HighVolumeHDF® with its numerous positive effects on cardiovascular risk factor in dialysis patients is acknowledged as the most effective dialysis treatment modality1, coming closer to the elimination profile of the natural kidney.
By achieving high substitution volumes, HighVolumeHDF® therapy is credited with more effective elimination of middle molecules. HighVolumeHDF® improves patient outcomes and exerts beneficial effects on the potential cardiovascular risk factors related to dialysis patients:
- Serum ß2-m and phosphate level2,3,4
- Inflammatory response5
- Intradialytic haemodynamic stability6
- Anaemia control7
These factors contribute to improved patient survival.8
1 Krick G, Ronco C (eds), Contrib Nephrol. (2011); 175: 93-109.
2 Canaud B., Contrib Nephrol (2007); 158: 216-224.
3 Penne L. et al., Clin J Am Soc Nephrol (2010); 5: 80-86.
4 Davenport A., Nephrol Dial Transplant (2010); 25: 897-901.
5 Pedrini L. et al., Nephrol Dial Transplant, advanced access published Jan 18, 2011.
6 Locatelli F. et al., J Am Soc Nephrol (2010); 21: 1798-1807.
7 Bonforte G. et al., Blood Purif (2002); 20: 357-363.
8 Maduell F. et al., J Am Soc Nephrol (2013); 24: 487-497.
- Reduced mortality risk with HighVolumeHDF®
- Fewer cardiovascular complications
In recent years several studies have confirmed the clinical benefits of HDF1-4. These studies have demonstrated that large convection volumes in post-dilution mode are required in order to achieve and maximise the benefits of HDF therapy. The Catalonian high-volume HDF study shows a significant 30% risk reducation in all-cause mortality for patients with high-efficieny post-dilution online HDF compared to HD1. The inverse relation between the magnitude of convection volume and mortality risk has been reinforced by the European Dialysis Working Group in their last meta-analysis5 and was confirmed by the HDF Pooling Project investigators6. The analysis showed that HDF reduces the risk of all-cause and cardiovascular mortality, especially with convection volumes of at least 23 L/session6.
More results of the Catalonian high-volume study see 2.0 Studies.
1 Maduell F. et al., J Am Soc Nephrol (2013); 24: 487-497.
2 Ok E. et al., Nephrol Dial Transplant (2013); 28: 192-202.
3 Grooteman M.P. et al., J Am Soc Nephrol (2012); 23: 1087-96.
4 Canaud B. et al., Kidney Int (2006); 69: 2087-93.
5 Mostovaya I.M. et al., Semin Dial (2014); 27(2): 119-127.
6 Peters S.A.E. et al., Nephrol Dial Transplant (2016); 31: 978-984.
Multiple risk factors contribute jointly to cardiovascular diseases, which may lead to rapid progression of atherosclerosis and left ventricular hypertrophy. These cardiovascular diseases are also associated with decreased tolerability of haemodialysis and other complications.
Inflammation and increased β2-microglobulin levels are important risk factors, which should be efficiently reduced during dialysis.
A large number of retained compounds are involved in uraemic toxicity. Among them are larger solutes and protein-bound compounds which seem to be associated with deleterious biological and clinical effects, but are difficult to remove by dialysis. Increased serum ß2-m levels are related to higher mortality.1
Results from a subgroup of patients from the CONvective TRAnsport STudy (CONTRAST) study show that after 6 months pre-dialytic serum ß2-m levels were decreased significantly in patients with HDF.2
1 Cheung A. et al., J Am Soc Nephrol (2006); 17: 546-555.
2 Penne L. et al., Clin J Am Soc Nephrol (2010); 5: 80-86.
Inflammation is an important cardiovascular risk factor for dialysis patients. Serum levels of inflammatory markers such as cytokines and C-reactive protein (CRP) are higher in these patients than in the general population. CRP has been identified as a predictor of all-cause and cardiovascular mortality in patients on haemodialysis.1
Patients being treated with online HDF benefit from significantly lower levels of CRP than patients on Low-Flux HD.2
1 Panichi P. et al., Nephrol Dial Transplant (2008); 23: 2337-2343.
2 Pedrini L. et al., Nephrol Dial Transplant (2011); 26 : 2617-2624.