Personalized Mean Arterial Pressure Management on Renal Function During Septic Shock (DORESEP)

This study is currently recruiting participants. (see Contacts and Locations)
Verified June 2014 by Assistance Publique - Hôpitaux de Paris
Sponsor:
Information provided by (Responsible Party):
Assistance Publique - Hôpitaux de Paris
ClinicalTrials.gov Identifier:
NCT01473498
First received: October 14, 2011
Last updated: June 13, 2014
Last verified: June 2014
  Purpose

Sepsis is the most severe complication of infections. Sepsis-associated Acute kidney injury (AKI) is commonly encountered in critically ill patients and independently predicts poor outcome. Unfortunately, no drug or management strategy was able to reduce incidence of AKI. To adapt the level of mean arterial pressure according to local renal hemodynamic evaluated by renal Doppler could lead to a better renal perfusion, and then less AKI.


Condition Intervention
Septic Shock
Acute Kidney Injury
Other: Haemodynamic management

Study Type: Interventional
Study Design: Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Open Label
Primary Purpose: Treatment
Official Title: Personalized Haemodynamic Management of Septic Shock: Influence of Mean Arterial Pressure Level on Renal Function: Randomized Controlled Trial

Resource links provided by NLM:


Further study details as provided by Assistance Publique - Hôpitaux de Paris:

Primary Outcome Measures:
  • Acute kidney injury according to RIFLE score [ Time Frame: at 7 days ] [ Designated as safety issue: No ]

Secondary Outcome Measures:
  • Need for renal replacement therapy [ Time Frame: during hospitalization ] [ Designated as safety issue: Yes ]
    including metabolic indications (Azotemia Serum urea ≥ 36mmol/L (100 mg/dL) ; Uremic complications : encephalopathy, pericarditis, bleeding ; Hyperkalemia K+ ≥ 6 mmol/L and/or electrocardiogram abnormalities ; Hypermagnesemia ≥4 mmol/L and/or anuria/absent deep tendon reflexes ; Acidosis Serum pH ≤ 7.15), Oligo-anuria Urine output <200mL/12 h or anuria, Fluid overload like Diuretic-resistant organ edema in the presence of acute kidney injury.

  • All cause mortality [ Time Frame: at 28 days ] [ Designated as safety issue: Yes ]
    All Cause mortality at 28 days, including refractory shock, refractory hypoxia, multiple organ failure, decisions to forgo life-sustaining therapies (DFLSTs)


Estimated Enrollment: 60
Study Start Date: January 2013
Estimated Study Completion Date: January 2015
Estimated Primary Completion Date: December 2014 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
Experimental: Test group

Patients will be treated with fluid and norepinephrine to achieve and maintain a mean arterial pressure of 65 mm Hg. Then they will be randomized in two groups.

In the first group (study group, n=30), mean arterial pressure will be increased to 85 mm Hg for 72 hours by increasing the dose of norepinephrine in patients. Key details, e.g., for drugs include dosage form, dosage, frequency and duration.

Other: Haemodynamic management

Patients will be treated with fluid and norepinephrine to achieve and maintain a mean arterial pressure of 65 mm Hg. Then they will be randomized in two groups.

In this group (control group, n=30), mean arterial pressure will be maintained at 65 mm Hg.

Active Comparator: Control group

Patients will be treated with fluid and norepinephrine to achieve and maintain a mean arterial pressure of 65 mm Hg. Then they will be randomized in two groups.

In this group (control group, n=30), mean arterial pressure will be maintained at 65 mm Hg.

Other: Haemodynamic management

Patients will be treated with fluid and norepinephrine to achieve and maintain a mean arterial pressure of 65 mm Hg. Then they will be randomized in two groups.

In the first group (study group, n=30), mean arterial pressure will be increased to 85 mm Hg for 72 hours by increasing the dose of norepinephrine in patients.


Detailed Description:

Acute Kidney Injury (AKI) is a frequent and serious complication of sepsis. Renal ischemia plays a major role in the pathophysiology of sepsis-associated AKI. There is currently no treatment to prevent or to treat AKI. It has been shown that a resistivity index (RI) greater than 0.74 of patients with septic shock could predict the occurrence of renal failure, and that increase mean arterial pressure (MAP) with norepinephrine could decrease RI. Hence, we propose to compare the frequency and the severity of the sepsis-associated AKI according to the early hemodynamic management of septic shock. Patients will be randomized in a classic group (MAP 65 mmHg) and an interventional group (MAP 85 mmHg). We can thus determine whether the level of MAP influences renal function, and whether this influence of MAP is dependent of renal perfusion assessed by renal Doppler.

Participants will be followed for the duration of hospital stay, an expected average of 4 weeks.

Primary endpoint:

-Presence and severity of sepsis-associated AKI at day 7.

Secondary endpoints:

  • Acute renal failure measured by Classification AKI at day 28.
  • Acute renal failure as measured by the RIFLE classification in the fourth to seventh day and 28th day.
  • Use of renal replacement therapy during hospitalization in intensive care unit
  • Mortality at day 28 Duration of study: Recruitment: 10 months, the patient monitoring: 28 days ± 3 days, total test duration: 11 months
  Eligibility

Ages Eligible for Study:   18 Years and older
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Criteria

Inclusion Criteria:

  • Any patient with septic shock in intensive care may be included in the next 6 to 16h
  • Age > 18 years old

Exclusion Criteria:

  • Chronic renal failure (Baseline serum creatinine > 120 mmol/L)
  • Chronic cardiac failure (Left ventricle ejection fraction < 40%)
  • Pregnancy
  • Urinary Tract Infection
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT01473498

Contacts
Contact: Jacques DURANTEAU, MD,PhD 01-45-21-39-36 jacques.duranteau@bct.aphp.fr
Contact: Adrien BOUGLE, MD 06-64-82-56-29 adrien.bougle@gmail.com

Locations
France
Reanimation Chirurgicale - Hôpital Kremlin Bicêtre Recruiting
Kremlin Bicêtre, France, 94275
Contact: Jacques DURANTEAU, MD,PhD    01-45-21-39-36    jacques.duranteau@bct.aphp.fr   
Principal Investigator: Jacques DURANTEAU, MD, PhD         
Sponsors and Collaborators
Assistance Publique - Hôpitaux de Paris
Investigators
Principal Investigator: Jacques DURANTEAU, MD,PhD Assistance Publique - Hôpitaux de Paris
  More Information

No publications provided

Responsible Party: Assistance Publique - Hôpitaux de Paris
ClinicalTrials.gov Identifier: NCT01473498     History of Changes
Other Study ID Numbers: P091103
Study First Received: October 14, 2011
Last Updated: June 13, 2014
Health Authority: France: Ministry of Health

Keywords provided by Assistance Publique - Hôpitaux de Paris:
Sepsis
Acute kidney injury
Mean arterial pressure
Catecholamines
Renal doppler

Additional relevant MeSH terms:
Acute Kidney Injury
Shock
Shock, Septic
Infection
Inflammation
Kidney Diseases
Pathologic Processes
Renal Insufficiency
Sepsis
Systemic Inflammatory Response Syndrome
Urologic Diseases
Norepinephrine
Adrenergic Agents
Adrenergic Agonists
Adrenergic alpha-Agonists
Autonomic Agents
Cardiovascular Agents
Molecular Mechanisms of Pharmacological Action
Neurotransmitter Agents
Peripheral Nervous System Agents
Pharmacologic Actions
Physiological Effects of Drugs
Sympathomimetics
Therapeutic Uses
Vasoconstrictor Agents

ClinicalTrials.gov processed this record on October 23, 2014