1. The effects of intravenous metoclopramide on baseline values and dopamine dose–response curves for renal haemodynamics and natriuresis were investigated in healthy volunteers and patients with renal disease. 2. Dopamine infusion alone, in doses ranging from 0.25 to 8 μg min −1 kg −1 , resulted in a dose-dependent increase in effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) with a fall in filtration fraction (FF) in eight hydrated healthy volunteers and, to a lesser degree, in 12 patients with renal disease. An increase in natriuresis (urinary excretion of sodium, U Na + V ), fractional excretion of sodium (FE Na + ) and diuresis (urine flow rate, UV ) was found in both groups for doses of 2 μg min −1 kg −1 and higher. 3. Metoclopramide infusion did not alter baseline values of GFR, ERPF or FF, but shifted the dopamine dose–response curve for ERPF and FF in the healthy volunteers. Metoclopramide induced a fall in U Na + V and FE Na + in both groups (fall in baseline FE Na + from 1.52 to 0.71 during metoclopramide in healthy volunteers and from 1.23 to 0.56 in patients; P < 0.01) and blunted the natriuretic response to subsequent dopamine infusion. The fall in U Na + V during metoclopramide infusion showed a strong correlation with baseline GFR ( r = −0.944). In the patients, the response for the fractional excretions of β 2 -microglobulin and γ-glutamyltransferase was comparable with that of FE Na + . 4. Dopamine infusion induced a fall, and metoclopramide led to rise, in plasma aldosterone concentration. 5. We conclude that metoclopramide acts as a dopamine antagonist at the renal level in man. Endogenous dopamine secretion does not seem to have a role in maintaining ERPF or GFR in hydrated healthy volunteers or in patients with renal disease, but is important for mediating natriuresis. Dopamine-induced changes in natriuresis were not found to depend on changes in renal haemodynamics.

1. In order to find out whether hyperoxaluria can be demonstrated in patients on chronic (twice a week) haemodialysis, a group of 13 patients was investigated. These included one patient with proven primary hyperoxaluria, one suspected of having this disease and 11 patients in whom no information was available as to their oxalate metabolism. 2. Oxalate concentrations in haemodialysate fractions and blood samples, taken before and after dialysis, were determined. 3. The patient with primary hyperoxaluria had a plasma oxalate concentration before dialysis above 100 μmol/l and after dialysis above 25 μmol/l, while the oxalate concentration in haemodialysate at the start of dialysis was above 25 μmol/l and at the end above 10 μmol/l. The patient suspected of hyperoxaluria had similar values. Of the remaining 11 patients, one was shown to exhibit a transient hyperoxaluria, but the others showed a normal oxalate metabolism. 4. A plasma oxalate/creatinine concentration ratio exceeding 0.1, and the calculated total quantity of oxalate removed by dialysis exceeding 2 mmol, also enabled a diagnosis of hyperoxaluria to be made. 5. Hyperoxaluria can still be demonstrated in patients, who because of renal failure are subjected to haemodialysis. Measurements of oxalate in haemodialysate and plasma are valuable in cases where kidney transplantations are considered, especially when the particular patient exhibits hyperoxaluria.