Dialysis Centre, ViaMedis Riesa, Germany
Received Date: March 30, 2016; Accepted Date: March 31, 2016; Published Date: April 07, 2016
Citation:Ryzlewicz T (2016) The Story of Tassin. J Nephrol Ther 6:e115. doi:10.4172/2161-0959.1000e115
Copyright: © 2016 Ryzlewicz T. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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In 1997 G. Laurent published extraordinary results of long-term treatment with Haemo-dialysis (NDT). The basics of this regime were 24 hours treatment time per week and a very low salt intake (2.0 g per day) by self-prepared cocking. There were nearly no antihypertensive drugs used. Many patients had treated 30 years RRT, another big group had done 40 years RRT. This has very well known by most of the nephrologists.
Not known are conditions of this treatment: Laurent had used the prescription of dialysis fluid of Shaldon (Acetate dialysis, Acetate as a buffer-precursor). There was no bicarbonate inside (> and no calcification!). Tassin had done this excellent quality of treatment by the known long treatment time and an only moderate dialyzer clearance. The last was very important, not to overrun the metabolic capacity of the liver to transform Acetate into Bicarbonate and CO2. So this form of treatment in Tassin had not the side-effects of Acetate, as the treatment time was long and the dialyzer clearance only moderate. For four tenyear decades, there was no reason to change this regime. It was an extraordinary result by excellent doctors!
The Bicarbonate dialysis started in 1978, using a second concentration pump and acidification with 3 mmol/l Acetate. From the very beginning, the problem of calcification if the dialysis fluid was present everywhere. That is why, the machine has to descale after every single treatment. Only the patient never will be descaled! Medical Societies had recognized the severe problem of calcification of coronary vessels and heart valves of CKD-5 patients, which is resulting in wellknown high rates of morbidity and of mortality. Now it is the time to stop this contribution of the calcifying Dialysis fluid to the patient’s calcification!
It is not my target, to re-introduce the buffer precursor Acetate. This is historic, whenever extraordinary doctors had splendid results with it. It is time, to exchange the acidification of bicarbonate dialysis fluid from 3 mmol/l Acetate to 1 mmol/l Citrate. At first, you have the same amount of CO2 production (> as Citrate is a three-fold base). At second, Citrate has a second principle of working, the chelate binding. The problematic ions for calcification (Ca++ and Mg++) will disguised by this in order to prevent any calcification at all!
As this is a problem of chemical solubility, it will not well understood by Medical doctors, even not by those of the Medical Societies. Official Authorities (FDA Dep. Medical Products (US) or BfArM Institut (Germany)) are not interested, as Dialysis concentrate is a Medical Product and there is no vigilance of it. So the interested nephrologist himself will kindly asked to think over this problem, as the Medical Societies neglect it.