, is a critical initial step towards understanding not only the overall burden of disease for each of the proposed CRS subtypes, but also their natural history, associated morbidity and mortality and potential health resource implications [1]. Importantly, these CRS subtypes may have important discriminating features in terms of predisposing or precipitating events, risk identification, natural history and outcomes. Likewise, a surveillance of the epidemiology is vital for determining whether there exist important gaps in knowledge and for the design of future epidemiologic investigations and clinical trials. Accordingly, this article will summarize the epidemiology of CRS.
12 March 2010 in Nephrology Dialysis Transplantation
FGfor the Acute Dialysis Quality Initiative (ADQI) consensus group
for the Acute Dialysis Quality Initiative (ADQI) consensus group
+23
Both cardiac and renal diseases are extremely common in the population and frequently coexist. Cardiac disease is often associated with worsening renal function and vice versa. The coexistence of cardiac and renal disease significantly increases mortality, morbidity and complexity and cost of care [1,2]. Syndromes describing the interaction between the heart and the kidney are recognized, but have never been clearly defined and classified. Several different definitions have been proposed [1,3–8] but none have been published as a result of a consensus process. As a result of the lack of consensus definition and classification, there is limited appreciation of its epidemiology, no standardized diagnostic criteria and no uniform approaches to prevention and treatment. Furthermore, treatment is often fragmented, single organ centred, with perceived competing priorities and specialty care is not necessarily integrated amongst relevant specialties. As a result, timing and appropriateness of care may suffer. In response to these issues, a consensus conference was organized under the auspices of the Acute Dialysis Quality Initiative (ADQI) by bringing together key opinion leaders and experts in the fields of nephrology, critical care, cardiac surgery, cardiology and epidemiology. A meeting was held in Venice, Italy from September 3 to 6, 2008. In this manuscript, we present the consensus document and the methodology by which a consensus definition and classification system for Cardio-Renal Syndromes was reached [9].
The cardiorenal syndrome (CRS) is a disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other. The general definition has been expanded into five subtypes reflecting the primacy of organ dysfunction and the time-frame of the syndrome: CRS type 1 = acute worsening of heart function leading to kidney injury and/or dysfunction; CRS type 2 = chronic abnormalities in heart function leading to kidney injury or dysfunction; CRS type 3 = acute worsening of kidney function leading to heart injury and/or dysfunction; CRS type 4 = chronic kidney disease leading to heart injury, disease and/or dysfunction, and CRS type 5 = systemic conditions leading to simultaneous injury and/or dysfunction of heart and kidney. Different pathophysiological mechanisms are involved in the combined dysfunction of heart and kidney in these five types of the syndrome.
Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) recently emerged in Wuhan, Hubei-China, as responsible for the coronavirus disease 2019 (COVID-19) and then spread rapidly worldwide. While most individuals remain asymptomatic or develop only mild symptoms, approximately 5% develop severe forms of COVID-19 characterized by acute respiratory distress syndrome (ARDS) and multiple-organ failure (MOF) that usually require intensive-care support and often yield a poor prognosis. Summary: The pathophysiology of COVID-19 is far from being completely understood, and the lack of effective treatments leads to a sense of urgency to develop new therapeutic strategies based on pathophysiological assumptions. The exaggerated cytokine release in response to viral infection, a condition known as cytokine release syndrome (CRS) or cytokine storm, is emerging as the mechanism leading to ARDS and MOF in COVID-19, thus endorsing the hypothesis that properly timed anti-inflammatory therapeutic strategies could improve patients’ clinical outcomes and prognosis. Key Messages: The objective of this article is to explore and comment on the potential role of the promising immunomodulatory therapies using pharmacological and nonpharmacological approaches to overcome the dysregulated proinflammatory response in COVID-19.