This research is in rats but the human research is here:
The Albumin in Acute Stroke Part 1 Trial
Did any protocol come from this? Ask your doctor, only 2013.
The latest rat research here:
Iso-Oncotic Albumin Mitigates Brain and Kidney Injury in Experimental Focal Ischemic Stroke
Renata de S. Mendes1, Gloria Martins1, 
Milena V. Oliveira1, 
Nazareth N. Rocha1, 
Fernanda F. Cruz1, Mariana A. Antunes1, 
Soraia C. Abreu1, 
Adriana L. Silva1, Christina Takiya2, 
Pedro M. Pimentel-Coelho3, 
Chiara Robba4, 
Rosália Mendez-Otero3, 
Paolo Pelosi4,5, 
Patricia R. M. Rocco1,6† and 
Pedro L. Silva1,6*†- 1Laboratory of Pulmonary Investigation, Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
- 2Laboratory of Imunophysiology, Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
- 3Laboratory of Cellular and Molecular Neurobiology, Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
- 4San Martino Policlinico Hospital, IRCCS for Oncology and Neurosciences, University of Genoa, Genoa, Italy
- 5Department of Surgical Sciences and Integrated Diagnostics (DISC), University of Genoa, Genoa, Italy
- 6Rio de Janeiro Network on Neuroinflammation, Carlos Chagas Filho Foundation for Supporting Research in the State of Rio de Janeiro (FAPERJ), Rio de Janeiro, Brazil
Background: There is widespread debate regarding the use of albumin in ischemic stroke. We tested the hypothesis that an iso-oncotic solution of albumin (5%), administered earlier after acute ischemic stroke (3 h), could provide neuroprotection without causing kidney damage, compared to a hyper-oncotic albumin (20%) and saline.
Objective: To compare the effects of saline, iso-oncotic albumin, and hyper-oncotic albumin, all titrated to similar hemodynamic targets, on the brain and kidney.
Methods: Ischemic stroke was induced in anesthetized male Wistar rats (n = 30; weight 437 ± 68 g) by thermocoagulation of pial blood vessels of the primary somatosensory, motor, and sensorimotor cortices. After 3 h, animals were anesthetized and randomly assigned (n = 8) to receive 0.9% NaCl (Saline), iso-oncotic albumin (5% ALB), and hyper-oncotic albumin (20% ALB), aiming to maintain hemodynamic stability (defined as distensibility index of inferior vena cava <25%, mean arterial pressure >80 mmHg). Rats were then ventilated using protective strategies for 2 h. Of these 30 animals, 6 were used as controls (focal ischemic stroke/no fluid).
Results: The total fluid volume infused was higher in the Saline group than in the 5% ALB and 20% ALB groups (mean ± SD, 4.3 ± 1.6 vs. 2.7 ± 0.6 and 2.6 ± 0.5 mL, p = 0.03 and p = 0.02, respectively). The total albumin volume infused (g/kg) was higher in the 20% ALB group than in the 5% ALB group (1.4 ± 0.6 vs. 0.4 ± 0.2, p < 0.001). Saline increased neurodegeneration (Fluoro-Jade C staining), brain inflammation in the penumbra (higher tumor necrosis factor-alpha expression), and blood-brain barrier damage (lower gene expressions of claudin-1 and zona occludens-1) compared to both iso-oncotic and hyper-oncotic albumins, whereas it reduced the expression of brain-derived neurotrophic factor (a marker of neuroregeneration) compared only to iso-oncotic albumin. In the kidney, hyper-oncotic albumin led to greater damage as well as higher gene expressions of kidney injury molecule-1 and interleukin-6 than 5% ALB (p < 0.001).
Conclusions: In this model of focal ischemic stroke, only iso-oncotic albumin had a protective effect against brain and kidney damage. Fluid therapy thus requires careful analysis of impact not only on the brain but also on the kidney.
Introduction
In ischemic stroke, maintenance of appropriate systemic perfusion is an important therapeutic goal (1). Fluids are often administered to achieve hemodynamic targets; however, there are controversies regarding the effects of different types of fluids on brain as well as kidney function. Even though normal saline (NaCl 0.9%) has been recommended in ischemic stroke (2, 3), it may lead to distal organ damage in critically ill patients (4–6).
Experimental studies have shown that the administration of hyper-oncotic (25%) albumin may have neuroprotective effects on brain ischemia by reducing infarct volume and cerebral edema (7, 8). Nevertheless, the potential benefits of hyper-oncotic albumin have not been confirmed in clinical trials (9, 10). The ALIAS II trial, which compared hyper-oncotic albumin (25%) with an equivalent volume of isotonic saline infusion within 5 h after onset of clinical signs of acute ischemic stroke, was stopped prematurely for futility (9). Since then, hyper-oncotic albumin has not been recommended for the treatment of patients with ischemic stroke (2, 3). Nevertheless, certain aspects that require special attention, such as: (1) the timing of albumin administration, which may be an important variable for which to control (11)—the earlier the intervention, the better the outcome might be; and (2) hyper-oncotic albumin may be associated with kidney damage proportional to its concentration, thus worsening prognosis (12, 13). Based on the foregoing, we tested the hypothesis that an iso-oncotic solution of albumin (5%), administered earlier after acute ischemic stroke (3 h), could provide neuroprotection without causing kidney damage, compared to a hyper-oncotic albumin (20%) and saline. Therefore, the effects of saline, 5% albumin, and 20% albumin were evaluated on neurodegeneration, blood-brain barrier permeability, as well as brain and kidney damage in experimental focal ischemic stroke.
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