Effect of Hyperthyroidism on the Renal Concentrating Mechanism in Humans

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Abstract
Previous studies regarding an impairment in renal concentrating capacity during thyrotoxicosis are conflicting. In the current study observations were made during both thyrotoxicosis and the eumetabolic state in 9 patients and 6 normal subjects made toxic with l-triiodothyronine. Measurement of the maximum urinary osmolality (Umax) was made following a 36-hr period of dehydration plus intramuscular vasopressin in oil and the net reabsorption of free water (TmcH2O) during an osmotic diuresis induced with hypertonic mannitol. During thyrotoxicosis a mean decrease of 200 and 199 mOsm/kg in Umax was noted in patients and subjects, respectively. The decrease in concentration of urinary solutes was about equally divided between urea and non-urea solutes in the thyrotoxic patients but was entirely due to a decrease in the non-urea solutes in the toxic subjects. Despite the decrease in Umax, TmcH2O was not significantly impaired in the majority of patients or subjects. Measurements of glomerular filtration rate and renal plasma flow were elevated during induced thyrotoxicosis in the subjects but there was no significant change in either of these parameters in thyrotoxic patients despite a striking increase in cardiac output in both study groups. The findings confirm prior observations of a mild concentrating defect in thyrotoxicosis and suggest that it is due primarily to a decrease in renal medullary sodium concentration. The decrease in medullary solute concentration is possibly caused by a relative increase in medullary blood flow.