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

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.

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Association of Proteinuria and Hematuria with Acute Kidney Injury and Mortality in Hospitalized Patients with COVID-19

Kidney & Blood Pressure Research ◽

10.1159/000511946 ◽

2020 ◽

Vol 45 (6) ◽

pp. 1018-1032

Author(s):

Imran Chaudhri ◽

Richard Moffitt ◽

Erin Taub ◽

Raji R. Annadi ◽

Minh Hoai ◽

...

Keyword(s):

Acute Kidney Injury ◽

Invasive Mechanical Ventilation ◽

Multivariable Analysis ◽

Kidney Injury ◽

Hospitalized Patients ◽

Hospital Death ◽

Study Cohort ◽

Icu Admission ◽

Risk Of Death ◽

Increased Risk

Introduction: Acute kidney injury (AKI) is strongly associated with poor outcomes in hospitalized patients with coronavirus disease 2019 (COVID-19), but data on the association of proteinuria and hematuria are limited to non-US populations. In addition, admission and in-hospital measures for kidney abnormalities have not been studied separately. Methods: This retrospective cohort study aimed to analyze these associations in 321 patients sequentially admitted between March 7, 2020 and April 1, 2020 at Stony Brook University Medical Center, New York. We investigated the association of proteinuria, hematuria, and AKI with outcomes of inflammation, intensive care unit (ICU) admission, invasive mechanical ventilation (IMV), and in-hospital death. We used ANOVA, t test, χ2 test, and Fisher’s exact test for bivariate analyses and logistic regression for multivariable analysis. Results: Three hundred patients met the inclusion criteria for the study cohort. Multivariable analysis demonstrated that admission proteinuria was significantly associated with risk of in-hospital AKI (OR 4.71, 95% CI 1.28–17.38), while admission hematuria was associated with ICU admission (OR 4.56, 95% CI 1.12–18.64), IMV (OR 8.79, 95% CI 2.08–37.00), and death (OR 18.03, 95% CI 2.84–114.57). During hospitalization, de novo proteinuria was significantly associated with increased risk of death (OR 8.94, 95% CI 1.19–114.4, p = 0.04). In-hospital AKI increased (OR 27.14, 95% CI 4.44–240.17) while recovery from in-hospital AKI decreased the risk of death (OR 0.001, 95% CI 0.001–0.06). Conclusion: Proteinuria and hematuria both at the time of admission and during hospitalization are associated with adverse clinical outcomes in hospitalized patients with COVID-19.

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Systolic Blood Pressure Reduction and Acute Kidney Injury in Intracerebral Hemorrhage

Stroke ◽

10.1161/strokeaha.120.030272 ◽

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.

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

Stroke ◽

10.1161/str.51.suppl_1.wp398 ◽

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.

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Contrast Associated Acute Kidney Injury and Mortality in Older Adults with Acute Coronary Syndrome: A Pooled Analysis of the FRASER and HULK Studies

Journal of Clinical Medicine ◽

10.3390/jcm10102151 ◽

2021 ◽

Vol 10 (10) ◽

pp. 2151

Author(s):

Rita Pavasini ◽

Matteo Tebaldi ◽

Giulia Bugani ◽

Elisabetta Tonet ◽

Roberta Campana ◽

...

Keyword(s):

Acute Kidney Injury ◽

Renal Function ◽

Multivariable Analysis ◽

Kidney Injury ◽

Coronary Intervention ◽

Pooled Analysis ◽

Coronary Syndrome ◽

Risk Of Mortality ◽

Increased Risk ◽

Short Term Mortality

Whether contrast-associated acute kidney injury (CA-AKI) is only a bystander or a risk factor for mortality in older patients undergoing percutaneous coronary intervention (PCI) is not well understood. Data from FRASER (NCT02386124) and HULK (NCT03021044) studies have been analysed. All patients enrolled underwent coronary angiography. The occurrence of CA-AKI was defined based on KDIGO criteria. The primary outcome of the study was to test the relation between CA-AKI and 3-month mortality. Overall, 870 older ACS adults were included in the analysis (mean age 78 ± 5 years; 28% females). CA-AKI occurred in 136 (16%) patients. At 3 months, 13 (9.6%) patients with CA-AKI died as compared with 13 (1.8%) without it (p < 0.001). At multivariable analysis, CA-AKI emerged as independent predictor of 3-month mortality (HR 3.51, 95%CI 1.05–7.01). After 3 months, renal function returned to the baseline value in 78 (63%) with CA-AKI. Those without recovered renal function (n = 45, 37%) showed an increased risk of mortality as compared to recovered renal function and no CA-AKI subgroups (HR 2.01, 95%CI 1.55–2.59, p = 0.009 and HR 2.71, 95%CI 1.45–5.89, p < 0.001, respectively). In conclusion, CA-AKI occurs in a not negligible portion of older MI patients undergoing invasive strategy and it is associated with short-term mortality.

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Does deeper hypothermia reduce the risk of acute kidney injury after circulatory arrest for aortic arch surgery?

European Journal of Cardio-Thoracic Surgery ◽

10.1093/ejcts/ezab044 ◽

2021 ◽

Author(s):

Andrew M Vekstein ◽

Babtunde A Yerokun ◽

Oliver K Jawitz ◽

Julie W Doberne ◽

Jatin Anand ◽

...

Keyword(s):

Acute Kidney Injury ◽

Circulatory Arrest ◽

Aortic Surgery ◽

Multivariable Analysis ◽

Kidney Injury ◽

Deep Hypothermia ◽

Moderate Hypothermia ◽

Bladder Temperature ◽

Increased Risk ◽

The Impact

Abstract OBJECTIVES The impact of hypothermic circulatory arrest (HCA) temperature on postoperative acute kidney injury (AKI) has not been evaluated. This study examined the association between circulatory arrest temperatures and AKI in patients undergoing proximal aortic surgery with HCA. METHODS A total of 759 consecutive patients who underwent proximal aortic surgery (ascending ± valve ± root) including arch replacement requiring HCA between July 2005 and December 2016 were identified from a prospectively maintained institutional aortic surgery database. The primary outcome was AKI as defined by Risk, Injury, Failure, Loss, End Stage Renal Disease (ESRD) criteria. The association between minimum nasopharyngeal (NP) and bladder temperatures during HCA and postoperative AKI was assessed, adjusting for patient-level factors using multivariable logistic regression. RESULTS A total of 85% (n = 645) of patients underwent deep hypothermia (14.1–20.0°C), 11% (n = 83) low-moderate hypothermia (20.1–24.0°C) and 4% (n = 31) high-moderate hypothermia (24.1–28.0°C) as classified by NP temperature. When analysed by bladder temperature, 59% (n = 447) underwent deep hypothermia, 22% (n = 170) low-moderate, 16% (n = 118) high-moderate and 3% mild (n = 24) (28.1–34.0°C) hypothermia. The median systemic circulatory arrest time was 17 min. The incidence of AKI did not differ between hypothermia groups, whether analysed using minimum NP or bladder temperature. In the multivariable analysis, the association between degree of hypothermia and AKI remained non-significant whether analysed as a categorical variable (hypothermia group) or as a continuous variable (minimum NP or bladder temperature) (all P > 0.05). CONCLUSIONS In patients undergoing proximal aortic surgery including arch replacement requiring HCA, degree of systemic hypothermia was not associated with the risk of AKI. These data suggest that moderate hypothermia does not confer increased risk of AKI for patients requiring circulatory arrest, although additional prospective data are needed.

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Evaluation of Acute Kidney Injury and Mortality After Intensive Blood Pressure Control in Patients With Intracerebral Hemorrhage

Journal of the American Heart Association ◽

10.1161/jaha.117.008439 ◽

2018 ◽

Vol 7 (8) ◽

Cited By ~ 6

Author(s):

L. Goodwin Burgess ◽

Nitin Goyal ◽

G. Morgan Jones ◽

Yasser Khorchid ◽

Ali Kerro ◽

...

Keyword(s):

Blood Pressure ◽

Acute Kidney Injury ◽

Intracerebral Hemorrhage ◽

Blood Pressure Control ◽

Kidney Injury ◽

Pressure Control ◽

Intensive Blood Pressure

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CIRP Secretion during Cardiopulmonary Bypass Is Associated with Increased Risk of Postoperative Acute Kidney Injury

The Thoracic and Cardiovascular Surgeon ◽

10.1055/s-0041-1730450 ◽

2021 ◽

Author(s):

Wenyan Liu ◽

Yang Yan ◽

Dan Han ◽

Yongxin Li ◽

Qian Wang ◽

...

Keyword(s):

Acute Kidney Injury ◽

Cardiac Surgery ◽

Cardiopulmonary Bypass ◽

Rna Binding ◽

Multivariable Analysis ◽

Kidney Injury ◽

Proinflammatory Response ◽

Increased Risk ◽

Before And After ◽

The Difference

Abstract Background Systemic inflammation contributes to cardiac surgery–associated acute kidney injury (AKI). Cardiomyocytes and other organs experience hypothermia and hypoxia during cardiopulmonary bypass (CPB), which induces the secretion of cold-inducible RNA-binding protein (CIRP). Extracellular CIRP may induce a proinflammatory response. Materials and Methods The serum CIRP levels in 76 patients before and after cardiac surgery were determined to analyze the correlation between CIRP levels and CPB time. The risk factors for AKI after cardiac surgery and the in-hospital outcomes were also analyzed. Results The difference in the levels of CIRP (ΔCIRP) after and before surgery in patients who experienced cardioplegic arrest (CA) was 26-fold higher than those who did not, and 2.7-fold of those who experienced CPB without CA. The ΔCIRP levels were positively correlated with CPB time (r = 0.574, p < 0.001) and cross-clamp time (r = 0.54, p < 0.001). Multivariable analysis indicated that ΔCIRP (odds ratio: 1.003; 95% confidence interval: 1.000–1.006; p = 0.027) was an independent risk factor for postoperative AKI. Patients who underwent aortic dissection surgery had higher levels of CIRP and higher incidence of AKI than other patients. The incidence of AKI and duration of mechanical ventilation in patients whose serum CIRP levels more than 405 pg/mL were significantly higher than those less than 405 pg/mL (65.8 vs. 42.1%, p = 0.038; 23.1 ± 18.2 vs. 13.8 ± 9.2 hours, p = 0.007). Conclusion A large amount of CIRP was released during cardiac surgery. The secreted CIRP was associated with the increased risk of AKI after cardiac surgery.

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

American Journal of Nephrology ◽

10.1159/000505447 ◽

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.

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Higher Ambient Nitrogen Dioxide Is Associated With An Elevated Risk Of Hospital-Acquired Acute Kidney Injury

Clinical Kidney Journal ◽

10.1093/ckj/sfab164 ◽

2021 ◽

Author(s):

Pinghong He ◽

Ruixuan Chen ◽

Liping Zhou ◽

Yanqin Li ◽

Licong Su ◽

...

Keyword(s):

Air Pollution ◽

Acute Kidney Injury ◽

Nitrogen Dioxide ◽

Multivariable Analysis ◽

Kidney Injury ◽

Onset Date ◽

Ambient Level ◽

Increased Risk ◽

Pm2.5 And Pm10 ◽

Hospital Acquired

Abstract Background Previous studies have suggested that long-term exposure to air pollution increased the risk of chronic kidney disease and its progression. However, the effect of air pollution on the risk of acute kidney injury (AKI) has not been studied. We aim to evaluate the transient effect of air pollution on the risk of hospital-acquired AKI (HA-AKI). Methods We selected from the Epidemiology of AKI in Chinese Hospitalized patients (EACH2 study) AKI cases of which the onset date could be unambiguously determined. We obtained city-specific daily averages of the ambient level of particulate matter (PM2.5 and PM10), carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2) and ozone (O3), from the Ministry of Environmental Protection of China. We used the time-stratified case crossover approach to examine the association between the ambient level of air pollutants and the risk of HA-AKI in the selected cases. Results A total of 11,293 AKI cases that met the inclusion and exclusion criteria were selected. In univariable analysis, the ambient levels of NO2 and SO2, were significantly associated with the risk of HA-AKI. In the multivariable analysis that incorporated all six pollutants in the same model, NO2 was the sole pollutant whose level remained to be associated with the risk of AKI (p < 0.001). The relationship between level of NO2 and the risk of HA-AKI appeared to be linear, with an estimated odds ratio of 1.063 (95% CI: 1.026, 1.101) for each increment of one median absolute deviance in the exposure. The association was consistent across the subgroups stratified by age, gender, baseline estimated glomerular filtration rate, AKI severity, need for intensive care, and season. Conclusions Higher ambient level of NO2 was associated with an increased risk of HA-AKI in hospitalized adults in China.

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