User login
TORONTO – Hospitalized patients with acute kidney injury had more than double the inpatient rate of venous thromboembolism as had patients without acute kidney injury in a prospective, observational study of more than 6,000 hospitalized U.S. soldiers.
“I think this should lower our threshold for investigating [possible cases of] venous thromboembolism in patients with acute kidney injury,” Michael McMahon, MD, said at the CHEST annual meeting. Acute kidney injury (AKI) “may require new prophylactic or diagnostic strategies” to prevent in-hospital venous thromboembolism (VTE) or to detect it early, said Dr. McMahon, a pulmonologist and critical care medicine physician at Walter Reed National Military Medical Center in Bethesda, Md.
He offered four possible mechanisms to explain a link between AKI and VTE:
- Patients with AKI are in a hypercoagulable state.
- AKI alters the pharmacodynamics or pharmacokinetics of VTE prophylactic treatments.
- AKI is a marker of an illness that causes VTE.
- VTE leads to an increased rate of AKI rather than the other way around.
Dr. McMahon’s analysis also revealed that two other clinical conditions that are generally believed to raise VTE risk – obesity and impaired overall renal function identified with stagnant measures – did not correspond with a significantly elevated VTE rate in this study.
The data came from 6,552 adults hospitalized for at least 2 days at Walter Reed between September 2009 and March 2011. The study excluded patients with VTE at the time of admission and also those who had been treated with an anticoagulant at the time of admission. The patients averaged 55 years of age and were hospitalized for a median of 4 days. About 22% of patients received VTE prophylaxis with unfractionated heparin, about 41% received prophylaxis with low-molecular-weight heparin, and about 39% received no VTE prophylaxis (percentages total 102% because of rounding).
About 16% of the patients had been diagnosed with AKI at the time of admission, and an additional 8% developed AKI while hospitalized, defined as an increase in serum creatinine during hospitalization of at least 50% above baseline levels or an increase of more than 0.3 mg/dL above the level at time of admission. During hospitalization, 160 patients (2%) developed a new onset VTE.
In an analysis that adjusted for baseline differences in type of surgery, body mass index, sex, age, and prior hospitalizations during the prior 90 days, the results showed that patients with preexisting or new onset AKI had a 2.2-fold higher rate of VTE, compared with patients without AKI, and this difference was statistically significant, Dr. McMahon reported.
The analysis also showed a significant 62% relatively higher rate of VTE among soldiers hospitalized for a deployment-related event, as well as a significant 63% relatively lower VTE rate among patients not receiving medical prophylaxis, compared with patients receiving an anticoagulant. Dr. McMahon suggested that this lower rate of VTEs among patients not on prophylaxis reflected success in identifying which patients had an increased risk for VTE and hence received prophylaxis.
[email protected]
On Twitter @mitchelzoler
TORONTO – Hospitalized patients with acute kidney injury had more than double the inpatient rate of venous thromboembolism as had patients without acute kidney injury in a prospective, observational study of more than 6,000 hospitalized U.S. soldiers.
“I think this should lower our threshold for investigating [possible cases of] venous thromboembolism in patients with acute kidney injury,” Michael McMahon, MD, said at the CHEST annual meeting. Acute kidney injury (AKI) “may require new prophylactic or diagnostic strategies” to prevent in-hospital venous thromboembolism (VTE) or to detect it early, said Dr. McMahon, a pulmonologist and critical care medicine physician at Walter Reed National Military Medical Center in Bethesda, Md.
He offered four possible mechanisms to explain a link between AKI and VTE:
- Patients with AKI are in a hypercoagulable state.
- AKI alters the pharmacodynamics or pharmacokinetics of VTE prophylactic treatments.
- AKI is a marker of an illness that causes VTE.
- VTE leads to an increased rate of AKI rather than the other way around.
Dr. McMahon’s analysis also revealed that two other clinical conditions that are generally believed to raise VTE risk – obesity and impaired overall renal function identified with stagnant measures – did not correspond with a significantly elevated VTE rate in this study.
The data came from 6,552 adults hospitalized for at least 2 days at Walter Reed between September 2009 and March 2011. The study excluded patients with VTE at the time of admission and also those who had been treated with an anticoagulant at the time of admission. The patients averaged 55 years of age and were hospitalized for a median of 4 days. About 22% of patients received VTE prophylaxis with unfractionated heparin, about 41% received prophylaxis with low-molecular-weight heparin, and about 39% received no VTE prophylaxis (percentages total 102% because of rounding).
About 16% of the patients had been diagnosed with AKI at the time of admission, and an additional 8% developed AKI while hospitalized, defined as an increase in serum creatinine during hospitalization of at least 50% above baseline levels or an increase of more than 0.3 mg/dL above the level at time of admission. During hospitalization, 160 patients (2%) developed a new onset VTE.
In an analysis that adjusted for baseline differences in type of surgery, body mass index, sex, age, and prior hospitalizations during the prior 90 days, the results showed that patients with preexisting or new onset AKI had a 2.2-fold higher rate of VTE, compared with patients without AKI, and this difference was statistically significant, Dr. McMahon reported.
The analysis also showed a significant 62% relatively higher rate of VTE among soldiers hospitalized for a deployment-related event, as well as a significant 63% relatively lower VTE rate among patients not receiving medical prophylaxis, compared with patients receiving an anticoagulant. Dr. McMahon suggested that this lower rate of VTEs among patients not on prophylaxis reflected success in identifying which patients had an increased risk for VTE and hence received prophylaxis.
[email protected]
On Twitter @mitchelzoler
TORONTO – Hospitalized patients with acute kidney injury had more than double the inpatient rate of venous thromboembolism as had patients without acute kidney injury in a prospective, observational study of more than 6,000 hospitalized U.S. soldiers.
“I think this should lower our threshold for investigating [possible cases of] venous thromboembolism in patients with acute kidney injury,” Michael McMahon, MD, said at the CHEST annual meeting. Acute kidney injury (AKI) “may require new prophylactic or diagnostic strategies” to prevent in-hospital venous thromboembolism (VTE) or to detect it early, said Dr. McMahon, a pulmonologist and critical care medicine physician at Walter Reed National Military Medical Center in Bethesda, Md.
He offered four possible mechanisms to explain a link between AKI and VTE:
- Patients with AKI are in a hypercoagulable state.
- AKI alters the pharmacodynamics or pharmacokinetics of VTE prophylactic treatments.
- AKI is a marker of an illness that causes VTE.
- VTE leads to an increased rate of AKI rather than the other way around.
Dr. McMahon’s analysis also revealed that two other clinical conditions that are generally believed to raise VTE risk – obesity and impaired overall renal function identified with stagnant measures – did not correspond with a significantly elevated VTE rate in this study.
The data came from 6,552 adults hospitalized for at least 2 days at Walter Reed between September 2009 and March 2011. The study excluded patients with VTE at the time of admission and also those who had been treated with an anticoagulant at the time of admission. The patients averaged 55 years of age and were hospitalized for a median of 4 days. About 22% of patients received VTE prophylaxis with unfractionated heparin, about 41% received prophylaxis with low-molecular-weight heparin, and about 39% received no VTE prophylaxis (percentages total 102% because of rounding).
About 16% of the patients had been diagnosed with AKI at the time of admission, and an additional 8% developed AKI while hospitalized, defined as an increase in serum creatinine during hospitalization of at least 50% above baseline levels or an increase of more than 0.3 mg/dL above the level at time of admission. During hospitalization, 160 patients (2%) developed a new onset VTE.
In an analysis that adjusted for baseline differences in type of surgery, body mass index, sex, age, and prior hospitalizations during the prior 90 days, the results showed that patients with preexisting or new onset AKI had a 2.2-fold higher rate of VTE, compared with patients without AKI, and this difference was statistically significant, Dr. McMahon reported.
The analysis also showed a significant 62% relatively higher rate of VTE among soldiers hospitalized for a deployment-related event, as well as a significant 63% relatively lower VTE rate among patients not receiving medical prophylaxis, compared with patients receiving an anticoagulant. Dr. McMahon suggested that this lower rate of VTEs among patients not on prophylaxis reflected success in identifying which patients had an increased risk for VTE and hence received prophylaxis.
[email protected]
On Twitter @mitchelzoler
AT CHEST 2017
Key clinical point:
Major finding: Inpatients with AKI had an adjusted 2.2-fold higher rate of VTE, compared with other inpatients.
Data source: Prospective, observational data from 6,552 inpatients at a single U.S. military hospital.
Disclosures: Dr. McMahon had no disclosures.