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. 2020 Oct;7(5):3219-3224.
doi: 10.1002/ehf2.12788. Epub 2020 Jun 24.

Mortality and pathophysiology of acute kidney injury according to time of occurrence in acute heart failure

Matthias Diebold  1   2 , Nikola Kozhuharov  1   3 , Desiree Wussler  1   2 , Ivo Strebel  1   3 , Zaid Sabti  1 , Dayana Flores  1 , Samyut Shrestha  1   2 , Jasmin Martin  1   2 , Daniel Staub  4 , Per Venge  5 , Christian Mueller  1   3 , Tobias Breidthardt  1   2
Affiliations

Mortality and pathophysiology of acute kidney injury according to time of occurrence in acute heart failure

Matthias Diebold et al. ESC Heart Fail. 2020 Oct.

Abstract

Aims: Acute kidney injury (AKI) during acute heart failure (AHF) is common and associated with increased morbidity and mortality. The underlying pathophysiological mechanism appears to have prognostic relevance; however, the differentiation of true, structural AKI from hemodynamic pseudo-AKI remains a clinical challenge.

Methods and results: The Basics in Acute Shortness of Breath Evaluation Study (NCT01831115) prospectively enrolled adult patients presenting with AHF to the emergency department. Mortality of patients was prospectively assessed. Haemoconcentration, transglomerular pressure gradient (n = 231) and tubular injury patterns (n = 253) were evaluated to investigate pathophysiological mechanisms underlying AKI timing (existing at presentation vs. developing during in-hospital period). Of 1643 AHF patients, 755 patients (46%) experienced an episode of AKI; 310 patients (19%; 41% of AKI patients) presented with community-acquired AKI (CA-AKI), 445 patients (27%; 59% of AKI patients) developed in-hospital AKI. CA-AKI but not in-hospital AKI was associated with higher mortality compared with no-AKI (adjusted hazard ratio 1.32 [95%-CI 1.01-1.74]; P = 0.04). Independent of AKI timing, haemoconcentration was associated with a lower two-year mortality. Transglomerular pressure gradient at presentation was significantly lower in CA-AKI compared to in-hospital AKI and no-AKI (P < 0.01). Urinary NGAL ratio concentrations were significantly higher in CA-AKI compared to in-hospital AKI (P < 0.01) or no-AKI (P < 0.01).

Conclusions: CA-AKI but not in-hospital AKI is associated with increased long-term mortality and marked by decreased transglomerular pressure gradient and tubular injury, probably reflecting prolonged tubular ischemia due to reno-venous congestion. Adequate decongestion, as assessed by haemoconcentration, is associated with lower long-term mortality independent of AKI timing.

Keywords: Acute heart failure; Acute kidney injury; Mortality and pathophysiology; NGAL.

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Conflict of interest statement

Dr Breidthardt received research grants from the Swiss National Science Foundation (PASMP3‐134362), University Hospital Basel, Abbott and Roche as well as speakers honoraria from Roche. Professor Mueller received research grants from the Swiss National Science Foundation and the Swiss Heart Foundation, the European Union, the Cardiovascular Research Foundation Basel, the University of Basel, 8sense, Abbott, ALERE, Astra Zeneca, Beckman Coulter, Biomerieux, BRAHMS, Critical Diagnostics, Nanosphere, Roche, Siemens, Singulex, and the University Hospital Basel, as well as speaker or consulting honoraria from Abbott, ALERE, Astra Zeneca, BG Medicine, Biomerieux, BMS, Boehringer Ingelheim, BRAHMS, Cardiorentis, Daiichi Sankyo, Novartis, Roche, Sanofi, Singulex, and Siemens. Dr Venge owns shares in Diagnostics Development (Uppsala, Sweden) and owns worldwide granted patents of measuring NGAL in human diseases. The other authors report no conflict of interest.

Figures

Figure 1
Figure 1
Adjusted mortality curves for community‐acquired (CA)‐AKI (green line), in‐hospital AKI (red line) and no AKI (blue line) in the whole cohort. Only CA‐AKI was significantly associated with higher mortality compared with no AKI patients. Adjusted for age, blood urea nitrogen, N‐terminal pro‐B‐type natriuretic peptide, high‐sensitivity troponin T, potassium, haemoglobin, mean arterial pressure, c‐reactive protein, New York Heart Association (NYHA) class IV, and delta creatinine between steady state and peak and beta blocker use at baseline. For all the covariates, the mean was used as constant value and beta‐blocker use at baseline was set as user for this plot. AKI, acute kidney injury.
See this image and copyright information in PMC

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