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NEWS Review

By Currents Editor posted 09-18-2018 14:25

 By Aimee Aysenne, MD (left), MPH, and Kyle Hobbs, MD (right)

Aimee_Aysenne_Headshot.jpgKyle_Hobbs_Headshot_2.jpgKidney 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.


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.


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


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.


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.

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