A. C. Kennedy

Total Body Potassium in Long-Term Frusemide Therapy: Is Potassium Supplementation Necessary?

Measurements of total body potassium (T.B.K.) were made by whole-body counting in four groups of patients receiving oral frusemide for one year. Patients in group 1 had essential hypertension and normal renal function and received 40 mg frusemide daily without potassium supplements. Patients in group 2 were similar but received oral potassium supplements for the first four months of treatment. Patients in group 3 had hypertension associated with renal disease and received 120 mg frusemide daily without potassium supplements. Patients in group 4 also had hypertension and renal impairment and in addition to 120 mg frusemide daily they received oral potassium supplements for four months. No evidence of depletion of T.B.K. was found in any of the groups after continuous treatment with frusemide for one year. It is questioned whether potassium supplementation in long term diuretic therapy with frusemide is necessary unless there is evidence of pre-existing potassium depletion or of some other factor such as cardiac failure, cirrhosis of the liver, or the nephrotic syndrome.

Renal Artery Stenosis, Hypertension, and Polycythaemia

In 27 subjects without any disorder of calcium metabolism the plasma calcium, measured four times daily, was significantly reduced when the calcium intake was reduced. The urine calcium also fell significantly. Eleven normal subjects received a normal and a low-calcium diet on successive days. The ultrafilterable calcium fell significantly on the day of the low calcium intake. There was a significant correlation between the changes in the plasma and urinary calcium produced by the alteration in the calcium intake. The relative magnitude suggests that if a maximum tubular reabsorptive capacity for calcium exists it was not exceeded under the conditions of these observations. Thus it would appear that changes in urine calcium brought about by variations in calcium intake could be accounted for by small but significant changes in plasma ultrafilterable calcium.

High Dosage Metolazone in Chronic Renal Failure

Metolazone is a modified quinazolinesulphonamide and in a dose of between 4 and 7·5 mg is an effective diuretic in man with normal renal function. Fourteen patients with non-oedematous stable chronic renal failure (creatinine clearance ranging from 1·2 to 12 ml/min) were given metolazone in doses ranging from 20-150 mg. A noticeable increase in urine flow and sodium excretion occurred, free water clearance increased, and there was a small but significant increase in potassium excretion. No side effects were noted.

Exchangeable and Total Body Potassium in Patients with Chronic Renal Failure

Total body potassium determined by whole-body monitoring and exchangeable body potassium estimated with 43K were measured simultaneously in 12 patients with stable chronic renal failure. Values for the exchangeable potassium were obtained after equilibration periods of 24, 48, and 64 hours. The exchangeable body potassium, expressed as a percentage of the total body potassium (mean ± S.E. of mean), gave values of 60·7 ± 3·3%, 83·6 ± 2·7%, and 85·9 ± 2·7% at 24, 48, and 64 hours respectively. It seems that the equilibration between radioactive and native potassium is incomplete after 24 hours; and that exchangeable potassium measured at this time is not an accurate index of the status of total body potassium in such patients. Furthermore, the finding that the value at 64 hours is significantly less than found in healthy subjects suggests that the exchangeable potassium is a smaller fraction of the total body potassium in patients with chronic renal failure.

Tuberculosis as a Continuing Cause of Renal Amyloidosis

In 40 patients with renal amyloidosis seen in a ten-year period tuberculosis was the major preceding disease in 20, though it was active in only two at diagnosis. Most patients presented with renal failure, and only two survived for five years. This experience (at least, in the west of Scotland) conflicts with the generally accepted view that rheumatoid arthritis is the commonest cause of renal amyloidosis.

Total Body Potassium in Non-Dialysed and Dialysed Patients with Chronic Renal Failure

Total body potassium was studied in 33 patients with chronic renal failure, 18 of whom had been receiving regular dialysis therapy for 1 to 48 months. In nondialysed patients body potassium was not significantly different from normal in the group as a whole, but was significantly greater than normal in three patients, and significantly less than normal in two patients. In 14 of the dialysed patients, both as individuals and as a group, body potassium was not significantly different from normal but in the remaining four it was less than normal. Potassium transfer during dialysis was studied in two patients. Uptake by these two patients of 43K added to the dialysate (1 mEq K/litre) was measured by whole-body monitoring. Transfer of administered 43K from the patients to the dialysate was measured by whole-body monitoring and by radioactive and chemical assay of the dialysate. A negative balance due to twice-weekly dialysis of 178 and 244 mEq K/week was found, which with weekly faecal and urine losses of 20-30 mEq K approximately equals the dietary intake of 210-315 mEq K.

Results of surgery in hypertension due to renal artery stenosis.

We have previously reported our exeriene on the detection af renovascular hypertension, a combination of intravenous 3yelography and isotope renography being used as a screening procedure in hypertensive patients (Kennedy et al., 1965; Luke et al., 1966). In this paper we give an account of the effect of surgical treatment in the 27 patients with renal artery stenosis operated on up to May 1966, so that the minimum follow-up period was at least one year. These 27 patients originated from group of 41 with functional renal artery stenosis found by screening about 1,000 patients with hypertension. We shall report separately the results of surgery in the slightly greater number of patients with unilateral chronic pyelonephritis and other forms of unilateral parenchymal renal disease originating from the same group of hypertensive patients.

Prevention and early management of acute renal failure.

ACUTE renal failure remains an important complication ofmany serious medical, surgical and obstetrical conditions. It still carries a considerable mortality, especially after trauma or surgery (Kennedy et al., 1963a; Merrill, 1965a; Shackman, 1966; Stewart et al., 1966). A suitable working definition of acute renal failure might be renal failure of sudden onset as manifested by insufficient bladder urine to prevent rising blood levels of nitrogenous end-products. This definition intentionally avoids defining acute renal failure purely in respect of urine volume since oliguria, although usually present, is not an invariable feature (Sevitt, 1959). Bladder urine means that acute retention is excluded. The only way to avoid overlooking the diagnosis of acute renal failure is to practise persistent vigilance in the presence of the appropriate clinical circumstances; these circumstances are commonplace in intensive care units. Acute renal failure may be pre-renal, renal, or post-renal in origin. Either pre-renal failure or postrenal failure may lead to intrinsic renal failure unless treated.

SUCCESSFUL TREATMENT OF THREE CASES OF VERY SEVERE BARBITURATE POISONING

Abstract Summar Three self-poisoned patients with extremely high serum-barbiturate levels (phenobarbitone 58 mg. per 100 ml., butobarbitone 15 mg. per 100 ml., and cyclobarbitone 14·8 mg. per 100 ml.) were successfully treated by prolonged haemodialysis and forced diuresis (combined, in one case, with peritoneal dialysis) besides standard supportive measures. The blood-levels are the highest ever recorded for these barbiturates. These cases illustrate the principles of management in very severe barbiturate intoxication.

Results of Nephrectomy in Hypertension Associated with Unilateral Renal Disease

Nephrectomy has been carried out in 34 patients with hypertension associated with unilateral parenchymal renal disease (28 with unilateral pyelonephritis, 3 tuberculosis, 2 hypoplasia, and 1 adenocarcinoma). In 13 of the patients the blood pressure was corrected, in four it was improved, and in 17 it was unaffected. The intravenous pyelogram (by the infusion technique with nephrotomography if necessary) and renogram give adequate information in most patients with unilateral parenchymal renal disease but may need to be supplemented by aortography, or retrograde pyelography, or divided renal function studies in a few special circumstances. When the function of the damaged kidney is less than 25% of the total (which is well maintained), and the contralateral kidney is intact, nephrectomy is recommended provided the hypertension is significant; success is more likely in younger patients with a short history of hypertension.