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      Recommendations for the use of tolvaptan in autosomal dominant polycystic kidney disease: a position statement on behalf of the ERA-EDTA Working Groups on Inherited Kidney Disorders and European Renal Best Practice

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          Abstract

          Recently, the European Medicines Agency approved the use of the vasopressin V2 receptor antagonist tolvaptan to slow the progression of cyst development and renal insufficiency of autosomal dominant polycystic kidney disease (ADPKD) in adult patients with chronic kidney disease stages 1–3 at initiation of treatment with evidence of rapidly progressing disease. In this paper, on behalf of the ERA-EDTA Working Groups of Inherited Kidney Disorders and European Renal Best Practice, we aim to provide guidance for making the decision as to which ADPKD patients to treat with tolvaptan. The present position statement includes a series of recommendations resulting in a hierarchical decision algorithm that encompasses a sequence of risk-factor assessments in a descending order of reliability. By examining the best-validated markers first, we aim to identify ADPKD patients who have documented rapid disease progression or are likely to have rapid disease progression. We believe that this procedure offers the best opportunity to select patients who are most likely to benefit from tolvaptan, thus improving the benefit-to-risk ratio and cost-effectiveness of this treatment. It is important to emphasize that the decision to initiate treatment requires the consideration of many factors besides eligibility, such as contraindications, potential adverse events, as well as patient motivation and lifestyle factors, and requires shared decision-making with the patient.

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          Most cited references 33

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

          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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            Volume progression in polycystic kidney disease.

            Autosomal dominant polycystic kidney disease (ADPKD) is characterized by progressive enlargement of cyst-filled kidneys. In a three-year study, we measured the rates of change in total kidney volume, total cyst volume, and iothalamate clearance in patients with ADPKD. Of a total of 241 patients, in 232 patients without azotemia who were 15 to 46 years old at baseline we used magnetic-resonance imaging to correlate the total kidney volume and total cyst volume with iothalamate clearance. Statistical methods included analysis of variance, Pearson correlation, and multivariate regression analysis. Total kidney volume and total cyst volume increased exponentially, a result consistent with an expansion process dependent on growth. The mean (+/-SD) total kidney volume was 1060+/-642 ml at baseline and increased by a mean of 204+/-246 ml (5.27+/-3.92 percent per year, P<0.001) over a three-year period among 214 patients. Total cyst volume increased by 218+/-263 ml (P<0.001) during the same period among 210 patients. The baseline total kidney volume predicted the subsequent rate of increase in volume, independently of age. A baseline total kidney volume above 1500 ml in 51 patients was associated with a declining glomerular filtration rate (by 4.33+/-8.07 ml per minute per year, P<0.001). Total kidney volume increased more in 135 patients with PKD1 mutations (by 245+/-268 ml) than in 28 patients with PKD2 mutations (by 136+/-100 ml, P=0.03). Kidney enlargement resulting from the expansion of cysts in patients with ADPKD is continuous and quantifiable and is associated with the decline of renal function. Higher rates of kidney enlargement are associated with a more rapid decrease in renal function. Copyright 2006 Massachusetts Medical Society.
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              Limitations of creatinine as a filtration marker in glomerulopathic patients.

              To determine the reliability of creatinine as a measure of the glomerular filtration rate (GFR), we compared the simultaneous clearance of creatinine to that of three true filtration markers of graded size in 171 patients with various glomerular diseases. Using inulin (radius [rs] = 15 A) as a reference marker, we found that the fractional clearance of 99mTc-DTPA (rs = 4 A) was 1.02 +/- 0.14, while that of a 19 A rs dextran was 0.98 +/- 0.13, with neither value differing from unity. In contrast, the fractional clearance (relative to inulin) of creatinine (rs = 3 A) exceeded unity, averaging 1.64 +/- 0.05 (P less than 0.001), but could be lowered towards unity by acute blockade of tubular creatinine secretion by IV cimetidine. Cross-sectional analysis of all 171 patients revealed fractional creatinine secretion to vary inversely with GFR. This inverse relationship was confirmed also among individual patients with either deteriorating (N = 28) or remitting (N = 26) glomerular disease, who were studied longitudinally. As a result, changes in creatinine relative to inulin clearance were blunted considerably or even imperceptible. We conclude that true filtration markers with rs less than 20 A, including inulin, are unrestricted in glomerular disease, and that creatinine is hypersecreted progressively by remnant renal tubules as the disease worsens. Accordingly, attempts to use creatinine as a marker with which to evaluate or monitor glomerulopathic patients will result in gross and unpredictable overestimates of the GFR.
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                Author and article information

                Journal
                Nephrol Dial Transplant
                Nephrol. Dial. Transplant
                ndt
                ndt
                Nephrology Dialysis Transplantation
                Oxford University Press
                0931-0509
                1460-2385
                March 2016
                29 January 2016
                29 January 2016
                : 31
                : 3
                : 337-348
                Affiliations
                [1 ]Department of Nephrology, University Medical Center Groningen, University of Groningen , Groningen, The Netherlands
                [2 ]Department of Nephrology, Hacettepe University Faculty of Medicine , Ankara, Turkey
                [3 ]Department II of Internal Medicine and Centre for Molecular Medicine Cologne, University of Cologne , Cologne, Germany
                [4 ]Department of Renal Medicine, Aarhus University Hospital , Aarhus, Denmark
                [5 ]Department of Biomedicine, Aarhus University , Aarhus, Denmark
                [6 ]Department of Nephrology, Second University of Naples , Naples, Italy
                [7 ]Nephrology Clinic, Dialysis and Renal Transplant Center, ‘C.I. PARHON’ University Hospital , and ‘Grigore T. Popa’ University of Medicine , Iasi, Romania
                [8 ]Institute of Physiology, University of Zurich , Zurich, Switzerland
                [9 ]Division of Nephrology, UCL Medical School , Brussels, Belgium
                [10 ]Renal Division, University of Würzburg , University Hospital , Wurzburg, Germany
                [11 ]Department of Nephrology and Hypertension, Friedrich-Alexander University Erlangen-Nürnberg (FAU) , Erlangen, Germany
                [12 ]Department of Nephrology and Urology, Bambino Gesù Children's Hospital-IRCCS , Rome, Italy
                [13 ]Department of Nephrology, Hôpital Necker , Paris Descartes University , Paris, France
                [14 ]Service de Néphrologie, Hémodialyse et Transplantation Rénale, Hôpital La Cavale Blanche, Centre Hospitalier Régional Universitaire de Brest , Brest, France
                [15 ]Division of Nephrology, Ambroise Paré Hospital, Assistance Publique Hôpitaux de Paris , Boulogne-Billancourt/Paris, France
                [16 ]Inserm U-1018, Equipe 5 , Villejuif, France
                [17 ]University of Paris Saclay and Paris Ouest—Versailles-Saint-Quentin-en-Yvelines (UVSQ) , France
                [18 ]Academic Nephrology Unit, University of Sheffield Medical School , Sheffield, UK
                [19 ]IIS-Fundacion Jimenez Diaz-UAM and REDINREN , Madrid, Spain
                [20 ]Pediatric Nephrology Division, Center for Pediatrics and Adolescent Medicine, Heidelberg University Hospital , Heidelberg, Germany
                [21 ]Inherited Kidney Diseases Nephrology Department, Fundació Puigvert Instituto de Investigaciones Biomédicas Sant Pau, Universitat Autònoma de Barcelona , Barcelona, Spain
                [22 ]REDINREN , Barcelona, Spain
                [23 ]Renal Division, Ghent University Hospital , Ghent, Belgium
                [24 ]Department of Nephrology, Transplantation and Internal Medicine, Medical University of Silesia in Katowice , Katowice, Poland
                [25 ]CNR-IFC Clinical Epidemiology and Pathophysiology of Renal Diseases and Hypertension Unit, Reggio Calabria c/o Ospedali Riuniti , Reggio Calabria, Italy
                Author notes
                Correspondence and offprint requests to: Ron T. Gansevoort; E-mail: r.t.gansevoort@ 123456umcg.nl
                Article
                gfv456
                10.1093/ndt/gfv456
                4762400
                26908832
                © The Author 2016. Published by Oxford University Press on behalf of ERA-EDTA.

                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

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                Categories
                Cutting-Edge Renal Science
                Ndt Perspectives

                Nephrology

                vasopressin v2 receptor antagonist, tolvaptan, adpkd

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