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increasing renal cortical blood flow, filtration rate, and
resulting solute load, mannitol can artificially reduce
medullary blood flow while simultaneously increasing
metabolic demand, further compromising renal tissue
These changes may potentiate the effects of ischemia
by decreasing the medullary protective mechanisms that
occur during oliguric renal failure, including reduction of
renal blood flow, thereby decreasing GFR and metabolic
load for solute reabsorption
Recent studies, including a meta-analysis of renal pro-
tective agents for contrast-induced nephropathy and
Cochrane analysis of the use of perioperative renal protective
agents, found no benefit from the use of mannitol in
preserving renal function in these settings .
A retrospective review at our institution evaluated the
use of intravenous mannitol during minimally invasive NSS
and found no evidence of clinically meaningful benefit in
patients who received mannitol intraoperatively eGFR
recovery models were similar between mannitol and
nonmannitol groups at any point in the postoperative
period. Several factors affected the ability of this retrospec-
tive study to definitively evaluate the use of mannitol as a
protective agent during renal ischemia.
Recently, Omae et al reported their retrospective
experience on the effect of mannitol in 55 patients with a
renal mass in a solitary kidney treated with open NSS.
Mannitol was given within 15 min before clamping the
renal artery, and ice-slush cold ischemia used. The mean
postoperative eGFR at 1 d, 1 mo, 3 mo, and 6 mo post-
operatively was similar in the 20 patients who received
mannitol and the 35 patients who did not. On multivariate
analysis, only ischemia time was associated with changes
in postoperative eGFR.
An international survey on the use of mannitol in partial
and living-donor nephrectomy in 92 high-volume urologic
centers reported the use of mannitol in 79% and 65% of
centers performing NSS and living-donor nephrectomy,
respectively, with an 83% overall rate of utilization of
mannitol In NSS, infused mannitol varied between
12.5 g in 30% of cases, 25 g in 49%, and other dosages in 22%.
This high degree of nonstandardized, variable application in
clinical practice combined with a lack of supporting clinical
evidence is a cautionary tale.
The strengths of our study include (1) the randomized,
double-blind, placebo-controlled design, (2) standardized
perioperative protocols, (3) robust follow-up at all study
visits, and (4) the comprehensive renal function evaluation.
Our finding provides the foundation for a change in clinical
practice, supporting standardized fluid management with-
out mannitol during NSS as the standard of care.
The limitations of our study include evaluating a single
dosage regimen of mannitol when results from a recent
survey suggest that 25 g is the most common practice.
Additionally, most patients had adequate preoperative
renal function and therefore the effect of mannitol in
patients with poor baseline kidney function is unknown.
Pre-enrolment selection bias is also a potential limitation
considering the number of patients who were not
approached for the study.
5. Conclusions
Intravenous mannitol infusion during NSS does not lead to
clinically relevant improvement in renal function outcomes,
and its use in patients with adequate renal function should
be discontinued.
Author contributions: Jonathan A. Coleman had full access to all the data
in the study and takes responsibility for the integrity of the data and the
accuracy of the data analysis.
Study concept and design: Power, Coleman, Russo, Sjoberg.
Acquisition of data: Coleman, Russo, Sjoberg, Bernstein, Spaliviero,
Murray, Benfante, Wren.
Analysis and interpretation of data: Sjoberg, Power, Spaliviero, Coleman,
Russo.
Drafting of the manuscript: Spaliviero, Power, Coleman, Sjoberg.
Critical revision of the manuscript for important intellectual content:
Spaliviero, Power, Coleman, Russo, Sjoberg, Murray, Wren.
Statistical analysis: Sjoberg, Benfante, Bernstein.
Obtaining funding: Coleman, Russo.
Administrative, technical, or material support: Spaliviero, Murray, Ben-
fante, Bernstein.
Supervision: Coleman, Russo.
Other: None.
Financial disclosures: Jonathan A. Coleman certifies that all conflicts of
interest, including specific fi nancial interests and relationships and
affiliations relevant to the subject matter or materials discussed in the
manuscript (eg, employment/affiliation, grants or funding, consultan-
cies, honoraria, stock ownership or options, expert testimony, royalties,
or patents filed, received, or pending), are the following: None.
Funding/Support and role of the sponsor: Memorial Sloan Kettering
Cancer Center and the NIH/NCI Cancer Center Support Grant P30
CA008748.
Acknowledgments: The authors acknowledge Alicia Fahrner and Brian
Kunzel for their outstanding research administrative assistance with the
trial and Carol Hoidra for her invaluable help in editing the manuscript.
ClinicalTrials.gov identifi er NCT01606787.
Appendix A. Supplementary data
Supplementary data associated with this article can be
found, in the online version, at
.
References
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