Iohexol plasma clearance for measuring glomerular filtration rate in clinical practice and research: a review. Part 2: Why to measure glomerular filtration rate with iohexol?

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Abstract

A reliable assessment of glomerular filtration rate (GFR) is of paramount importance in clinical practice as well as epidemiological and clinical research settings. It is recommended by Kidney Disease: Improving Global Outcomes guidelines in specific populations (anorectic, cirrhotic, obese, renal and non-renal transplant patients) where estimation equations are unreliable. Measured GFR is the only valuable test to confirm or confute the status of chronic kidney disease (CKD), to evaluate the slope of renal function decay over time, to assess the suitability of living kidney donors and for dosing of potentially toxic medication with a narrow therapeutic index. Abnormally elevated GFR or hyperfiltration in patients with diabetes or obesity can be correctly diagnosed only by measuring GFR. GFR measurement contributes to assessing the true CKD prevalence rate, avoiding discrepancies due to GFR estimation with different equations. Using measured GFR, successfully accomplished in large epidemiological studies, is the only way to study the potential link between decreased renal function and cardiovascular or total mortality, being sure that this association is not due to confounders, i.e. non-GFR determinants of biomarkers. In clinical research, it has been shown that measured GFR (or measured GFR slope) as a secondary endpoint as compared with estimated GFR detected subtle treatment effects and obtained these results with a comparatively smaller sample size than trials choosing estimated GFR. Measuring GFR by iohexol has several advantages: simplicity, low cost, stability and low interlaboratory variation. Iohexol plasma clearance represents the best chance for implementing a standardized GFR measurement protocol applicable worldwide both in clinical practice and in research.

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Most cited references 36

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Decline in estimated glomerular filtration rate and subsequent risk of end-stage renal disease and mortality.

Josef Coresh, Tanvir Turin, Kunihiro Matsushita … (2014)

The established chronic kidney disease (CKD) progression end point of end-stage renal disease (ESRD) or a doubling of serum creatinine concentration (corresponding to a change in estimated glomerular filtration rate [GFR] of −57% or greater) is a late event. To characterize the association of decline in estimated GFR with subsequent progression to ESRD with implications for using lesser declines in estimated GFR as potential alternative end points for CKD progression. Because most people with CKD die before reaching ESRD, mortality risk also was investigated. Individual meta-analysis of 1.7 million participants with 12,344 ESRD events and 223,944 deaths from 35 cohorts in the CKD Prognosis Consortium with a repeated measure of serum creatinine concentration over 1 to 3 years and outcome data. Transfer of individual participant data or standardized analysis of outputs for random-effects meta-analysis conducted between July 2012 and September 2013, with baseline estimated GFR values collected from 1975 through 2012. End-stage renal disease (initiation of dialysis or transplantation) or all-cause mortality risk related to percentage change in estimated GFR over 2 years, adjusted for potential confounders and first estimated GFR. The adjusted hazard ratios (HRs) of ESRD and mortality were higher with larger estimated GFR decline. Among participants with baseline estimated GFR of less than 60 mL/min/1.73 m2, the adjusted HRs for ESRD were 32.1 (95% CI, 22.3-46.3) for changes of −57% in estimated GFR and 5.4 (95% CI, 4.5-6.4) for changes of −30%. However, changes of −30% or greater (6.9% [95% CI, 6.4%-7.4%] of the entire consortium) were more common than changes of −57% (0.79% [95% CI, 0.52%-1.06%]). This association was strong and consistent across the length of the baseline period (1 to 3 years), baseline estimated GFR, age, diabetes status, or albuminuria. Average adjusted 10-year risk of ESRD (in patients with a baseline estimated GFR of 35 mL/min/1.73 m2) was 99% (95% CI, 95%-100%) for estimated GFR change of −57%, was 83% (95% CI, 71%-93%) for estimated GFR change of −40%, and was 64% (95% CI, 52%-77%) for estimated GFR change of −30% vs 18% (95% CI, 15%-22%) for estimated GFR change of 0%. Corresponding mortality risks were 77% (95% CI, 71%-82%), 60% (95% CI, 56%-63%), and 50% (95% CI, 47%-52%) vs 32% (95% CI, 31%-33%), showing a similar but weaker pattern. Declines in estimated GFR smaller than a doubling of serum creatinine concentration occurred more commonly and were strongly and consistently associated with the risk of ESRD and mortality, supporting consideration of lesser declines in estimated GFR (such as a 30% reduction over 2 years) as an alternative end point for CKD progression.

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The hyperfiltration theory: a paradigm shift in nephrology.

Barry Brenner, Elizabeth Lawler, Harald Mackenzie (1996)

Experimental studies incriminate glomerular hypertension in mediating progressive renal damage after any of a variety of initiating injuries. Prevention of glomerular hypertension by dietary protein restriction or antihypertensive therapy lessens progressive glomerular damage in several experimental models of chronic renal disease. Glomerular hypertension and hyperfiltration also occur in humans with diabetes mellitus, solitary or remnant kidneys, and various forms of acquired renal disease. Clinical studies indicate that dietary protein restriction and antihypertensive therapy also slow progression in many of these disorders. Large multicenter trials confirm the beneficial effects of these therapeutic maneuvers on the rate of progression of chronic renal disease.

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Costimulation blockade with belatacept in renal transplantation.

, Royce W. Zhou, Gilles Blancho … (2005)

Renal transplantation is the standard of care for patients with end-stage renal disease. Although maintenance immunosuppression with calcineurin inhibitors yields excellent one-year survival, it is associated over the long term with high rates of death and graft loss, owing in part to the adverse renal, cardiovascular, and metabolic effects of these agents. The use of potentially less toxic agents, such as belatacept, a selective blocker of T-cell activation, may improve outcomes. We randomly assigned renal-transplant recipients to receive an intensive or a less-intensive regimen of belatacept or cyclosporine. All patients received induction therapy with basiliximab, mycophenolate mofetil, and corticosteroids. The primary objective was to demonstrate the noninferiority of belatacept over cyclosporine in the incidence of acute rejection at six months (with an upper bound of the 95 percent confidence interval around the treatment difference of less than 20 percent). At six months, the incidence of acute rejection was similar among the groups: 7 percent for intensive belatacept, 6 percent for less-intensive belatacept, and 8 percent for cyclosporine. At 12 months, the glomerular filtration rate was significantly higher with both intensive and less-intensive belatacept than it was with cyclosporine (66.3, 62.1, and 53.5 ml per minute per 1.73 m2, respectively), and chronic allograft nephropathy was less common with both regimens of belatacept than with cyclosporine (29 percent, 20 percent, and 44 percent, respectively). Lipid levels and blood-pressure values were similar or slightly lower in the belatacept groups, despite the greater use of lipid-lowering and antihypertensive medications in the cyclosporine group. Belatacept, an investigational selective costimulation blocker, did not appear to be inferior to cyclosporine as a means of preventing acute rejection after renal transplantation. Belatacept may preserve the glomerular filtration rate and reduce the rate of chronic allograft nephropathy. Copyright 2005 Massachusetts Medical Society.

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Author and article information

Journal

Journal ID (nlm-ta): Clin Kidney J

Journal ID (iso-abbrev): Clin Kidney J

Journal ID (publisher-id): ckj

Journal ID (hwp): ndtplus

Title: Clinical Kidney Journal

Publisher: Oxford University Press

ISSN (Print): 2048-8505

ISSN (Electronic): 2048-8513

Publication date (Print): October 2016

Publication date (Electronic): 09 September 2016

Publication date PMC-release: 09 September 2016

Volume: 9

Issue: 5

Pages: 700-704

Affiliations

[1 ]Department of Nephrology, Dialysis and Transplantation, University of Liège Hospital (ULg CHU) , 4000 Liège, Belgium

[2 ]Metabolic and Renal Research Group, UiT The Arctic University of Norway and Section of Nephrology, University Hospital of North Norway , Tromsø, Norway

[3 ]Charité University Medicine, Institute of Public Health, Berlin, Germany

[4 ]Department of Clinical Chemistry, Skåne University Hospital , Lund, Sweden

[5 ]Department of Nephrology, Dialysis, Transplantation and Hypertension, CHU Hôpital Nord, University Jean Monnet, PRES Université de LYON , Saint-Etienne, France

[6 ]Department of Clinical Chemistry, University of Liège Hospital (ULg CHU) , Liège, Belgium

[7 ]Department of Occupational and Environmental Medicine, Lund University , Lund, Sweden

[8 ]Department of Nephrology, Skåne University Hospital , Lund, Sweden

[9 ]Department of Translational Medicine, Division of Medical Radiology, Skåne University Hospital , Malmö, Sweden

[10 ]University of La Laguna, CIBICAN-ITB, Faculty of Medicine, Hospital Universtario de Canarias , Tenerife, Spain

[11 ]Centro di Ricerche Cliniche per le Malattie Rare ‘Aldo e Cele Daccò ’, Istituto di Ricerche Farmacologiche Mario Negri, Centro Anna Maria Astori, Science and Technology Park Kilometro Rosso , Bergamo, Italy

[12 ]Unit of Nephrology, Azienda Socio Sanitaria Territoriale (ASST) Ospedale Papa Giovanni XXIII , Bergamo, Italy

[13 ]Department of Medical Sciences, Uppsala University , Uppsala, Sweden

[14 ]Department of Nephrology, Skåne University Hospital , Malmö, Sweden

[15 ]IRCCS - Istituto di Ricerche Farmacologiche ‘Mario Negri', Centro di Ricerche Cliniche per le Malattie Rare ‘Aldo e Cele Daccò', Ranica, Bergamo, Italy

Author notes

Correspondence and offprint requests to: Pierre Delanaye; E-mail: pierre_delanaye@ 123456yahoo.fr

Article

Publisher ID: sfw071

DOI: 10.1093/ckj/sfw071

PMC ID: 5036903

PubMed ID: 27679716

SO-VID: 9afe9dd2-045f-421f-97ca-29235d551ce3

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

History

Date received : 18 May 2016

Date accepted : 11 July 2016

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Iohexol plasma clearance for measuring glomerular filtration rate in clinical practice and research: a review. Part 2: Why to measure glomerular filtration rate with iohexol?

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Karger: Cardiovascular System

Most cited references 36

Decline in estimated glomerular filtration rate and subsequent risk of end-stage renal disease and mortality.

The hyperfiltration theory: a paradigm shift in nephrology.

Costimulation blockade with belatacept in renal transplantation.

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Cited by 55

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