Prevalence and Determinants of Acute Renal Failure Following Cardiopulmonary Resuscitation

Mattana, Joseph

doi:10.1001/archinte.1993.00410020085007

Cited by 59 publications

(20 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…AKI is quite common after CA, occurring in up to 30% of survivors 32. CA is itself an extreme example of whole body ischemia, which is a common precedent for AKI 33.…”

Section: Discussionmentioning

confidence: 99%

Estrogen Is Renoprotective via a Nonreceptor-dependent Mechanism after Cardiac Arrest In Vivo

et al. 2010

View full text Add to dashboard Cite

Background Severe ischemia induces renal injury less frequently in women than men. In this study, cardiac arrest and cardiopulmonary resuscitation were used to assess whether estradiol is renoprotective via an estrogen receptor (ER)-dependent mechanism. Materials and Methods Male and female C57BL/6 and ER gene-deleted mice underwent 10 min of cardiac arrest followed by cardiopulmonary resuscitation. Serum chemistries and renal stereology were measured 24 h after arrest. Results Estrogen did not affect mean arterial pressure, regional renal cortical blood flow, and arterial blood gases. Hence, female kidneys were protected (mean ± SEM: blood urea nitrogen, 65 ± 21 vs.149 ± 27 mg/dl, P = 0.04; creatinine, 0.14 ± 0.05 vs. 0.73 ± 0.16 mg/dl, P = 0.01; volume of necrotic tubules, 7 ± 1% vs. 10 ± 0%, P = 0.04). Estrogen also reduced renal injury. In intact females (n = 5), ovariectomized/vehicle-treated (n = 8), and ovariectomized/estrogen-treated (n = 8) animals, blood urea nitrogen was 65 ± 21, 166 ± 28, and 50 ± 14 mg/dl (P = 0.002); creatinine was 0.14 ± 0.05, 0.74 ± 0.26, and 0.23 ± 0.27 mg/dl (P = 0.014); necrotic tubules were 2.5 ± 0.25%, 12.0 ± 1.9%, and 5.0 ± 1.6% (P = 0.004), respectively. In ER-α and ER-β gene-deleted mice and controls estradiol-reduced functional injury (blood urea nitrogen: estradiol 117 ± 71, vehicle 167 ± 56, P = 0.007; creatinine: estradiol 0.5 ± 0.5, vehicle 1.0 ± 0.4, P = 0.013), but the effect of estradiol was not different between ER-α or ER-β gene-deleted mice. Adding ICI 182,780 to estradiol did not alter injury. Conclusions In women, kidneys were protected from cardiac arrest through estrogen. Estradiol-mediated renoprotection was not affected by ER deletion or blockade. Estradiol is renoprotective after cardiac arrest. The results indicate that estradiol renoprotection is ER-α and ER-β independent.

show abstract

“…AKI is quite common after CA, occurring in up to 30% of survivors 32. CA is itself an extreme example of whole body ischemia, which is a common precedent for AKI 33.…”

Section: Discussionmentioning

confidence: 99%

Estrogen Is Renoprotective via a Nonreceptor-dependent Mechanism after Cardiac Arrest In Vivo

et al. 2010

View full text Add to dashboard Cite

show abstract

“…In another study, profound hypothermia to 20°C in patients undergoing cardiopulmonary bypass increased GFR and increased flow of hypo-osmolar urine 15, but general anesthesia used has itself been found to confounding effects on renal function and urine output 21,22. Cardiac arrest survivors treated with hypothermia to 32–34°C had a relative delay in the post-arrest return of normal creatinine clearance 18, but renal dysfunction is a common occurrence in survivors of cardiac arrest, and manifests as acute renal failure in up to a third of patients 23,24. Cold water immersion results in a diuresis of dilute urine 25,26, but immersion in water itself, regardless of temperature, induces humoral and hemodynamic changes that may increase urine output more significantly than the hypothermia itself 26,27,28.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic hypothermia is associated with a decrease in urine output in acute stroke patients

et al. 2010

View full text Add to dashboard Cite

Aims-It is unclear what effect therapeutic hypothermia may have on renal function, because its effect has so far been primarily evaluated in settings in which there may be possible confounding perturbations in cardiovascular and renal physiology, such deep intra-operative hypothermia, general anesthesia, and post-cardiac arrest. We sought to determine if therapeutic hypothermia affects renal function in awake patients with normal renal function who were enrolled into a clinical trial of hypothermia plus intravenous thrombolysis for acute ischemic stroke.Methods-Eleven patients with normal renal function were cooled to 33°C for 24 hours using an endovascular catheter, and then re-warmed over 12 hours to 36.5°C, while hourly temperature, Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Previous presentation:Early portions of this work were presented at the 32th International Stroke Conference, San Francisco, CA at a poster session, NIH Public Access Author ManuscriptResuscitation. Author manuscript; available in PMC 2011 December 1. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript blood pressure, and fluid status data was recorded. Blood samples for blood urea nitrogen (BUN), creatinine, and hematocrit were drawn prior to treatment (baseline), immediately after hypothermia and re-warming (day 2), and again at day 7 or discharge, and values compared. Conclusion-Inducing hypothermia in patients with relatively unperturbed renal physiology results in a decrease in urine output that is linearly correlated with the decrease in core temperature. This has important implications for fluid management in patients undergoing therapeutic hypothermia. Results-On

show abstract

“…However, even when a patient suffers a witnessed, in‐hospital arrest, the chance of survival to discharge after cardiopulmonary resuscitation (CPR) is very poor. In fact, moderate‐to‐severe heart failure is one of the strongest independent predictors of in‐hospital mortality after CPR [6–10]. The small opportunity of saving and prolonging life should also be weighed against the negative effects associated with the procedure.…”

Section: Introductionmentioning

confidence: 99%

Should cardiopulmonary resuscitation be performed on patients with heart failure? The role of the patient in the decision‐making process

Ågård

Hermerén

Herlitz

2000

Journal of Internal Medicine

View full text Add to dashboard Cite

show abstract

Prevalence and Determinants of Acute Renal Failure Following Cardiopulmonary Resuscitation

Cited by 59 publications

References 22 publications

Estrogen Is Renoprotective via a Nonreceptor-dependent Mechanism after Cardiac Arrest In Vivo

Estrogen Is Renoprotective via a Nonreceptor-dependent Mechanism after Cardiac Arrest In Vivo

Therapeutic hypothermia is associated with a decrease in urine output in acute stroke patients

Should cardiopulmonary resuscitation be performed on patients with heart failure? The role of the patient in the decision‐making process

Contact Info

Product

Resources

About