DIURETICS AND BODY POTASSIUM

DIURETICS AND BODY POTASSIUM

1413 basis of their total exchangeable potassium, even when the plasma-potassium was normal. Dr Davidson and his colleagues’ criticism of total excha...

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1413 basis of their total

exchangeable potassium, even when the plasma-potassium was normal. Dr Davidson and his colleagues’ criticism of total exchangeable potassium as a measure for body potassium is valid if patients with oedema are studied or if complete equilibration is not allowed. We studied ten such patients who were all in a stable state clinically and whose therapy had been unchanged for more than a year. All had normal plasma-potassium values. The exchangeable potassium was measured with the 43K radioisotope allowing 44 h for equilibration. When the results were compared with normal values predicted from the data of Body et al. the patients fell into two groups. In six patients (aged 60-69) the exchangeable potassium was 1.5—26% below the predicted value and this was confirmed by two more measurements made 2 months apart. In the other four patients (age 38-80) the exchangeable potassium was less than 7% below the predicted value. These data suggest that in the second group the potassium supplements were either unnecessary or were adequate to prevent depletion. However, similar supplements were inadequate in the first group. It may be that these patients were more susceptible to potassium depletion or that some other contributing factors may be present such as magnesium deficiency, which we are now studying.

Plasma Angiotensin n Concentration pg/ml.

Correlation of P.R.C. and

angiotensin

II in normal and obese

subjects before and after stimulation of renin. r=O.74, r<0001. circulates

Renin

in

plasma

in

active

and

University Department of Medicine and Department of Chemical Pathology, Bristol Royal Infirmary, and Department of Medical Physics, Bristol General Hospital

M. HOMEIDA G. WALTERS

G. STADDON A. E. READ

inactive

forms.2-3 13 After stimulation, active renin increases while inactive renin decreases3 or remains unchanged.3 14 P.R.C. is a measure of active and inactive components together.2 Why then should it usually correlate so well with angiotensin 11 if the two components sometimes dissociate? The answer, we suspect, is that dissociation is temporary and that within a few hours their relation is restored as in the steady state.3 Supporting this we find a close correlation of P.R.C. and angiotensin n in an obese subject when serial samples were taken every 24 h or more during marked stimulation of renin by sodium deprivation and fasting (n=ll, r=0.91, P<0001). Close correlation of P.R.C. and angiotensin n is not invariable : in normal pregnancy there is no significant correlation in our experience12 and in nephrotic syndrome the slope of the relation is shifted.8 To summarise, Professor Swales is concerned that Glasgow and Rotterdam studies measure renin in different ranges and that the former does not show a correlation between renin and angiotensin n in the lower part of the range. He can be reassured on both points.

Medical Research Council Blood Pressure Unit, Western Infirmary,

Glasgow G11

6NT

B. LECKIE J. J. BROWN A. F. LEVER J. J. MORTON J. I. S. ROBERTSON M. TREE

DIURETICS AND BODY POTASSIUM

SIR,-We read the article

on the effect of long-term diuretic in heart-disease by Dr Davidson potassium body and his colleagues (Nov. 13, p. 1044) with great interest. Our studies on patients with chronic heart-disease receiving diuretics and potassium supplements yielded different results from theirs. We divided the patients into two distinct groups on the

therapy

on

12. Weir, R. J., and others J. clin. Endocrin. Metab. 1975, 40, 1. 13. Skinner, S. L., Cran, E. J., Gibson, R., Taylor, R., Walters, W A. W., Catt, K J. Am. J. Obstet. Gynec. 1972, 121, 626. 14. Leckie, B. J., McConnell, A., Grant, J., Tree, M., Brown, J. J. Circulation Res. (in the press).

LYMPHOMAS AND ANIMAL-PROTEIN CONSUMPTION

SiR,—Iread with great interest Dr Cunningham’s survey

(Nov. 27, p. 1184). He draws attention to an important but neglected aspect of cancer epidemiology. In 1966 my colleagues and I reported that in various countries the incidence of leukaemia and consumption of animal protein seemed to be correlated. Taking into account the signs of hepatic dysfunction in acute leukaemia, we suggested that in this disease the basic lesion may be an enzymatic blocking of the metabolic processes involved in synthesis occurring in the bone-marrow. This would be characteristic of a preleuksemic state. When excessive loading with the substrate for the blocked pathway (presumably protein or concomitant substance) is taking place, pathological proliferation of the cells in the bone-marrow may develop. Based on this hypothesis, a low-protein purine-free diet was introduced as an adjunct in the treatment of acute leukaemia in children.2 On different grounds, a similar diet was used by Hilson,3 also with encouraging results. A possible beneficial effect was reported in acute leukaemia in which aminoacid imbalance was induced by supplementing the diet with excess phenylalanine and tyrosine.4 Later experimental work has focused on the immunological aspects of a low-protein diet. In mice fed diets containing between 5% and 10% casein normal cellular cytotoxic responses to the immunising tumour developed while serumblocking activity was absent. A 10-fold greater target-cell damage occurred in mice on 3% casein diet than in normally fed mice tested under the same conditions. Comparable results could be obtained by deficiency or imbalance of certain aminoacids in the diet.6 Whatever the mechanism(s) might be operating, it seems essential to investigate the possible role of low-protein diet in 1. 2. 3. 4. 5. 6.

King, P. C. , Davies, D L Eur J. clin Invest 1973, 3, 188. Halikowski, B., Armata, J , Garwicz, S Br med. J. 1966, i, 519.

Body, K.,

Hilson, D. ibid. p. 979. Allan, J. D., Ireland, J. T., Milner, J., Moss, A. D. Lancet, 1965, i, 302.

Jose, D. G.. Good, R. A. Cancer Res. 1973, 33, 807. Jose, D G., Good, R. A. J. exp Med. 1973, 137, 1.