Discussion 261 



(less than 20 g. daily). I have no comparison with a group of patients 

 who continued eating normal amounts of protein. I have the impression 

 that our patients can continue longer with their ordinary work. Their 

 nausea usually disappears, they often gain weight, and in other respects 

 are also in better condition. We have the paradox that reducing the 

 protein intake often results in a rise in serum albumin and sometimes in 

 a slight rise in serum haemoglobin. The protein-poor diet does not 

 prevent a gradual reduction of the kidney function. However this decline 

 is usually slow and the patients may have several years of useful life. 

 A high diastolic blood pressure is a very bad prognostic factor. As long 

 as we have no control group we cannot produce convincing evidence 

 that an untreated patient will not live as long as our 'maltreated' 

 patients. 



Kennedy : Have you done any liver function tests in a situation where 

 serum albumin is falling in spite of a high protein intake, Prof. Borst? 

 There may be a possible connexion with the increased liver protein 

 breakdown when one removes the kidney (Sellers, Katz and Marmorston, 

 (1957). Amer. J. Physiol., 191, 345). 



Borst: No liver function tests were done, and we only have data on 

 the serum proteins. There is no increased y-globulin as is usually found 

 in chronic hepato-cellular disease. We had, however, some evidence of a 

 deleterious effect of the low protein diet. More cases of tuberculosis were 

 seen than would be expected in similar patients on a normal protein diet, 

 and two patients died from miliary tuberculosis. Probably the extremely 

 low protein diet reduces the resistance against the tubercle bacillus in 

 spite of the fact that the patients do not lose weight. 



Talbot: How do you define a low protein diet? 



Borst: It is less than 20 g./day. To control the diet and determine 

 whether or not the patient adheres to it, 24-hour urine portions are 

 regularly examined for nitrogen excretion. We also determine creatinine 

 excretion to be sure that urine collection is complete. The 24-hour 

 creatinine output is very constant. This output is determined for every 

 kidney patient during clinical observation, and we use the figures for 

 comparison with the nitrogen output when the patients are under control 

 in the out-patient department. Many adhere to the diet and go along 

 very well for several years. 



Fejfar: We have had similar experiences in Czechoslovakia. This 

 treatment originated in the experiments of Thomas Addis (1948. 

 Glomerulonephritis : Diagnosis and Treatment. New York : Macmillan), 

 who showed that partially nephrectomized rats kept on a higher protein 

 intake could not survive as long as the animals with a low protein 

 diet. We therefore started to use a low protein diet in all patients with 

 chronic glomerulonephritis. Usually we give • 5-0 • 7 g./kg. body weight 

 per day in the diet (but no less than 0-5 g./kg.), plus the amount lost in 

 the urine. Of course, children and those with the nephrotic syndrome 

 are given larger amounts of protein. It is very difficult to judge long-term 

 results as we have no control group for this treatment. Nevertheless we 

 do think we can prolong the life of patients with chronic nephritis on 

 this low-protein diet. 



