Cimetidine for pruritus in Hodgkin's disease.

our patients. Our results, however, indicate that conflicting reports2 3 about the diurnal rhythm of water and salt excretion in renal allograft recipients are explicable by the fact that the patients were studied at different times after transplantation. Although nocturia is common in renal failure, our results clearly show that renal failure alone cannot account for nocturia in patients who have recently undergone transplantation since these patients had significantly lower D :N ratios of urine volume than those with renal failure with comparable creatinine clearances (p< 005); the patient with the severest nocturia (case 1) had normal renal function; and the patients studied at least a year after transplantation had normal D :N ratios of urine volume, although their mean creatinine clearance was significantly lower than that in the normal subjects (p< 001). Other possible causes of the nocturia are discussed below. Autonomic neuropathy-Autonomic dysfunction4 produces nocturnal polyuria and saluresis. It is tempting to postulate that autonomic dysfunction, which is common in patients receiving dialysis,5 might account for the nocturia in the first few months after transplantation and that as the allograft continues to function the autonomic dysfunction is corrected, thereby normalising water and salt excretion. None of our patients, however, had postural hypotension or other clinical signs of autonomic neuropathy, and the cardiovascular reflex in eight patients in the recent-transplant group as assessed by the Valsalva ratio was not significantly different from that in 42 healthy volunteers. While a normal Valsalva ratio probably excludes gross autonomic dysfunction, an abnormal ratio does not establish the presence of autonomic neuropathy, since the ratio is reduced in cardiac insufficiency.' Allograft positions-Although the allograft's position may have some unknown haemodynamic influence on its function, it cannot be responsible for the early nocturnal polyuria since the abnormality corrects itself with time while the kidney remains in the same position. Influence of drugs-Since all our patients who had received transplants took prednisolone at 2000 the mineralocorticoid activity of the drug would be expected to reduce nocturnal sodium excretion, whereas the opposite was observed. The nocturnal kaliuresis in patients in the recent-transplant group was probably caused by the combined effects of urine volume and steroids given at night. Postural influence-The reported normal diurnal rhythm of water excretion in renal allograft recipients when the influence of posture has been eliminatedf6 suggests that the denervated kidney is unduly sensitive to postural changes. This is supported by our observation that when the patient in case 1 remained recumbent for 24 hours the nocturia was almost completely abolished (D :N urine-volume ratio changed from 035 to 090) while the dose of immunosuppressive drugs remained unaltered. It is not known why this supersensitivity to postural changes disappeared at least a year after transplantation, although gradual adaptation of the denervated vasculature is possible. Whether or not re-enervation of the graft7 plays a part remains speculative. Our study has shown that renal allograft recipients often have nocturia, which abates spontaneously, usually within a year after operation. It is not due to renal insufficiency, autonomic neuropathy, or immunosuppressive drugs but is related to postural influences. Patients who have received transplants and who complain of nocturia should be reassured that it will eventually disappear.