Abstract WP398: Occurrence of Acute Kidney Injury in Patients With Intracerebral Hemorrhage Undergoing Systolic Blood Pressure Reduction

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Adnan I Qureshi ◽  
Wei Huang ◽  
Iryna Lobanova ◽  
Hunain Aslam ◽  
Werdah Zafar
Keyword(s):  
Blood Pressure ◽  
Acute Kidney Injury ◽  
Intracerebral Hemorrhage ◽  
Serum Creatinine ◽  
Systolic Blood Pressure ◽  
Standard Treatment ◽  
Blood Pressure Reduction ◽  
Kidney Injury ◽  
Hematoma Expansion ◽  
Open Label

Background: Aggressive systolic blood pressure (SBP) reduction may precipitate acute kidney injury (AKI) because of underlying hypertensive nephropathy, in subjects with intracerebral hemorrhage (ICH). Rate and determinants of AKI during acute hospitalization among ICH subjects were analyzed using a post hoc analysis of randomized, multicenter, two-groups, open-label clinical trial. Methods: Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH) 2 trial data was analyzed. Subjects with ICH (volume <60 cm 3 ) and a Glasgow Coma Scale (GCS) score of 5 or more were randomized to a SBP target of 110 to 139 mm Hg (intensive treatment) or a target of 140 to 179 mm Hg (standard treatment). IV nicardipine was given within 4.5 hours of symptom onset to lower SBP. Serum creatinine was ascertained at baseline, 24, 48 and 72 hours after randomization. AKI was classified based on increase in serum creatinine levels from baseline, stage 1 ≥ 0.3 mg/dl (≥ 26.4umol/L) or (>1.5 to 2-fold), stage 2 (>2 to 3-fold) and stage 3 (>3-fold) were identified. Results: Of 1000 randomized subjects, 158 developed AKI (65% were men; mean age of 61.5±13.2 years). Severity of AKI was grade I, II, III in 15.3%, 0.1%, and 0.4% patients, respectively. The rate of AKI was similar in intensive and standard treatment group (16.4% versus 15.2%, P=N.S). AKI incidence was significantly higher in subjects with baseline creatinine greater than 1.2 mg/dl (36% compared to 14%, OR 3.4, 95% CI 2.3-4.9, P= <0.0001). There was no significant association between subjects with AKI and hypertension (RR 1.1, 95% CI 1-1.2, P=0.15) or diabetes mellitus type 2 (RR 0.72, 95% CI 1.5-1.1, P=0.12). Patients with GCS ≤ 12 had significantly lower chances of developing AKI (RR 0.5, 95% CI 0.4-0.9, P=0.01). The incidence of hematoma expansion (OR 2.5, 95% CI 0.6-11, P=0.2) was not significantly higher in the subjects with AKI. No significant association was observed between occurrence of AKI and death or disability (modified Rankin score 4-6) at 3 months post randomization (RR 1.1, 95% CI 0.9-1.3, P=0.44). Conclusions: Mild AKI is frequent among intracerebral hemorrhage subjects undergoing SBP reduction. However, the rate of AKI was not different between subjects who were randomized to intensive or standard treatments.

scholarly journals Systolic Blood Pressure Reduction and Acute Kidney Injury in Intracerebral Hemorrhage

Stroke ◽  
2020 ◽  
Vol 51 (10) ◽  
pp. 3030-3038
Author(s):  
Adnan I. Qureshi ◽  
Wei Huang ◽  
Iryna Lobanova ◽  
Daniel F. Hanley ◽  
Chung Y. Hsu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Acute Kidney Injury ◽  
Intracerebral Hemorrhage ◽  
Serum Creatinine ◽  
Systolic Blood Pressure ◽  
Odds Ratio ◽  
Blood Pressure Reduction ◽  
Kidney Injury ◽  
Pressure Reduction ◽  
Baseline Serum

Background and Purpose: We determined the rates and predictors of acute kidney injury (AKI) and renal adverse events (AEs), and effects of AKI and renal AEs on death or disability in patients with intracerebral hemorrhage. Methods: We analyzed data from a multicenter trial which randomized 1000 intracerebral hemorrhage patients with initial systolic blood pressure ≥180 mm Hg to intensive (goal 110–139 mm Hg) over standard (goal 140–179 mm Hg) systolic blood pressure reduction within 4.5 hours of symptom onset. AKI was identified by serial assessment of daily serum creatinine for 3 days post randomization. Results: AKI and renal AEs were observed in 149 patients (14.9%) and 65 patients (6.5%) among 1000 patients, respectively. In multivariate analysis, the higher baseline serum creatinine (≥110 μmol/L) was associated with AKI (odds ratio 2.4 [95% CI, 1.2–4.5]) and renal AEs (odds ratio 3.1 [95% CI, 1.2–8.1]). Higher area under the curve for intravenous nicardipine dose was associated with AKI (odds ratio 1.003 [95% CI, 1.001–1.005]) and renal AEs (odds ratio 1.003 [95% CI, 1.001–1.006]). There was a higher risk to death (relative risk 2.6 [95% CI, 1.6–4.2]) and death or disability (relative risk 1.5 [95% CI, 1.3–1.8]) at 90 days in patients with AKI but not in those with renal AEs. Conclusions: Intracerebral hemorrhage patients with higher baseline serum creatinine and those receiving higher doses of nicardipine were at higher risk for AKI and renal AEs. Occurrence of AKI was associated higher rates of death or disability at 3 months. Registration: URL: https://clinicaltrials.gov . Unique identifier: NCT01176565.

Abstract WP396: Analysis of Patients With Excessively High Pre-Randomization Systolic Blood Pressure and Effect of Intensive Systolic Blood Pressure Reduction in Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH) 2

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Adnan I Qureshi ◽  
Lydia D Foster ◽  
Iryna Lobanova ◽  
Wei Huang ◽  
Jose I Suarez ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Treatment Effect ◽  
Standard Treatment ◽  
Blood Pressure Reduction ◽  
Intensive Treatment ◽  
Hematoma Expansion ◽  
Disability Score ◽  
Modifying Effect ◽  
Current Guidelines

Background: Current guidelines recommend for intracerebral hemorrhage (ICH) patients with the systolic blood pressure (SBP) >220 mmHg, unlike those with initial SBP 150-220 mm, Hg, the efficacy of aggressive reduction of SBP is less well established and further studies are recommended. Methods: We analyzed data from ATACH 2 trial which randomized patients with initial SBP >180 mm Hg to intensive (goal 110-139 mmHg) and standard (goal 140-179 mmHg) SBP reduction using IV nicardipine within 4.5 hours of symptom onset. We compared the characteristics and outcomes between patients with pre- randomization SBP ≥220 mm Hg and those with initial SBP <220 mm Hg. We analyzed the modifying effect (interaction test) of pre-randomization SBP ≥220 mm Hg on treatment effect (intensive versus standard) on death or disability (score 4-6 on modified Rankin scale) at 3-months post-randomization ascertained by a blinded investigator. Results: Of 1000 randomized subjects, 48 subjects had a pre-randomization SBP ≥ 220 mm Hg (mean age 57.8 years, 65% men); 24 were assigned to intensive-treatment and standard-treatment each. The rate of death or disability at 3 months (47.9% versus 37.7%, odds ratio (OR): 1.52, 95% confidence interval (CI): 0.43 to 1.5, 0.85 to 2.72) and hematoma expansion within 24 hours (30.0% versus 21.2%, OR: 1.60; 95% CI: 0.80 to 3.20) was not different among subjects with SBP≥220 mm Hg SBP and those with SBP < 220 mm Hg. Rates of hematoma expansion (19% and 27.3%, OR: 0.63; 95% CI: 0.15 to 2.6) and neurological deterioration (8.7% versus 17.4%, OR: 0.45; 95% CI: 0.07 to 2.8) within 24 hours were not different between those randomized to intensive treatment and those to standard treatment in patients with SBP≥220 mm Hg. The interaction between initial SBP ≥220 mm Hg and treatment effect on death or disability was significant (p=0.0111). Conclusions: Patients with pre-randomization SBP ≥220 mm Hg did not have higher rates of hematoma expansion or death or disability compared to those with SBP <220 mm Hg. The interaction of pre- randomization SBP ≥220 mm Hg with the treatment effect and a non-significantly higher rate of death or disability associated with intensive treatment requires further studies.

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.

P1581Early blood pressure reduction by intravenous vasodilators associates with acute kidney injury in patients with hypertensive acute decompensated heart failure

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
Y Arao ◽  
A Sawamura ◽  
M Nakatochi ◽  
H Oishi ◽  
H Kato ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Acute Kidney Injury ◽  
Logistic Regression ◽  
Serum Creatinine ◽  
Acute Decompensated Heart Failure ◽  
Blood Pressure Reduction ◽  
Kidney Injury ◽  
Decompensated Heart Failure ◽  
Regression Analyses

Abstract Background In patients with hypertensive acute decompensated heart failure (ADHF), intravenous vasodilators are commonly used. However, little is known about optimal use in blood pressure (BP) management to avoid acute kidney injury (AKI). Purpose To investigate the association between systolic BP (SBP) changes in first 6 h and incidence of AKI within 48 h in patients with hypertensive ADHF. Methods Post-hoc analysis was performed on a prospectively enrolled cohort. We investigated 245 patients with ADHF and SBP >140 mmHg on arrival (mean age, 76 years; 40% female). We defined “SBP-fall” as maximum percent reduction in SBP 6h after intravenous treatment. AKI was defined as serum creatinine (SCr) ≥0.3 mg/dL, or urine output <0.5 mL/kg/h at 48 h. Results Mean SBP, SBP-fall and SCr level at arrival were 180 mmHg, 29.4%, and 1.21 mg/dL, respectively. Sixty-six patients experienced AKI. There were no significant differences in age, NYHA functional class, SBP and SCr at admission between AKI and Non-AKI group. AKI group had the greater SBP-fall compared with Non-AKI (36.7%versus 27.2%, p≤0.0001). Logistic regression analyses revealed that SBP-fall had an independent predictor of AKI (Table). In addition, SBP-fall had positive association with the number of concomitant used intravenous vasodilators in first 6 h (Figure). Logistic regression analyses for AKI Univariate Multivariate AUC OR 95% CI P OR 95% CI P Ages, years, per 10 years 1.04 0.82–1.33 0.17 0.75 SBP at arrival, per 10 mmHg 1.01 0.93–1.11 0.77 SBP-fall, per 10% 1.49 1.22–1.81 <0.001 1.54 1.24–1.91 <0.001 HR, per 10 beat/min 1.12 1.00–1.25 0.049 1.07 0.95–1.21 0.28 COPD 2.95 1.06–8.21 0.04 3.06 0.99–9.43 0.054 SCr, per 1 mg/dL 1.40 0.83–2.37 0.21 Furosemide i.v. 1.12 0.42–2.95 0.82 Carperitide 3.22 1.69–6.13 0.0002 4.39 2.16–8.93 <0.001 NTG/ISDN i.v. 0.97 0.54–1.74 0.92 CCB i.v. 1.86 0.76–4.53 0.18 OR, odds ratio; CI, confidence interval; AUC, area under the curve; SBP, systolic blood pressure; COPD, chronic obstructive pulmonary disease; SCr, serum creatinine; i.v., intravenous; NTG, nitroglycerin; ISDN, isosorbide dinitrate; CCB, calcium channel blocker. SBP-fall odds ration for AKI Conclusion In the first 6h of management for hypertensive ADHF patients, aggressive SBP reduction by the combination use of vasodilator agents predicted the incidence of AKI.

scholarly journals Acute hypertensive response in patients with intracerebral hemorrhage pathophysiology and treatment

2017 ◽  
Vol 38 (9) ◽  
pp. 1551-1563 ◽  
Author(s):  
Adnan I Qureshi ◽  
Mushtaq H Qureshi
Keyword(s):  
Blood Pressure ◽  
Intracerebral Hemorrhage ◽  
Systolic Blood Pressure ◽  
Cerebral Hemorrhage ◽  
Blood Pressure Reduction ◽  
Systemic Blood Pressure ◽  
Current Evidence ◽  
Hematoma Expansion ◽  
Pressure Reduction ◽  
Small Magnitude

Acute hypertensive response is a common systemic response to occurrence of intracerebral hemorrhage which has gained unique prominence due to high prevalence and association with hematoma expansion and increased mortality. Presumably, the higher systemic blood pressure predisposes to continued intraparenchymal hemorrhage by transmission of higher pressure to the damaged small arteries and may interact with hemostatic and inflammatory pathways. Therefore, intensive reduction of systolic blood pressure has been evaluated in several clinical trials as a strategy to reduce hematoma expansion and subsequent death and disability. These trials have demonstrated either a small magnitude benefit (second intensive blood pressure reduction in acute cerebral hemorrhage trial and efficacy of nitric oxide in stroke trial) or no benefit (antihypertensive treatment of acute cerebral hemorrhage 2 trial) with intensive systolic blood pressure reduction compared with modest or standard blood pressure reduction. The differences may be explained by the variation in intensity of systolic blood pressure reduction between trials. A treatment threshold of systolic blood pressure of ≥180 mm with the target goal of systolic blood pressure reduction to values between 130 and 150 mm Hg within 6 h of symptom onset may be best supported by current evidence.

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.

Systolic Blood Pressure Reduction and Risk of Acute Renal Injury in Patients with Intracerebral Hemorrhage

2012 ◽  
Vol 125 (7) ◽  
pp. 718.e1-718.e6 ◽  
Author(s):  
Adnan I. Qureshi ◽  
Yuko Y. Palesch ◽  
Renee Martin ◽  
Jill Novitzke ◽  
Salvador Cruz Flores ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Intracerebral Hemorrhage ◽  
Systolic Blood Pressure ◽  
Renal Injury ◽  
Blood Pressure Reduction ◽  
Pressure Reduction ◽  
Acute Renal Injury
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