Graves’ Disease and the Manifestations of Thyrotoxicosis
DeGroot LJ.
ncbi.nlm.nih.gov/books/NBK2...
URINARY TRACT
Polyuria and occasionally glycosuria are seen in uncomplicated thyrotoxicosis. Standard clinical renal function tests give normal results. Glycosuria may reflect accelerated absorption of sugar from the intestine and glucose intolerance.
In hyperthyroid animals and humans, the glomerular filtration rate and renal blood flow are on average increased, as are tubular transfer maxima for glucose and diodrast. The glomerular filtration rate and renal blood flow alterations probably are secondary to increased cardiac output, whereas the increased tubular activity may be a direct effect of thyroid hormone on renal function [381]. Polyuria does not indicate insensitivity to vasopressin, for the kidney responds normally to vasopressin with an increase in concentration of urine [382].
Hypercalcemia is a feature of severe thyrotoxicosis, but it rarely injures the kidneys. Occasionally hyposthenuria and uremia occur [307, 308], or more selective renal damage takes place. Huth et al [383] reported a patient with renal tubular acidosis coincident with hyperthyroidism. Circumstantial evidence suggested that hyperthyroidism led to hypercalcemia, which in turn had damaged the renal medulla and produced acidosis.
ENDOCRINE SYSTEM:
( TABLE 10-7)
Table 7Changes in Endocrine Function in Graves' Disease
• FTI and T3 increased, TSH reduced
• Prolactin normal
• Growth hormone normal
• Parathyroid hormone suppressed
• Cortisol normal, urinary 17-OHCS increased, urinary free cortisol normal
• Free testosterone reduced in males
• Diabetic control worsened