scholarly journals Uncontrolled hypertension and elevated NT-proBNP predict acute kidney injury and cardiac death in all-comer patients 1 year after acute coronary syndromes

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Denegri ◽  
L Raeber ◽  
S Windecker ◽  
B Gencer ◽  
F Mach ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Acute Kidney Injury ◽  
Cardiac Death ◽  
Acute Coronary Syndromes ◽  
Kidney Injury ◽  
Composite Endpoint ◽  
Uncontrolled Hypertension ◽  
Increased Risk ◽  
Coronary Syndromes ◽  
One Year

Abstract Background Hypertension is a recognized cardiovascular (CV) risk factor and, although many highly effective antihypertensive drugs have been developed, most patients fail to achieve recommended blood pressure target levels. This may increase major adverse CV events after acute coronary syndromes (ACS) such as acute kidney injury (AKI) and cardiac death (CD). Purpose We assessed the prognostic value of uncontrolled hypertension (UH) and elevated NT-proBNP among 2,168 all-comer patients admitted to 4 Swiss University Hospitals for acute coronary syndromes (ACS) enrolled in the prospective multicenter SPUM registry. Methods Patients with UH defined as a systolic blood pressure≥140 mmHg, and a NT-proBNP>900 ng/l were considered for the analysis. The composite primary endpoint was AKI and CD. Adjusted Cox proportional hazards regression models were implemented to determine risk prediction for UH and elevated NT-proBNP levels. Results Out of 2,168 ACS patients, 235 patients (10.8%) showed UH and NT-proBNP>900 ng/l (Fig. 1A). Compared to the general ACS population, those with UH and elevated NT-proBNP were more likely to be older (41.7% vs 20.0%, p<0.001), of female sex (36.2% vs 19.7%, p<0.001) and with a more complex history of CV disease, such as hypertension (77.0% vs 56.2%, p<0.001), diabetes (24.7% vs 17.5%, p=0.006), peripheral artery disease (9.4% vs 5.2%, p=0.011), cerebrovascular disease (6.8% vs 3.4%, p=0.013), chronic heart failure (3.4% vs 1.3%, p=0.025), dialysis (2.1% vs 0.3%, p=0.004) as well as prior CABG (9.4% vs 5.2%, p=0.010) and more often admitted as NSTEMIs (59.6% vs 40.9%, p<0.001). Although these patients were on a more aggressive antihypertensive therapy at admission (all p<0.05 for ACEi, ARB, Beta-blockers, calcium antagonists, nitrates and diuretics), there was a higher rate of death (OR 1.83, 95% CI 1.07–3.14, p=0.027), CD (OR 2.13, 95% CI 1.19–3.81, p=0.009), AKI (OR 2.83, 95% CI 1.41–5.67, p=0.002) and composite endpoint AKI+CD (OR 2.46, 95% CI 1.56–3.90, p<0.001) at one year. This combined risk persisted after adjustment for baseline differences, with a 71% (Adj. HR 1.71, 95% CI 1.44–1.84, p=0.003) increase for the composite endpoint (Fig. 1B). Conclusions Among a real-world cohort of ACS patients, coexistence of UH with elevated levels of NT-proBNP confers increased risk for AKI and CD up to one year after ACS. These observations might help clinicians to identify ACS patients at risk using simple clinical parameters and biomarkers and to target them for more intense preventive therapies. Figure 1. A: GRADE1 = 140–159 mmHg and/or 90–99 mmHg; GRADE2 = 160–179 mmHg and/or 100–109 mmHg; GRADE3 = ≥180 mmHg and/or ≥110 mmHg; ISH (isolate systolic hypertension) = ≥140 mmHg and <90 mmHg; NT-proBNP = N-terminal-pro B-type natriuretic peptide. B: UH = uncontrolled hypertension; AKI = acute kidney injury; CD = cardiac death. Funding Acknowledgement Type of funding source: None

Prognostic value of inflammatory biomarkers and GRACE score for cardiac death and acute kidney injury after acute coronary syndromes

2021 ◽  
Author(s):  
Valentina A Rossi ◽  
Andrea Denegri ◽  
Alessandro Candreva ◽  
Roland Klingenberg ◽  
Slayman Obeid ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Neutrophil Count ◽  
Cardiac Death ◽  
Acute Coronary Syndromes ◽  
Kidney Injury ◽  
Inflammation Markers ◽  
Aldosterone Antagonists ◽  
Index Procedure ◽  
Coronary Syndromes ◽  
Grace Score

Abstract Aims  The aim of this study was to analyse the role of inflammation and established clinical scores in predicting acute kidney injury (AKI) after acute coronary syndromes (ACS). Methods and results  In a prospective multicentre cohort including 2034 patients with ACS undergoing percutaneous coronary intervention, high-sensitivity C-reactive protein (hsCRP), neutrophil count, neutrophil-to-lymphocyte ratio (NL-ratio), and creatinine were measured at the index procedure. AKI (n = 39, defined according to RIFLE criteria) and major cardiovascular and cerebrovascular events were adjudicated after 1 year. Associations between inflammation, AKI, and cardiac death (CD) were assessed by C-statistics and Cox proportional hazard models with log-rank test to compare survival. Patients with ACS with elevated neutrophil count >7.8 × 109/L, NL-ratio >5, combined neutrophil-count/creatinine, or NL-ratio/creatinine at baseline showed a higher incidence of AKI (all P < 0.05) and CD (all P < 0.001). The risk of AKI, CD, and their combination was increased in patients with higher neutrophil count/creatinine (heart rate (HR) = 3.7, 95% cardiac index (CI) 1.9–7.1; HR = 2.7, 95% CI 1.6–4.6; HR = 3.2, 95% CI 2.1–4.9); NL-ratio/creatinine (HR = 2.1, 95% CI 1.6–4.1; HR = 2.2, 95% CI 1.3–3.8; HR = 2.3, 95% CI 1.5–3.5); and hsCRP (HR = 1.8, 95% CI 0.9–3.5; HR = 2.2, 95% CI 1.3–3.6; HR = 1.9, 95% CI 1.2–2.8) after adjustment for age, diabetes, hypertension, previous heart failure, kidney function, haemodynamic instability at admission, statin, and renin–angiotensin–aldosterone antagonists use. Subjects with higher GRACE score 1.0/NL-ratio had higher rate of AKI, CD, and both (HR = 1.4, 95% CI 0.5–4.2; HR = 2.7, 95% CI 1.3–5.9; HR = 2.1, 95% CI 1–4.3). Conclusions  Inflammation markers may predict AKI after correction for renal function at the index procedure. hsCRP performed better than the NL-ratio. However, the integration of inflammation markers to traditional risk factors or scores does not add prognostic information. Trial registration  ClinicalTrials.gov, NCT01000701.

scholarly journals Management of Presumed Acute Kidney Injury during Hypertensive Therapy: Stay Calm and Carry on?

2020 ◽  
Vol 51 (2) ◽  
pp. 108-115
Author(s):  
Teresa K. Chen ◽  
Chirag R. Parikh
Keyword(s):  
Blood Pressure ◽  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Blood Pressure Control ◽  
Kidney Injury ◽  
Pressure Control ◽  
Intensive Treatment ◽  
Urinary Biomarkers ◽  
Increased Risk ◽  
Intensive Blood Pressure

Background: Recent studies have demonstrated that intensive blood pressure control is associated with improved cardiovascular outcomes. Acute kidney injury (AKI), however, was more common in the intensive treatment group prompting concern in the nephrology community. Summary: Clinical trials on hypertension control have traditionally defined AKI by changes in serum creatinine. However, serum creatinine has several inherent limitations as a marker of kidney injury, with various factors influencing its production, secretion, and elimination. Urinary biomarkers of kidney injury and repair have the potential to provide insight on the presence and phenotype of kidney injury. In both the Systolic Blood Pressure Intervention Trial and the Action to Control Cardiovascular Risk in Diabetes study, urinary biomarkers have suggested that the increased risk of AKI associated with intensive treatment was due to hemodynamic changes rather than structural kidney injury. As such, clinicians who encounter rises in serum creatinine during intensification of hypertension therapy should “stay calm and carry on.” Alternative explanations for serum creatinine elevation should be considered and addressed if appropriate. When the rise in serum creatinine is limited, particularly if albuminuria is stable or improving, intensive blood pressure control should be continued for its potential long-term benefits. Key Messages: Increases in serum creatinine during intensification of blood pressure control may not necessarily reflect kidney injury. Clinicians should evaluate for other contributing factors before stopping therapy. Urinary biomarkers may address limitations of serum creatinine as a marker of kidney injury.

B-Type Natriuretic Peptide and Risk of Acute Kidney Injury in Patients Hospitalized With Acute Coronary Syndromes*

2014 ◽  
Vol 42 (3) ◽  
pp. 619-624 ◽  
Author(s):  
Marco Moltrasio ◽  
Angelo Cabiati ◽  
Valentina Milazzo ◽  
Mara Rubino ◽  
Monica De Metrio ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Natriuretic Peptide ◽  
Acute Coronary Syndromes ◽  
Kidney Injury ◽  
Coronary Syndromes

scholarly journals Acute kidney injury in acute coronary syndromes – An important multifactorial consequence

2016 ◽  
Vol 35 (7-8) ◽  
pp. 415-421
Author(s):  
David Neves ◽  
Adriana Belo ◽  
Ana Filipa Damásio ◽  
João Carvalho ◽  
Ana Rita Santos ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Acute Coronary Syndromes ◽  
Kidney Injury ◽  
Coronary Syndromes

Abstract WMP100: Excessive Blood Pressure Reduction Increases the Risk of Acute Kidney Injury After Intracerebral Hemorrhage

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Kenichi Irie ◽  
Kaori Miwa ◽  
Kanta Tanaka ◽  
Hajime Ikenouchi ◽  
Masafumi Ihara ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Acute Kidney Injury ◽  
Intracerebral Hemorrhage ◽  
Characteristic Curve ◽  
Blood Pressure Reduction ◽  
Multivariable Analysis ◽  
Kidney Injury ◽  
Hospital Death ◽  
Stroke Registry ◽  
Increased Risk

Background: Elevated blood pressure (BP) in the first 24 hours of admission of acute intracerebral hemorrhage (ICH) has been the focus of intensive therapeutic investigation, although early intensive BP lowering addresses a concern about development of acute kidney injury (AKI). However, it is unclear as to the effect of BP measure including the absolute BP reduction and increased BP variability on AKI in patients with acute ICH. Methods: We retrieved data of consecutive patients with acute ICH from our prospective stroke registry between July 2015 and August 2017. We excluded patients with preexisting end-stage renal disease or in-hospital death within 24 hours. The primary outcome was AKI within 7days after admission defined using the AKI Network criteria. We recorded BP on emergency department arrival and for every 1 hour from 1 to 24 hours after admission (25 measurements). We measured mean systolic BP (SBP) and maximum minus minimum SBP within both 12 hours and 24 hours, and also quantified SBP variabilities (SBPV) including standard deviation, coefficient of variation, successive variation, and average real variability. Results: Among 361 patients with ICH (age 72.7±12.8, male 55%, non-lobar 76%), 31 (9%) developed AKI. For all SBP measure, the 12-hour SBP reduction was associated with the increased risk of AKI in multivariable analysis (odds ratio [per10 mmHg increase] 1.30; 95% CI 1.10-1.35). There was no significant association between the SBP variability and risk of AKI. The area under the receiver operating characteristic curve of the 12-hour SBP reduction for predicting AKI was 0.75. The association between the 12-hour SBP reduction and AKI was not modified by preexisting chronic kidney disease (interaction P=0.40). Conclusion: Early BP reduction in the first 12 hours of admission contributed to the risk of AKI in acute ICH. This may have clinical implication to avoid excess absolute BP reduction in patients with acute ICH.

Acute kidney injury in patients with acute coronary syndromes

Heart ◽  
2015 ◽  
Vol 101 (22) ◽  
pp. 1778-1785 ◽  
Author(s):  
Giancarlo Marenzi ◽  
Nicola Cosentino ◽  
Antonio L Bartorelli
Keyword(s):  
Acute Kidney Injury ◽  
Acute Coronary Syndromes ◽  
Kidney Injury ◽  
Coronary Syndromes

scholarly journals Associations of Intraoperative Radial Arterial Systolic, Diastolic, Mean, and Pulse Pressures with Myocardial and Acute Kidney Injury after Noncardiac Surgery

2020 ◽  
Vol 132 (2) ◽  
pp. 291-306 ◽  
Author(s):  
Sanchit Ahuja ◽  
Edward J. Mascha ◽  
Dongsheng Yang ◽  
Kamal Maheshwari ◽  
Barak Cohen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Acute Kidney Injury ◽  
Pulse Pressure ◽  
Renal Injury ◽  
Myocardial Injury ◽  
Kidney Injury ◽  
Noncardiac Surgery ◽  
Complex Signal ◽  
Discriminative Ability ◽  
Increased Risk

Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Arterial pressure is a complex signal that can be characterized by systolic, mean, and diastolic components, along with pulse pressure (difference between systolic and diastolic pressures). The authors separately evaluated the strength of associations among intraoperative pressure components with myocardial and kidney injury after noncardiac surgery. Methods The authors included 23,140 noncardiac surgery patients at Cleveland Clinic who had blood pressure recorded at 1-min intervals from radial arterial catheters. The authors used univariable smoothing and multivariable logistic regression to estimate probabilities of each outcome as function of patients’ lowest pressure for a cumulative 5 min for each component, comparing discriminative ability using C-statistics. The authors further assessed the association between outcomes and both area and minutes under derived thresholds corresponding to the beginning of increased risk for the average patient. Results Out of 23,140 patients analyzed, myocardial injury occurred in 6.1% and acute kidney injury in 8.2%. Based on the lowest patient blood pressure experienced for greater than or equal to 5 min, estimated thresholds below which the odds of myocardial or kidney injury progressively increased (slope P < 0.001) were 90 mmHg for systolic, 65 mmHg for mean, 50 mmHg for diastolic, and 35 mmHg for pulse pressure. Weak discriminative ability was noted between the pressure components, with univariable C-statistics ranging from 0.55 to 0.59. Area under the curve in the highest (deepest) quartile of exposure below the respective thresholds had significantly higher odds of myocardial injury after noncardiac surgery and acute kidney injury compared to no exposure for systolic, mean, and pulse pressure (all P < 0.001), but not diastolic, after adjusting for confounding. Conclusions Systolic, mean, and pulse pressure hypotension were comparable in their strength of association with myocardial and renal injury. In contrast, the relationship with diastolic pressure was poor. Baseline factors were much more strongly associated with myocardial and renal injury than intraoperative blood pressure, but pressure differs in being modifiable.

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