Aimee Aysenne,
MD, MPH
Kyle Hobbs, MD
Kidney injury is common
in the neurocritical care
unit. It has a significant
impact on ICU length of
stay and ultimate recovery,
and can be aggravated by
interventions undertaken
for neurologic disease. The
reviewed studies below
investigate the effect of
aggressive blood pressure
control in acute
spontaneous intracerebral hemorrhage on renal function, as well
kidney protection strategies in patients undergoing angiography.
Aggressive BP lowering in intracerebral hemorrhage is associated
with acute kidney injury in severely hypertensive patients.
Neurocrit Care 28(3):344-352, 2018.
Summary
Optimal targets for acute blood pressure lowering in spontaneous
intracerebral hemorrhage remain controversial. This single-center
retrospective study evaluated the impact of degree of admission
hypertension on the development of acute kidney injury (AKI)
with intensive blood pressure lowering. Four hundred one adult
patients with acute spontaneous ICH were classified as having
mild (SBP 141-179 mmHg), moderate (180-219 mmHg) and
severe (> 220 mmHg) hypertension prior to CT scan confirming
ICH. The primary outcome was development of AKI (rise in serum
creatinine > 0.3 mg dL or > 150 percent above baseline) within
seven days of hospital admission. All patients were initially treated
with a SBP goal of < 140 per institutional protocol. Patients with
chronic kidney disease (SCr > 2.0 mg/dL or pre-existing ESRD on
renal dialysis) were excluded. There were 177 patients in the mild
group, 124 moderate and 100 severe. Patients in the severe group
were slightly younger, more likely to be African-American and had
a higher total body weight compared to mild patients. The severe
group had a lower percentage of SBP readings at goal than the
moderate or severe groups. Overall, AKI rates varied significantly
between groups (28 versus 37 versus 56 percent, p < 0.001). AKI
rate was significantly increased in the severe group compared to
the other groups, but there was no difference between mild and
moderate groups. Resolution of AKI by discharge did not vary
between groups. The likelihood of severe renal failure was higher
in the severe group, but there were no differences in need for renal
replacement therapy. There were no differences seen in mortality
between groups, but the severe group did have longer ICU and
hospital lengths of stay than the mild group. In univariate analysis,
patients experiencing AKI had significantly higher mortality and
longer ICU and hospital length of stay compared to those who
did not develop AKI. Severe hypertension on admission was an
independent predictor of developing AKI.
Comments
ICH patients treated with aggressive rapid blood pressure
lowering had much higher rates of AKI when presenting with
severe compared to mild or moderate hypertension, and severe
admission hypertension was an independent predictor of
AKI development. This study suggests that BP targets after
acute ICH are not one-size-fits-all; however, this study does
not address whether the higher rates of AKI seen in severe
hypertension were due to overly aggressive BP lowering,
or whether these patients would have still suffered higher
rates of AKI even at a higher BP control target. A randomized
prospective trial would better answer this question.
No benefit to IV sodium bicarbonate or acetylcysteine for
prevention of contrast-associated acute kidney injury in high
risk patients.
NEJM 378(7):603-614 2018
Summary
Acute kidney injury resulting from the administration of
contrast during angiography is associated with morbidity and
mortality. Use of IV sodium bicarbonate and acetylcysteine
for renal protection is widespread, despite definitive evidence
of effectiveness. This multi-site, international, double-blind,
placebo- and drug-controlled randomized controlled trial enrolled
patients with baseline decreased GFR who were scheduled to
undergo coronary or non-coronary angiogram. Patients were
randomized two by two to receive either IV sodium bicarbonate
or sodium chloride (NS) and oral acetylcysteine (NAC) or
placebo capsules. IV fluids were dosed based on weight before,
during and after angiography. The primary endpoint was a
composite of death, need for dialysis and persistent increase in
serum creatinine > 50 percent above baseline 90 to 104 days after
angiography. 5177 patients were randomized (184 withdrawn
as they did not undergo angiography); 90 percent underwent
coronary angiography. There were no demographic differences
between groups. There was no interaction seen between sodium
bicarbonate and NAC. The primary endpoint occurred in 4.4
percent versus 4.7 percent in the sodium bicarb versus NS group
(OR 0.93; 95 percent CI, 0.72-2.22; p=0.62) and 4.6 percent
versus 4.5 percent in the NAC versus placebo group (OR 1.02;
95 percent CI, 0.78-1.33; p=0.88). There was no difference in
AKI in either group during admission or at 90 days. The study
was stopped early as the preplanned interim analysis showed no
difference in primary endpoint between groups.
Comments
The PRESERVE trial is the largest randomized trial to evaluate
IV sodium bicarbonate and acetylcysteine for prevention of
contrast-induced nephropathy. One particular strength of this
trial over prior trials is that only high-risk patients with baseline
impaired renal function were included. A limitation of this trial
was that the median volume of contrast administration was
small; the benefit of NAC and sodium bicarbonate in patients
undergoing higher volumes of contrast administration is unclear.
While sodium bicarbonate and NAC have few side effects, this
trial indicates there is no benefit from their usage over hydration
with normal saline.
NEWS Review
By Aimee Aysenne, MD, MPH, and Kyle Hobbs, MD
22