NON-RENIN-MEDIATED RENOVASCULAR HYPERTENSION

1312 tients who had high concentrations. Did they have any evidence of thromboembolism? It is hard to justify Dr O’Brien’s inference that a plasma-j3thromboglobulin is not useful in pregnancy when he studied only 13 well women in the third trimester. In a study of 157 women Pepper and 12 recorded a rise in p!asma-j3-thromboglobulin between the first and second trimesters, and 16 women had high values. Before the value of &bgr;-thromboglobulin testing in pregnancy is dismissed it would be interesting to know what happens in pre-eclampsia, a condition possibly associated with intravascular platelet aggregation. What is needed are large, well-controlled clinical trials to assess the value of the plasma-p-thromboglobulin in various disease states.

Department of Hæmatology, University Hospital of Wales,

C. A. LUDLAM

Cardiff CF4 4XW

NON-RENIN-MEDIATED RENOVASCULAR HYPERTENSION

SIR,-,-Dr Marks and his colleagues have reported non-laterrenal-vein-renin ratios in four patients with renalartery stenosis, two of whom had a positive (vasodepressor) response to saralasin infusion2 and two a negative one (March 19, p. 615). In the earlier report,2 they concluded that saralasin testing was more reliable than renal-vein-renin determinations as a means of detecting renin-mediated hypertension. Our experience, and that of others,3,4 leads us to the opposite

alising

RESULTS OF SARALASIN

TESTS,

RENAL-VEIN

SURGERY IN FOUR CASES OF UNILATERAL

RATIOS,

AND

(RIGHT-SIDED)

RENAL-ARTERY STENOSIS

tive

success

in renovascular

hypertension

than the saralasin

test. Medical Research Department, Kanematsu Memorial Institute,

Sydney Hospital, Sydney, New South Wales, Australia

PAUL MACCARTHY GORDON STOKES

RAISED SERUM-AMYLASE IN DIABETIC KETOACIDOSIS

SIR,-Dr Warshaw and his colleagues (April 30, p. 929) report that the pancreas is usually not the origin of the raised serum-amylase often seen in diabetic ketoacidosis. We have investigated 20 patients with diabetic coma (14 with diabetic ketoacidosis and 6 with non-ketoacidotic coma). 13 (65%) had hyperamylasaemia. We found no correlation between raised serum-amylase activity and abdominal pain or tenderness, hepatic involvement (judged by raised serum glutamic-oxaloacetic transaminase and alkaline phosphatase), renal failure (judged by blood-urea-nitrogen), or degree of dehydration (estimated by raised serum-osmolality). 3 of the 13 patients with raised serum-amylases died. Necropsy revealed, macroscopically and microscopically, no evidence of acute pancreatitis, oedema of the pancreas, or disease of the liver and biliary tract. Two patients died from acute myocardial infarction and one from sepsis and acute tubulointerstitial nephropathy. We agree with Dr Warshaw and his colleagues that the raised serumamylase often seen in diabetic ketoacidosis is not usually of pancreatic or hepatic origin but may be caused by systemic derangement of carbohydrate metabolism. Steno Memorial

Hospital,

Gentofte, Denmark

K. KØLENDORF

Renal Unit, Hvidovre Hospital,

B. B. MØLLER

Copenhagen

METHYLPREDNISOLONE IN URÆMIC PERICARDITIS

*And analgesic nephropathy.

conclusion. Further, we join with Dr Skrabal (May 21, p. 1103) in questioning the conclusions they reached from renalvein-renin values obtained after slight sodium depletion. We doubt whether such results constitute valid evidence that their patients had "non-renin-mediated renovascular hypertension". We have studied four patients with operatively proven renal-artery stenosis using the protocol of Streeten et al. for saralasin infusion and that of Stokes et al. for measurement of renal-vein-renin concentrations (see table). Three of these patients had a negative saralasin response, despite significant prior sodium depletion with intravenous frusemide 40 mg. All four patients had non-lateralising renal-vein-renin ratios, which lateralised correctly after intravenous diazoxide; this accords with our previous finding that diazoxide stimulation of renal-vein-renin release helps to lateialise correctly a surgically remediable lesion.6 Thus, in Dr Marks’ patients it is possible that renal-vein ratios would have lateralised had diazoxide stimulation been used. We suggest that the diazoxide-stimulated renal-vein-renin ratio is a better method for predicting opera2.

Marks, L. S., Maxwell, M. H., Smith, R. B., Cahill, P. J., Kaufman, J. J. J. Urol. 1976, 116, 406. 3. Williams, G. H., Hollenberg, N. K. in Systemic Effects of Antihypertensive Agents (edited by M. P. Sambhi); p. 531. New York, 1976. 4. Thomas, R. D., Ball, S. G., Lee, M. R. Lancet, 1977, i, 724. 5. Streeten, D. H. P., Dalakos, T. G., Anderson, G. H. Progr. biochem. Pharmac. 1976, 12, 214. 6. Stokes, G. S., Weber, M. A., Gain, J., Scott, A. J., Roberts, B. A., Sheil, A. G. R. Aust. N.Z.

Jl Med. 1976, 6, 26.

SIR,-In your editorial (April 30, p. 941) you discuss the problem of uraemic pericarditis. We would like to record our experience with systemic corticosteroids in treating this dangerous complication. As soon as uraemic pericarditis is diagnosed, methylprednisolone 0.5-1 mg/kg body-weight is RESULTS OF STEROID TREATMENT IN URAMIC PERICARDITIS

the dose is tapered off in 10-14 days to 16 mg daily for another 2 weeks. This results in the rapid relief of chest pain, fever, and tachycardia (see table). Pericardial tamponade is prevented in most cases, and pericardiocentesis is rarely needed. Our results, which will be published in full elsewhere, accord with those of Eliasson and Murphy’ and Compty et al.1 Pericardiectomy is very rarely needed, if ever, in early diagnosed cases treated by steroids. No serious side-effects from this steroid treatment were seen in our patients.

given;

2nd Propedeutic Department of Medicine, Aristotelian University of Thessaloniki, Dimosion Meeftirion Hospital, Thessaloniki, Greece

1. 2.

M. PAPADIMITRIOU C. RAIDIS P. METAXAS

Eliasson, G., Murphy, J. F. J. Am. med. Ass. 1974, 229, 12. Compty, C. M., Cohen, S. L., Shapiro, F. L. Ann intern. 173.

Med.

1971, 75,