Meprobamate in the Treatment of Stuttering
Authors: R. D. H. Maxwell, J. W. Paterson
Journal: BMJ (1958)

Brm 873 -~~~~~~~~~~~~~~~~~MIA ORA Although mercury salts in large amounts can cause a full-blown tubular necrosis, the effect of small amounts of mercurials, such as are in question here, is to produce an epithelial necrosis limited to the proximal tubule and not involving the basement membrane (Oliver et al., 1951).The first patient had had a full course of mercurials while on a low-salt diet, so that iatrogenic sodium depletion is a possible additional cause of lowered renal blood flow; against this possibility is the absence of hyponatraemia in the early anuric stage, and the restoration of urine flow spontaneously, while on a sodium-free intake.Arterial desaturation may well aggravate the effects of renal ischaemia; but hypercapnia is probably not a critical factor, as it was absent in the first patient.We have not observed anuria in other forms of cardiac failure.In the last few days of illness both patients had hyper- kalaemia (7 mEq/l.);one had a definitely low plasma sodium (130 mEq/l.)and the other a low-normal value (138 mEq/l.).We have recently seen another patient with terminal cor pulmonale, but without anuria, whose plasma sodium was 130 mEq/l.and potassium 7.6 mEq/l.Anoxia and acidosis are recognized causes of a shift of potassium from cells to extracellular fluid; so that the obvious ex- planation of hyperkalaemia in terms of diminished renal output of potassium may be less important than internal shifts of potassium, and possibly also of sodium.This is a question which could only be settled by full balance-studies, which are not likely to be made.It is relevant, however, to mention that Moore et al. (1954), studying other types of acute renal failure, found that patients whose total ex- changeable potassium was low quite often had a high plasma potassium; and one of us (D. A. K. B.) has seen a patient with corrosive sublimate poisoning whose plasma potassium fell from 8 to 3.5 mEq/l. in 24 hours, during which time metabolic acidosis had been corrected by infusion of 200 ml. of molar sodium lactate.Acute renal failure occurring in such circumstances may well be regarded as almost the least of a patient's troubles; while it constitutes an additional therapeutic problem, the situation may sometimes be met by conservative treatment, which is more likely to succeed if the condition is promptly recognized.More important, perhaps, than the treatment of established renal failure is the recognition that it can occur in patients with lung disease, whose cor pulmonale has been complicated by a lowering of cardiac output, often associated with acute respiratory infection.These observa- tions perhaps reinforce in some small degree the already strong case for the prompt and vigorous treatment of sus- pected acute respiratory infection in patients with bronchitis and emphysema; in this way, the dangerous situation of peripheral circulatory failure may be prevented or cut short.Summary Two patients with terminal respiratory failure had in addition acute oliguric renal failure; in one the urine flow returned before death, while the other died before this could happen.It is suggested that a terminal fall in cardiac output in patients with cor pulmonale may on occasion produce ischaemic tubular necrosis.We are grateful to Professor R.