Serum Tests for Measurement of Thyroid Function

219

A B S T R A C T Thyroid function was evaluated in 46patients with end-stage kidney disease and 42 normal subjects. Patients were studied before and after the institution of maintenance hemodialysis (HD) and after renal transplantation (RT). Serum total triiodothyronine concentrations (TT3, ng/100 ml, mean± SD) were 63±17 and 83±22 in the non-HD and HD groups, respectively. Values from normal subjects were 128±25 and from RT patients 134±20. The TT3 was in the hypothyroid range (<78 ng/100 ml; 2 SD below normal mean) in 80% of non-HD and 43% of HD patients. Mean serum total thyroxine concentration (TT4), although within the normal range, was lower than the control value. T4-binding globulin capacity was also slightly lower but the difference was not statistically significant. Among patients whose TT4 was 1 SD below the normal mean, the free T4 index was equally depressed, suggesting that factors other than decreased binding capacity might be responsible for the low TT4. In addition, there was a 37% incidence of goiter. Mean serum thyroid-stimulating hormone (TSH) was not elevated and the TSH response to thyrotropinreleasing hormone (TRH) was distinctly blunted, suggesting the possibility of pituitary dysfunction as well. In vivo '25I-L-T4 and 13'I-L-T3 kinetics during 0.2 mg/day of L-T4 replacement showed marked reduction in T3 turnover rate in the uremic patients, both before and during HD; the values (,tg T3/day, mean±SD) for the different groups were as follows: normal, 33.8+6.1; non-HD, 13.5±2.6; HD, 12.9±3.1; and RT, 30.3±7.1.The low T3 turnover rate was due to impaired extrathyroidal conversion of T4 to T3. The mean perThis work was presented in part at the 50th Annual

Section: Methodsmentioning

confidence: 99%

Thyroid Dysfunction in Chronic Renal Failure

Lim¹,

Fang²,

Katz³

et al. 1977

219

“…Resin sponge triiodothyronine uptake (R-Ts) was determined using the Triosorb-kit,5 and serum total protein (TP) by refractometry.6 The FT4 index was obtained from the product of the PBI and R-Ts expressed as fraction of a normal control (37), and the TBG index from the ratio of the R-Ts expressed as per cent of the normal control, and the PBI (2). When the PBI was unavailable the TT4 was used for the estimation of these indexes (38).…”

Section: Methodsmentioning

confidence: 99%

Study of Four New Kindreds with Inherited Thyroxine-Binding Globulin Abnormalities POSSIBLE MUTATIONS OF A SINGLE GENE LOCUS

Refetoff¹,

Robin²,

Alper³

1972

A B S T R A CT Five families with inherited thyroxinebinding globulin (TBG) abnormalities were studied. On the basis of serum thyroxine (T4)-binding capacity of TBG in affected males, three family types were identified: TBG deficiency, low TBG, and high TBG capacity. In all families evidence for X-linked inheritance was obtained and in one family all criteria establishing this mode of inheritance were met. Only females were heterozygous, exhibiting values intermediate between affected males and normals. Overlap in heterozygotes was most commonly encountered in families with low TBG.Quantitative variation in the serum concentration of functionally normal TBG was demonstrated by: (a) failure of serum from TBG-deficient subjects to react with anti-TBG antibodies; (b) normal kinetics of To and triiodothyronine-binding to TBG in sera from subjects with low TBG and high TBG capacity; (c)

“…Serum TT4 was measured by a competitive binding assay and the results of a resin T4 uptake test were used to calculate FT4I. as described (28).…”

Section: Analytical Proceduresmentioning

confidence: 99%

Thyroid Function in a Uremic Rat Model

Lim¹,

Henriquez²,

Seo³

et al. 1980

A B S T R A C T The main objective of this study was to determine whether the principal abnormality of thyroid function observed in patients with chronic renal failure, low serum triiodothyronine (T3) concentration, causes hypothyroidism at the tissue level. A partially nephrectomized (Nx) uremic rat model was developed and the following parameters of thyroid function were assessed: serum total thyroxine (TT4), total T3 (TT3), and thyrotropin and liver T3 content, and activity oftwo thyroid hormone-dependent enzymes, mitochondrial a-glycerophosphate dehydrogenase (aGPD) and cytosol malate dehydrogenase (MDH). The results were compared to those of intact control (C), thyroidectomized (Tx), and nephrectomized-thyroidectomized (NxTx) littermates.Results expressed as mean+SEM showed that Nx rats had a fivefold increase in blood urea nitrogen, (112±20 mg/dl in Nx, and 22±1 mg/dl in C) and manifested all the changes of of thyroid function observed in uremic men, including a low serum TT3 level (30±7 ng/dl in Nx and 50±6 ng/dl in C). In the liver, T3 was significantly reduced (18±2 ng/total liver in Nx and 35±3 ng/total liver in C) as well as the activities of aGPD (8.8± 1.0 and 16.1± 1.5 AOD/min per total liver in Nx and C, respectively) and MDH (6.3±1.6 and 12.6±2.2 U/total liver in Nx and C, respectively). The reduction in liver enzyme activities correlated significantly with the decrease in T3 content.The changes in Tx rats were as expected, showing a profound reduction in serum hormone levels, liver T3 content, and liver enzyme activities. Serum thyrotropin was markedly elevated to 2,390±212 ng/ml as compared to 703±61 in C and 441±87 ng/ml in Nx rats. 946The NxTx rats showed the combined effects ofnephrectomy and thyroidectomy; blood urea nitrogen was elevated to 203, and serum levels of TT4, TT3, and thyrotropin were 0.4, < 10, and 2,525, respectively. Total liver T3 and aGPD and MDH were strikingly low; the corresponding values were 3.5, 2.4, and 2.5.L-triiodothyronine replacement (0.4 ,ug/100 g body wt/d) for 4 wk in the Nx rats resulted in significant increases in liver enzyme activities, aGPD and MDH rose by 70 and 60% over their respective basal values without alteration in the severity of azotemia.From these data, we conclude that the reduction of liver T3 content in the uremic rats, accompanied by a decrease in aGPD and MDH activity, indicates the presence ofhypothyroidism at the tissue level. Restoration of enzyme activities toward normal levels after T3 administration provided further supporting evidence that the diminution in liver enzyme activity was causally related to tissue T3 deficiency.