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The retinoid status of kidney transplant recipients.

Dr. G.E. Kelly, The University of Sydney, Department of Surgery, Sydney, NSW 2006 (Australia) Dear Sir, Renal function has an important influence on vitamin A (retinol) metabolism in as much as plasma retinol which is usually complexed to retinol binding protein (RBP) and transthyretin (TTR), is filterable through the glomerulus but normally is efficiently reabsorbed in the renal tubules [1, 2]. Hence, dysfunction of glomerular filtration may lead to disordered retinol metabolism. Patients with chronic renal failure and patients on long-term hemodialysis have been reported to have elevated plasma levels of both retinol and RBP [3–6]. In some of these patients, blood and liver levels of retinol were sufficiently high as to cause concern. Also, the skin of some uremic patients is reported to have high retinol levels and in these patients symptoms such as pruritis, xerosis and hair loss have been ascribed in part to hyper-vitaminosis A [5]. Given the susceptibility of long-term surviving kidney transplant recipients (KTxR) to progressive impairment of kidney function, we were interested to study the retinoid status of these patients. We studied 42 KTxR and 42 control subjects who were healthy volunteers; the two groups were matched for age and sex. The KTxR were between 4 and 15 years posttransplantation and were on maintenance immunosuppressive therapy (azathioprine and prednisone). All subjects were studied for plasma levels of vitamin A, ß-carotene and α-tocopherol using high-performance reversed-phase chromatotraphy, and RBP and TTR using immunoturbidometric technique. All subjects were tested on 2–3 occasions and a mean result determined for each subject. The statistical significance of differences between patient groups was tested by one-way analysis of variance. KTxR, compared to the control subjects, had significantly higher plasma levels of vitamin A, TTR and RBP (table I) and the levels of these three parameters were related directly to serum creatinine levels (table II). Table I. Plasma chemistry levels (mean ± SD) in control, healthy subjects and KTxR