Multicompartmental analysis of thyroxine (T4) and 3,5,3'-triiodothyronine (T3) kinetics based on the plasma disappearance curves of the two tracer hormones (J. J. DiStefano III, M. Jang, T. K. Malone, and M. Broutman. Endocrinology 110: 198-213, 1982 and J. J. DiStefano III, T. K. Malone, and M. Jang. Endocrinology 111: 108-117, 1982) was extended to include additional experimental data, namely, the appearance curve in plasma of labeled T3 generated in vivo from precursor T4. Kinetic analysis of data obtained in 14 studies carried out in normal subjects by using a composite six-pool model made it possible to quantify the contributions of the thyroid (3.3 micrograms.day-1.m-2) and the periphery (12.7 micrograms.day-1.m-2) to T3 production. T4 monodeiodination occurred mainly in peripheral tissues rapidly exchanging with plasma (10.7 micrograms T3.day-1.m-2), whereas only 2.0 micrograms T3.day-1.m-2 arose in slowly exchanging tissues. In contrast, if plasma disappearance curves only were analyzed, a value of 10.9 micrograms T3.day-1.m-2 was calculated for peripheral conversion in slowly exchanging tissues; this underscores the need for additional data, such as the [125I]T3 plasma appearance curve for the partition of central and peripheral production of T3.
Chromogranin A (CGA) is a low MW (49,000) acidic hydrophilic protein. It is synthesized in the chromaffm granules of the neuroendocrine cells, and has been found circulating in the blood of healthy subjects. The aim of this study was to assess the relationship between serum levels of CGA and renal function. One hundred two renal patients (45 M and 57 F; age 14-76 years, mean 52) participated in the study. Glomerular filtration rate (GFR) was measured by the bladder cumulative method, using 99mTc-DTPA as a tracer. Blood CGA was determined by RIA. Plasma creatinine, beta2microglobulin (beta2m) and tumor associated trypsin inhibitor (TATI) were also determined. The reduction in renal function was associated with an increase in all of the above studied parameters. In patients with advanced renal failure (GFR <20 mL/min) CGA levels increased by 22-fold as compared to the patients with normal renal function (GFR> 100 mL/min). The other studied parameters were also increased but to a lesser degree, e.g., TATI 14-, beta2m 8- and creatinine 5-fold. The results of this study demonstrate that renal handling of the CGA is similar to other low MW proteins, and it accumulates in the blood in renal failure.
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