We compared the effects of intravenous infusions of 0.9% saline ([Cl−] 154 mmol/L) and Plasma-Lyte 148 ([Cl−] 98 mmol/L, Baxter Healthcare) on renal blood flow velocity and perfusion in humans using magnetic resonance imaging (MRI).
Animal experiments suggest that hyperchloremia resulting from 0.9% saline infusion may affect renal hemodynamics adversely, a phenomenon not studied in humans.
Twelve healthy adult male subjects received 2-L intravenous infusions over 1 hour of 0.9% saline or Plasma-Lyte 148 in a randomized, double-blind manner. Crossover studies were performed 7 to 10 days apart. MRI scanning proceeded for 90 minutes after commencement of infusion to measure renal artery blood flow velocity and renal cortical perfusion. Blood was sampled and weight recorded hourly for 4 hours.
Sustained hyperchloremia was seen with saline but not with Plasma-Lyte 148 (P < 0.0001), and fall in strong ion difference was greater with the former (P = 0.025). Blood volume changes were identical (P = 0.867), but there was greater expansion of the extravascular fluid volume after saline (P = 0.029). There was a significant reduction in mean renal artery flow velocity (P = 0.045) and renal cortical tissue perfusion (P = 0.008) from baseline after saline, but not after Plasma-Lyte 148. There was no difference in concentrations of urinary neutrophil gelatinase–associated lipocalin after the 2 infusions (P = 0.917).
This is the first human study to demonstrate that intravenous infusion of 0.9% saline results in reductions in renal blood flow velocity and renal cortical tissue perfusion. This has implications for intravenous fluid therapy in perioperative and critically ill patients. NCT01087853
This is the first study in humans to show that the intravenous infusion of 2 L of 0.9% saline over 60 minutes results in reductions in renal blood flow velocity and renal cortical tissue perfusion, changes not observed after infusion of a balanced crystalloid.
*Division of Gastrointestinal Surgery, Nottingham Digestive Diseases Centre National Institute for Health Research Biomedical Research Unit, Nottingham University Hospitals, Queen's Medical Centre
†Sir Peter Mansfield Magnetic Resonance Centre, School of Physics and Astronomy, University of Nottingham, Nottingham, UK.
Reprints: Dileep N Lobo, DM, FRCS, FACS, Division of Gastrointestinal Surgery, Nottingham University Hospitals, Queen's Medical Centre, Nottingham NG7 2UH, UK. E-mail: firstname.lastname@example.org.
Disclosure: A.H.C. received a travel grant from Baxter Healthcare to present the data. D.N.L. has received unrestricted research funding, travel grants, and speaker's honoraria from Baxter Healthcare, Fresenius Kabi, and BBraun. E.F.C. and S.T.F. have no conflicts of interest to declare. A.H.C. also received research fellowships from the Royal College of Surgeons of England and the Nottingham Digestive Diseases Centre National Institute for Health Research Biomedical Research Unit. The running costs of this investigator-initiated study were met by a grant from Baxter Healthcare. The sponsors of the study had no role in the study design, data collection, data analysis, data interpretation, or in the writing of the report.
This paper has been presented to the International Surgical Congress of the Association of Surgeons of Great Britain and Ireland, Bournemouth, May 2011 and to the Annual Congress of the European Society for Clinical Nutrition and Metabolism, Gothenburg, September 2011. It has been published in abstract form: Br J Surg 2011;98(S3):45–46 and Clin Nutr Suppl 2011;6(1):3–4.