The Salt Wars

Francesca Trebelli | 12 Sep 2008, 10:12:57

A recent issue of NDT in July 2008 has highlighted what I will chose to call “the salt wars.” In that issue, I was invited to write an editorial on why all ESRD patients should be instructed to follow a salt restricted intake of 5g/day or less. I was motivated to write this editorial (1) as I had been puzzled for 40 years about an observation we made in 1964 (2), when we observed a secondary drop in mainly diastolic blood pressure of 8 patients who has been treated by haemodialysis and a 5g/day salt diet for 6 months. This second drop following the classical response to volume reduction by progressive ultrafiltration over the first few weeks and could not be explained by anything dreamed of in Guyton’s philososophy. The “lag phenomenon” as it was later called by Charra, Bergstrom and Scribner (3), clearly was not related to volume change as the extracellular volume (Bromide space) and exchangeable Na 23 and total body water by H 3 (Tritium) were constant. The recent evidence of a non osmotically active sodium space (4), together with in vitro work suggesting that sodium could stimulate the MAPK38 (HOG1) gene (5) leads to the possibility that inflammation mediated through IL-1 could be the basis of the vascular pathology now recognised as the major killing agent throughout the world\s population as the eating habits change from home cooking to processed food. The fact that the July issue of NDT (6) gives more room for the salt council’s defence of salt rather than the science of molecular biology on excess salt speaks to the powerful lobby of food and drink manufacturers that fund the salt council.

Dr Qais Al-Awqati’s editorial from Kidney International highlights this important issue in what undoubtedly merits the name of the salt wars. Read this article here.

As it appears that Science is losing the battle of the salt wars, this blog has been conceived to highlight the issue. Let battle commence.

References

1. Shaldon S, Vienken J.The long forgotten salt factor and the benefits of using
a 5-g-salt-restricted diet in all ESRD patients. Nephrol Dial Transplant 2008; 23: 2118–2120

2. Comty C, Rottka H, Shaldon S. Blood pressure control in patients with end stage renal disease treated by intermittent haemdialysis. Proc EurDial Transplant Assoc 1964; 1: 209–213

3. Charra B, Bergstrom J, Scribner BH. Blood pressure control in dialysis patients: importance of the lag phenomenon.
Am J Kidney Dis. 1998; 32: 720-724.

4.Titze J, Shakibaei M, Schaffihuber M et al. Glycosaminoglycan
polymerisation may enable osmotically inactive Na storage in the skin. AmJ Physiol Heart Circ Physiol. 2004; 287: H203-H20

5. Shapiro L, Dinarello CA. Osmotic regulation of cytokine synthesis in vitro. Proc. Natl. Acad. Sci. USA. 1995; 92:12230-12234.

6. Nephrology Dialysis Transplantation: Volume 23, Number 7, July 2008

7. Titze J. Water-free Na retention: interaction with hypertension and tissue hydration.Blood Purif.2008;26(1):95-9

8. Schafflhuber M, Volpi N, Dahlmann A, Hilgers KF, Maccari F, Dietsch P, Wagner H, Luft FC, Eckardt KU, Titze J. Mobilization of osmotically inactive Na by growth and by dietary salt restriction in rats.Am J Physiol Renal Physiol. 2007 May;292(5):F1490-500

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1.

At 13:00:20 on 18/09/2008, arwa shuhaibar wrote:

What I do not understand why we use full strength of normal saline as a wash back in haemodialysis patients even if they are hypertensive?

2.

At 02:53:39 on 19/09/2008, AYMORE CELESTE TOLEDO JUNIOR wrote:

THE RESTRICTION SALT INTAKE AND HBP CAN BE SHOWED IN PEOPLE WHO LOW SALT INTAKE IS PRESENT ON DAY BY DAY. WHAT HAPPENS IN LOCAL VASCULAR SYSTEM SHOW US THE EFFECT OF HIGH SALT INTAKE IN FOODS. FREE RADICALS ARE SHOWING US THAT IT´S THE MAINLY COMPOUND TO DEVELOP HBP. I HAVE BEEN NOTICED IN MINE CLINICAL PRACTICE THAT OTHERS ANTI-HYPERTENSIVE DRUGS ARE MOST EFFECTVE AFTER DIURETICS AND SALT RESTRICTION DIET A LONG TIME AGO. I AGREE IN SALT RESTICTION DIET IN ERSD PATIENTS TO BLOOD PRESSURE CONTROL AND DRY WEIGHT. I BELIEVE THAT IN THE HUMAN EVOLUTION SPECIES THE RENIN-ANGIOTENSIN SYSTEM WAS THE ORIGIN TO RETENTION SALT IN HUMAN ORGANISMS AND NOWADAYS THE HIGH SALT`S CONCENTRATION IN FOODS MUST BE AVAILABLE. BEST REGARDS A.C.TOLEDO JUNIOR,M.D

3.

At 15:36:11 on 19/09/2008, Carmine Zoccali wrote:

Dereck Denton's experiments in chimpanzees were revealing in demonstrating the effect of changes in salt intake on BP in these primates. Randomized studies in hypertensive subjects where up to 4 levels of salt intake were tested show that 24h ambulatory blood pressure monitoring captures a linear relationship between BP and salt intake, a response pattern which was partly obscured in corresponding (standard) clinic measurments ( Clinical Science 1994; 87: 635-639).

4.

At 21:18:35 on 19/09/2008, Stanley Shaldon wrote:

I believe that the focus of salt in relationship to blood pressure and the idea that therefore the benefit of restricting salt is achieved via blood pressure maybe misleading. There is animal evidence in strains of rats that are resistant to hypertension that salt independently of blood pressure has a damaging effect on the endothelium. The 25% reduction in incidence of CVS disease seen in Cook et al BMJ 2007 was in a normotensive population and cannot be explained by a better control of hypertension.

5.

At 22:58:53 on 19/09/2008, Diego Novo wrote:

When we can really discourage our patients in depressed the daily salt consumption, in any stage of the CKD, we are teaching them and their families,and they themselves tell us "at home anybody use salt". That's a good notice!

6.

At 08:29:39 on 20/09/2008, wim van biesen wrote:

Dear sir,I believe there should be little doubt about the negative salt intake in patients with kidney disease. THe most neglected point in this pro-con discussion is the fact that salt is maybe not harmful in "normal" persons (and in these people a lack of salt can even provoke damage by activation of the RAAS system), as the healthy kidney is very good in regulating our "saltcontent" .This is certainly not the case in people where normal kidney function is disturbed. IN these patients, sodium intake leads to sodium retention. This in its turn, leads to upregulation of endothelin (Modesti et al, Am J Physiol, 1998), a potent vasoconstrictor, enhanced cardiac fibrosis (Frohlich et al, Nature Clinical Practice), a faster decline of residual renal function (Cianciaruso et al, Mineral elektrolyte metabolism, 1998) induced by a TGF beta mediated glomerulofibrosis (Ying et al, Am J Physiology and renal Phsyiology, 1998). IN addition, sodium intake leads to osteoporosis (Titze et al, J Hypertension, 2004). It should also not be forgotten that kidney disease patients have a down regulation of their eNOS, making them more sensitive for the negative effects of salt loading through an impaired capacity for vasodilation (Ohashi et al, Hypertension, 2006). It should also be stressed that the effects of salt intake and salt retention are enahnced in patients with hyperinsulinaemia, as insulin will induce a decrease in fractional salt excretion in the tubulus (Skott P., Diabetologia, 1991). At the end, it is very clear that in dialysis patients, salt intake induces hyperosmolarity and thus thirst, and thus weight gain and hypervolemia. Several studies have pointed out that weight reduction and interdialytic weight gain decrease can be achieved in dialysis patients simply by stressing more the need for sodium intake restriction. As a consequence, all these studies showed a decrease in blood pressure, and even in left ventricular mass (Gunal et al, AJKD, 37, 2001, 588-593).We have now accumulating evidence in our rat model that salt intake leads to substantia changes in peritoneal membrane structure, independent of the PD practice, potentially leading to a vicious circle of more volume intake (indiuced by thirst and hyperosmolarity)and decreased removal by damage of the PD membrane.

7.

At 10:50:35 on 20/09/2008, Saeed Abdelwhab wrote:

in study by Timothy D higher percentage of eosinophils, neutrophils, and levels of ECP were found in induced sputum following exercise on the normal and high salt intake compared with the low salt intake in asthmatic patients, is another evidence for the hazardous effects of salt other than blood pressure elevation.ref Med Sci Sports Exerc. 2005;37(6):904-914

8.

At 13:15:23 on 22/09/2008, Roland E. Winkler wrote:

Dear Stanley, dear Joerg,
It is very interesting that after 40 years the discussion about salt is new opened. There are differences in the look about salt. In CKD stage 3-4 patients with diuretic drug therapy and a bilanced fluid distribution and without arterial hypertension the salt ingestion is necessary to get a Blood Sodium near 135- 138 mmol/l because of the residual renal function. In anuric patient you have to decide between sodium sensitive hypertensive patients (about 35%) and patients with a reduced intradialytic refilling and arterial hypotension (less than 85 mmHg before dialysis without any antihypertensive drug therapy and without dilatative cardiomyopathy). It is very difficult to describe and to treat such patients. Well, you can prolong dialysis time, well, you can treat those patients with convective- diffusive procedures but eevery time you have a look onto the blood volume and the restricted refilling (atherosclerosis (?), arteriosclerosis (?), reduced kinetic between compartiments (?)). In that patients Sodium is a substance to improve the refilling temporarily. The Sodium concentration after dialysis session could be between 135- 138 mmol/l. Sodium restriction is very important but you have to decide individually.
Best wishes from the baltic coast and the old Hansestadt Rostock, Roland

9.

At 15:44:39 on 23/09/2008, Carmine Zoccali wrote:

Of course dr. Shaldon is right in reiterating that low salt has BP independent effects. However, heart failure apart, these effects are not so well documented in clinical trials. Patients in Cook's study were pre-hypertensives (not normotensives) and the CV risk reduction observed in TOHP I and II was adjusted for trial, clinic, age, race, and sex, baseline sodium excretion and weight but not for BP, a fundamental adjustment to prove that the risk reduction is BP independent. The (correct) conclusion by Cook was "Sodium reduction, previously shown to lower blood pressure, may also reduce long term risk of cardiovascular events". In fact the effect of low salt on BP was not even reported in this BMJ paper.

10.

At 11:35:41 on 24/09/2008, Stanley Shaldon wrote:

I would like to reply to certain comments made recently. Firstly, Dr Zoccali, Cook selected a study population defined as an individual with a relative (sibling or parent or parents's sibling with proven hypertension. She described them as prehypertensive NORMALS. Other workers have used other definitions for prehypertensive. Therefore when I used the normal I believe I was correct. The issue is important as there is a mistaken belief even amongst full professors of nephrology that an individual with normal kidney function may eat as much salt as he likes and the kidney will take care of it. The WHO Recomendations on salt intate for normals.Sodium Dietary intake of sodium, from all sources, influences blood pressure levels in populations and should be limited so as to reduce the risk of coronary heart disease and both forms of stroke. Current evidence suggests that an intake of no more than 70 mmol or 1.7 grams of sodium per day is beneficial in reducing blood pressure. The special situation of individuals who may be adversely affected by sodium reduction needs to be kept in mind (pregnant women and non-acclimated people who perform strenuous physical activity in hot environments). Limitation of dietary sodium intake to meet these goals should be achieved by restricting daily salt (sodium chloride) intake to less than 5 grams per day. This should take into account total sodium intake from all dietary sources, for example additives such as monosodium glutamate and preservatives. Use of potassium-enriched low-sodium substitutes is one way to reduce sodium intake. The need to adjust salt iodization, depending on observed sodium intake and surveillance of iodine status of the population, should be recognized. (WHO FAO expert report Summary of strength of evidence on lifestyle factors and risk of developing cardiovascular diseases 2005,545 p65) The centre for Science in the public interest has a lengthy and well documented booklet entitled "SALT the Forgotten killer". I will be happy to email the booklet and the WHO recommendations to any interested participants. My email address is stanley.shaldon@libello.com. I think attempts to justify a salt intake in normals in excess of 5g/day is unethical and almost akin to malpractice.

11.

At 08:17:09 on 26/09/2008, Carmine Zoccali wrote:

With BP what matters is risk and the risk of BP is linear. The wording normal vs abnormal makes little sense here. The category of pre-hypertension was proposed by the JNC VII because of evidence of a measurable increase in risk. That said, it is not my intention to polemize with dr. Shaldon mostly because, like him, I sit among those who believe that reducing salt intake is a public health priority. A few years ago a meritorius world-wide initiative - the CASH (Consensus Action on salt and health) was launched by Graham McGregor (St.George University BP Unit, London UK). Thanks to this initiative the salt intake in UK has fallen 8.6g/day. In Italy because of the pressure on the Ministry of Health by CASH members of that country, the salt content of bread was reduced by the 15%. Nephrologists who would like become "low salt" advocates are invited to join CASH (http://www.actiononsalt.org.uk/).

12.

At 16:23:34 on 26/09/2008, philip klemmer wrote:

The article "Of snakes and men: the evolution of ACE inhibitors" by Dr Andrew Bomback and myself recently appeared in the Journal of the Renin angiotensin Aldosterone System. We believe that nothing in biology makes sense except in light of evolutionary biology. I totally agree that Alderman's assertion that low salt is harmful is based on the erroneous interpretation of RAAS activation in severe heart failure. The Yanamami and chimps do just fine on a DASH-2 diet.. Philip J Klemmer MD

13.

At 13:50:51 on 27/09/2008, Stanley Shaldon wrote:

Whilst not wishing to continue a semantic dialogue with dr.Zoccali, I cannot accept his dogma relating to blood pressure. Firstly, I was brought up to believe that hypertension was a symptom and not a disease. Secondly, salt can produce endothelial lesions indepenently of blood pressure in certain strains of rat. Finally the danger of Dr Zoccali's approach is that there will be a tendency to opt for the easy way out , namely to use a control of blood pressure by the use of antihypertensive medication without restricting salt intake as this is a far more acceptable treatment in patients with normal kidney function and by extrapolation in patients with ESRD today. In fact this is now state of the art in the dialysis patient. Only lip service is paid to salt restriction today.

14.

At 18:26:43 on 27/09/2008, Carmine Zoccali wrote:

Dr. Shaldon has always been the most brilliant intellectual fighter in the realm of nephrology. Here he over-interprets (?) what I say, even though I at large share his view. I have never said nor at any stage implied that hypertension per se is a disease. High BP is a fundamental intermediate mechanism which may be activated by various factors (including salt) and which in concert with other factors may induce cardiovascular and renal damage. I hope dr.Shaldon agrees on this. As a final conciliatory note, I agree that salt excess in "sensitive" individuals can elicit endothelial dysfunction. Beyond animal models (food for thought not drivers of clinical decisions), the interference of salt excess with endothelial function was shown in several human studies ( e.g. Hypertension. 2001;37, 2 Part 2:444-8).

15.

At 17:31:49 on 13/10/2008, Saeed Abdelwhab wrote:

I think we have to emphasize the importance of sodium / potassium ratio of diet in addition to the amount of salt intake. This Ratio may be more important than the absolute amount of salt intake especially there is unavoidable amount of salt in our diet and till we reach a regulation to control sodium content of preserved food. The disturbed potassium-sodium imbalance had been blamed to be the cause of high blood pressure (essential hypertension), the main cause of stroke, and contributes to heart disease, memory decline, osteoporosis, asthma, ulcers, stomach cancer, kidney stones, and cataracts, and possibly be involved with erectile dysfunction and rheumatoid arthritis. Ref The Salt Solution by Herb Boynton, Mark F. McCarty, Richard Moore , Richare D. (2001)

16.

At 08:14:29 on 18/10/2008, Stanley Shaldon wrote:

David A McCarron has either given up his post as a consultant of the salt Instiitute or has deliberately forgotten to mention it in his defense of salt in the recent battle with Graham MacGregor (Nephrol Dial Transplant 2008 3:3382-3385). In his previous contribution- Nephrol Dial Transplant 2008 23:2133-2137 he declared HE WAS A CONSULTANT TO THE SALT INSTITUTE. I think it is appropriate to ask why he has forgotten to declare this serious conflict and why the editors of NDT allowed it to occur. A deliberate error like this suggests that the real battle is just beginning and that the Salt Council are now considering underground tactics and ridiculous suggestions of expensive and wasteful trials to prove/disprove by evidence based medicine what is already accepted by the majority of scientific opinion on a world wide basis, namely, that the human need for salt is no more than 5-6g per day and that excess of salt is associated with a significantly higher incidence of cardiovascular disease and mortality by mechanisms that involve inflammatory blood vessel changes with or without hypertension. The salt wars have only just begun, it has taken over 50 years since Doll first published on the dangers of smoking tobacco for the world to accept the dangers of passive smoking associated disease, and it will probably take another 50 yeaars before the processed food industry is obliged to remove this addictive substance from their food products. Unfortunately, the altered taste bud sensation of the "salt addict" will make this even more difficult to achieve.

17.

At 23:46:35 on 21/10/2008, Marianne Vennegoor wrote:

Dear Colleagues, The Journal of Renal Nutrition, January 2009 and following editions will include the proceedings of the 14th International Congess on Renal Nutrition and Metabolism, held in June 2008, Marseilles, France. One of the sessions was devoted to Salt (Sodium) pro's and con's of salt restriction and practical aspects to reducing salt intake including CKD patients. Salt reduction is a global issue and the World Health Organisation's mandate is to gradually reduce salt intake to 5 or 6 g and even lower if possible. Some countries are aiming at 4g. Marianne Vennegoor Renal Dietitian.

18.

At 21:34:29 on 24/10/2008, Helen Lewis wrote:

I am social researcher in renal medicine, not a nephrologist: as a carer of a dialysis patient for 25 years, I/we found that reducing sale intake was directly related to blood pressure reduction in young patients, and conversely restaurant food high in salt, resulted in raised bp...

19.

At 18:51:51 on 26/10/2008, George Dunea wrote:

Thank you for conducting this important survey on the issue of salt intake in dialysis patients. It is important because in so many patients the systolic blood pressure is poorly controlled. If were able to reduce their salt intake they would not require anti-hypertensive medications. I indeed remember the days when Dr Kolff did not prescribe anti-hypertensive drugs, so that it was either salt restriction or bilateral nephrectomy!! The problem nowadays is that patients, at least in Chicago, are totally unable to limit their salt intake. We think they eat enormous amounts. We try to instruct them, but to no avail. They eat what they want!!! Sometimes I ponder that we might be better off trying to understand, or at least exploit, the relation between salt and the sympathetic system. Here in Chicago we still use a lot of sympathetic system blockers, mostly clonidine but also alpha-methyl dopa, sometimes combined with a small dose of minoxidil, 2.5 mg at night and seem to control the blood pressure even in the most avid salt eaters Regards to all George Dunea MD, FACP, FRCP (Lond

20.

At 10:35:12 on 27/10/2008, Stanley Shaldon wrote:

I would like to quote a dialogue I had with Dr Kolff in 1964 during the first meeting of the EDTA in Amsterdam. Proc.Eur.dial.Transplant 1964,1,220 as on readind Dr Dunea's comment "19" I feel little has changed in over 44 years, and indeed the situation has become even worse. I wonder if diabetic dietary compliance is as bad in US as ESRD patient compliance. S. SHALDON (London): I should just like to say that in my opinion - and I think I can quote Dr. Scribner here - it has not proved necessary to do a bilateral nephrectomy in any patient to achieve blood pressure control where the patient has been properly treated on a regular haemodialysis regimen. I think that this statement should be made positively, because other centres have attempted to control blood pressure by bilateral nephhrectomy when chronic haemodialysis has, perhaps, failed. I think that one very important endocrine potential of the kidney may be removed by this, namely the erythropoietin production, and there is some evidence that this may persist even in the absence of excretory function. I would strongly suggest that nobody need take out the kidneys to control the blood pressure in these patients. W. J. KOLFF (Cleveland): I think we are exaggerating the differences here but I take exception to the last statement of my good friend, Shaldon. I would say that if you have such charming associates as has Dr. FunckkBrentano, who has at his disposal Dr. Zingraff-Kok, or if, like Dr. Shaldon you have Dr.Comty, then you can make patients eat anything. You can even reconcile them to a life in which they are allowed to drink, let us say approximately 600 grammes of water a day. But for most people I know, at least in Cleveland, Ohio, life under those circumstances would not be worth living, and they would much rather die. I have never denied that if patients are willing to go through many months of severe dietary restricction, and if you threaten them with death and hell if they ever exceed their water and salt intake, and if they go through many months of crippling invalidity during which they have to be kept in hospital, it is probably possible then to control the blood pressure of these patients. However, before you have them regulated, which may take many months, you go through several months of a state which I have called sub- dehydration, and this state of sub-dehydration is most uncomfortable. I would invite you people, since you have just said that these kidneys are virtually not excreting any urine, to take them out.

21.

At 14:56:56 on 30/10/2008, Lillian Pickering wrote:

Hello all, I am a hemodialysis nurse with 37 years of experience. In the last 15 years, in our program, the use of sodium modeling (also known as ramping) has become popular to prevent low BPs and cramping. Many nurses are convinced that the "step" sodium profile is the best to use, and I cannot convince them that they are giving their patients much too much sodium, and that they are probably increasing their patients' thirst and interdialytic weight gains.What are your thoughts on the use of sodium modeling in hemodialysis?Thanks in advance for your advice.Lillian Pickering, RN, BS

22.

At 18:53:36 on 01/11/2008, Stanley Shaldon wrote:

In answer to comment 21, I believe sodium modelling is another way of giving patients a higfh salt intake and should be avoided. I believe the secret of a easy well tolerated dialysis comes from an adherence to a low salt dier. However, Patient compliance with dietary salt restriction (5g salt per day) is very variable and difficult to assess unless the patient is anuric. The accurate measure of interdialytic weight gain (IDWG) has been the backbone method of assessing patient compliance to salt restriction in the anuric ESRD patient. Briefly, the following rule of thumb has proven to be reliable provided that the patient is eating normally. The 70Kg anuric patient on 3 x week haemodialysis should have a mean IDWG of 1.5Kg. Significant excess of this usually represents an increase in dietary salt intake. Accurate measurement of patient�s predialysis weight is rarely done today and so this parameter is oftrn inaccurately measured. The recent ERA-EDTA salt survey revealed a 94% positive reply regarding the value of dietary salt restriction in ESRD patients. No mention of IDWG was made in the questions and answers in this survey indicating that this well tried assessment of estimating salt intake indirectly has largely been abandoned. This has lead many nephrologists to believe that an arbitrary determined dry body weight removes the salt accumulated during the interdialytic period. No direct measurements of sodium balance have been made in dialysis patients since the 1960�s. Recently, it was of interest to note that in one publication (in press) the population of the centre exercising strict salt restriction need to use antihypertensive medication in only 7% of their population (n=190 :MEAN IDWG 2,3Kg) compared to another centre with a similar population vintage ( paying only lip service to salt restriction) used anti hypertensive medication in 43% of their population(n=202: MEAN IDWG 3.3Kg). The cardiac status of the latter centre was significantly poorer tha the former one as evidenced by ECG and radiographic evidence of left ventricular enlargement. This land mark comparative study of 2 populations clearly demonstrated the superiority of adhering to a salt restricted regime rather than relying on antihypertensive medication to control hypertension. The difficulty in achieving this results lies in the amount of patient education that is necessary to achieve it and the persistent follow up based upon a correct IDWG accurately measured. The benefit is associated with a smoother tolerance of dialysis itself with less post dialysis fatigue.Thus when a patient has experienced the benefit and comfort associated with the reduced IDWG, the low salt diet adherence becomes habitual. The problem lies in the time expenditure in the initial months of dialysis to achieve this goal and is compounded today by the change in social eating habits where home cooking is less and less a feature of modern life and processed take-away food has an ever increasing amount of salt added to satisfy the salt addicts taste buds. Reference:Kayicgioglu M et al . The benefit of salt restriction in the treatment of End stage renal disease by haemodialysis Nephrol Dial Transplant 2008 in press.

23.

At 00:17:09 on 02/11/2008, George Dunea wrote:

Dr. Kolff is a great man, and the statements of great men have often proved to be wrong (in retrospect!!). In the early 1960s, however, blood pressure control was difficult in the vasoconstricted hypertensive patient, who was already dry and in whom further ultrafiltration only increased blood pressure by stimulating more renin production. In such patients bilateral nephrectomy could be life-saving; it became unnecessary after the introduction of minoxidil, especially as in the nephrectomized (�renoprival�) state blood pressure was shown to be directly related to the total exchangeable body sodium,

24.

At 16:01:20 on 02/11/2008, Stanley Shaldon wrote:

My personal experience of controlling hypertension in dialysis patients was that it was not necessary to use bilateral nephrectomy. The difference between my experience and the ezperience of Seattle compared to centres east of the Mississipi in the early 60's was not just the use of a low salt diet. The dialysis technique was completely different and perhaps that is why Kolff needed to use bilateral nephrectomy where as at Seattle and the Royal Free London this operation was never used to control hypertension. In fact the only reason I ever used bilateral nephrectomy was for severe infection in polycyctic kidneys. I find the use of the adjective great in a scientific discussion to be inappropriate. If I were to admire a pioneer of haemodialysis , I would sasy that Alwall contributed more than Kolff but was not such a good marketing man.

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