triiodothyronine--reverse and Acute-Kidney-Injury

Topics: Acute Kidney Injury; Humans; Kidney Diseases; Nephrotic Syndrome; Thyroid Hormones; Thyroxine; Thyroxine-Binding Proteins; Triiodothyronine; Triiodothyronine, Reverse

The aim of this study is to analyze thyroid hormone parameters in large homogenous patient cohorts with preterminal (stage 4) and terminal (stage 5) renal failure in an area of low iodine intake.. Thyroid parameters were measured in healthy controls (n=48), patients with preterminal renal failure (n=48) and patients with terminal renal failure undergoing hemodialysis (n=288). All patients were assessed by measurement of TSH, T4, T3, fT4, rT3, Tg and TPO-antibodies.. There was a significant decrease of T4 and fT4 from healthy controls to patients with preterminal renal failure and to patients with terminal renal failure. T3 showed a decrease from healthy controls to patients with preterminal renal failure and to patients with terminal renal failure (1.54+/-0.06 microg/l VS. 1.05+/-0.05 microg/l VS. 1.09+/-0.23 microg/l, p<0.001 VS. controls). rT3 was significantly decreased in patients with terminal renal failure (0.24+/-0.01 microg/l VS. 0.25+/-0.02 microg/l VS. 0.16+/-0.01 microg/l, p<0.001). The rT3/T3 ratio was significantly elevated in patients with preterminal renal failure (p<0.01). TSH concentrations were in the normal range in all groups.. Our data suggest different T4 degradation pathways in patients with preterminal and terminal renal failure.

Topics: Acute Kidney Injury; Adult; Cohort Studies; Diet; Disease Progression; Female; Humans; Iodine; Kidney Failure, Chronic; Kidney Transplantation; Male; Middle Aged; Thyrotropin; Thyroxine; Triiodothyronine; Triiodothyronine, Reverse

Abnormalities in thyroid function are observed in patients with end stage renal disease. However, there are no data available evaluating sequential changes of thyroid function after renal transplantation. Therefore, we have studied thyroid hormone function in the immediate post-operative period after renal transplantation in order to determine the relationship between improving renal function and changes in thyroid hormone economy.. Thyroid function was evaluated in 22 patients before and on days 1, 3, 7 and 15 after renal transplantation. All patients received prednisone and cyclosporin as immunosuppressive therapy. Twelve patients with normal renal function undergoing comparable surgical procedures served as a control group.. Serum creatinine and thyroid hormone parameters (total T4, total T3, free T4, free T3, thyroxin binding globulin (TBG), reverse T3, T3 sulphate and TSH) were measured.. According to post-operative kidney function after renal transplantation, patients could be subdivided into three groups: five patients had primary graft function (group I); seven patients had delayed graft function because of acute renal failure (group II); 10 patients had delayed graft function requiring high doses of prednisone and some also of OKT3 because of acute rejection (group III). There was a significant fall in T3 and T4 concentrations with a concomitant rise in reverse T3 in all patients up to 3 days after renal transplantation. However, only patients in group I reached pre-operative values on day 15 after renal transplantation (serum creatinine 167 +/- 52 microM), whereas patients in group II (creatinine 609 +/- 118 microM) and group III (creatinine 839 +/- 71 microM) continued to have T3 concentrations well in the hypothyroid range (group I, 1.68 +/- 0.28 nM) vs 0.87 +/- 0.09 nM in group II and 0.76 +/- 0.10 nM in group III; P < 0.01). Serum T4 concentrations were also low in group III (47.7 nM vs 100.2 nM in group I; P < 0.05) 15 days after renal transplantation. These changes were accompanied by a concomitant fall in T3/TBG ratio and in free T3. Elevated reverse T3 returned to normal values in all groups on the 15th day after renal transplantation. TSH fell significantly on the first post-operative day, but did not return to pre-operative values in renal transplantation patients. In the control group, TSH did not change during the study period. T3 sulphate, known to be elevated in chronic renal failure, remained above normal in all patients irrespective of graft function during this study period.. T3 concentrations reflect renal graft function after renal transplantation. T3 is below normal in patients with delayed graft function (acute renal failure or acute rejection). The post-operative period (up to 3 days after renal transplantation) is associated with a low T3 syndrome. TSH does not return to pre-operative values even in patients with primary graft function. This might be due to the administration of prednisone. T3-sulphate is elevated before and after renal transplantation irrespective of graft function.

Topics: Acute Kidney Injury; Adult; Biomarkers; Cyclosporine; Female; Graft Rejection; Humans; Immunosuppressive Agents; Kidney; Kidney Transplantation; Male; Middle Aged; Postoperative Period; Prednisolone; Thyroid Gland; Thyrotropin; Thyroxine; Thyroxine-Binding Proteins; Triiodothyronine; Triiodothyronine, Reverse

The effects of exertional heat stroke (ExHS), with or without acute renal failure (ARF), on thyroid hormone metabolism were investigated. Eighteen ExHS patients were recruited and divided into two groups based on the presence or absence of ARF. Eleven age-matched healthy subjects served as a control group. Serum values of T3, T4, TSH, free T4 (FT4), rT3, and sulfated T3 (T3S) were measured in these groups during the acute and recovery stages of ExHS. Serum T3, T4, and FT4 levels were reduced, with reciprocal increases in rT3 and T3S levels as the severity of ExHS increased. The following mean levels of thyroid hormones were found (controls vs. ExHS without ARF vs. with ARF): T3, 1514 vs. 1164 vs. 393 pmol/L (P < 0.05 each); T4, 97 vs. 79 vs. 49 nmol/L (P = NS and P < 0.05, respectively); FT4, 20.5 vs. 19.5 vs. 19.0 pmol/L (P = NS each); rT3, 371 vs. 617 vs. 805 pmol/L (P < 0.05 and P = NS, respectively); and T3S, 30.1 vs. 34.2 vs. 71.1 pmol/L (P = NS and P < 0.05, respectively). The serum TSH levels were not significantly different among the three groups. Significantly negative correlations were found between serum creatinine and T3 (r = -0.75; P < 0.001) and T4 levels (r = -0.65; P < 0.001), whereas no relationship was noted between serum creatinine and rT3 values (r = 0.11; P < 0.05). In contrast, a correlation was observed between serum glutamic pyruvic transaminase and rT3 (r = 0.45; P < 0.01). Thyroid function tests returned to normal after patients recovered. In conclusion, our results show that patients suffering from ExHS, with or without ARF, displayed altered serum thyroid function in proportion to the severity of their condition. No significant changes in serum levels of rT3 were observed between the two groups, whereas a positive relationship was observed between serum rT3 and serum glutamic pyruvic transaminase values, suggesting that the changes in serum rT3 levels were more dependent on extrarenal illness than on renal disease per se. The moderate increase in serum T3S levels found in patients suffering from both ExHS and ARF may represent a decrease in tissue 5'-monodeiodinase activity as found in other nonthyroidal illnesses. A return of serum thyroid function tests to normal values after recovery from ExHS suggests that the low T3 state may play a protective role to prevent undesirable catabolic effects. Replacement therapy is thus not recommended.

Topics: Acute Kidney Injury; Adult; Alanine Transaminase; Blood Urea Nitrogen; Creatinine; Heat Stroke; Humans; Military Personnel; Physical Exertion; Thyroid Hormones; Thyrotropin; Thyroxine; Triiodothyronine; Triiodothyronine, Reverse

In order to examine the effects of developing renal failure on circulating thyroid hormones, serum concentrations of thyroxine (T4), free T4 (FT4), triiodothyronine (T3) and reverse T3 (rT3) and TBG capacity were measured in 9 baboons before and during the progress of acute (mean survival 12 days), subacute (32 days) and chronic (120 days) renal failure following allogeneic renal transplantation. Irrespective of the rate of development of renal failure, there were significant, non linear (power functions) negative correlations between serum creatinine or urea concentrations and levels of T4, FT4 and T3; rT3 levels remained unchanged, but the T4: rT3 molar ratio fell from 236.5 +/- 61 (+/- SE) to 121.8 +/- 30.9 (p less than 0.05). T4 and T3 levels were invariably subnormal at creatinine concentrations greater than 250 mumol/l (2.8 mg/dl), but FT4 was subnormal only in chronic renal failure. Thyroxine binding globulin (TBG) capacity did not change significantly; thus the TBG: T4 ratio increased from 3.4 +/- 0.2 (basal) to 10.4 +/- 3.4 before death (p less than 0.05). In animals which survived for greater than 25 days after transplantation, a significant linear correlation between FT4 and T3 was found as uremia progressed. Polyacrylamide gel electrophoresis (pH 7.4) of (125I)-T4 labelled preoperative and uremic serum showed a consistent decline in the proportion of tracer bound to TBG, from 67.0 +/- 0.8% to 58.9 +/- 1.0% (p less than 0.001), with a 48% reduction in TBG saturation (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acute Kidney Injury; Animals; Creatinine; Electrolytes; Electrophoresis, Polyacrylamide Gel; Kidney Transplantation; Papio; Serum Albumin; Thyroid Hormones; Thyroxine; Thyroxine-Binding Proteins; Triiodothyronine; Triiodothyronine, Reverse; Urea

Thyroid function tests were obtained from 335 consecutive patients admitted to an intensive care unit. Twenty patients suffering from severe non-endocrine diseases (septicaemia, fulminant hepatic and renal failure, acute pancreatitis, polytrauma, cerebral haemorrhage) were found to have serum thyroxine levels in the hypothyroid range (less than 4 micrograms/dl). Serum concentrations of total thyroxine (2.3 +/- 0.2 micrograms/dl), triiodothyronine (0.23 +/- 0.03 ng/ml), and thyroxine binding globulin (15.1 +/- 1.3 micrograms/ml) were reduced, but were above normal for reverse triiodothyronine (0.43 +/- 0.06 ng/ml). Response of TSH secretion to iv TRH was found to be either normal, lowered or absent. Primary hypothyroidism was excluded, as no enhanced TSH response was observed in any case. Although decreased thyroxine levels may be due to increased thyroid hormone degradation it appears that associated impaired TSH responsiveness to TRH may result from illness-related inhibition of pituitary TSH release. Although the finding of decreased thyroid hormone levels is not rare in care patients, it represents an index of poor prognosis. Differentiation between this "low-T4 syndrome" and true hypothyroidism depends essentially on clinical symptoms and course of disease.

Topics: Acute Disease; Acute Kidney Injury; Adolescent; Adult; Aged; Critical Care; Female; Hepatic Encephalopathy; Humans; Hypothyroidism; Male; Middle Aged; Pancreatitis; Pituitary Gland; Sepsis; Thyroid Function Tests; Thyroid Gland; Thyrotropin; Thyroxine; Thyroxine-Binding Proteins; Triiodothyronine; Triiodothyronine, Reverse; Wounds and Injuries

Thyroid function was evaluated in a group of 36 patients with acute renal failure (ARF) during the oliguric/anuric, polyuric and postpolyuric phase. Serum thyroxine (T4) and triiodothyronine (T3) concentrations were significantly decreased in the oliguric/anuric phase, as compared with the mean values obtained in the post-polyuric phase and with controls. In contrast to T3 and T4, the concentration of serum reverse triiodothyronine (rT3) was elevated in the oliguric/anuric phase and normal in the polyuric phase. The sephadex-T3-binding index (T3I) was significantly increased in oliguric/anuric patients and in the polyuric phase. The levels of serum thyreotropin were significantly elevated during all phases of ARF as compared with the controls. From the results obtained it is concluded that abnormal peripheral metabolism of T4 seems to be the primary cause of altered plasma concentrations of thyroid hormones in patients with ARF.

Topics: Acute Kidney Injury; Adolescent; Adult; Aged; Creatinine; Female; Humans; Male; Middle Aged; Thyroid Hormones; Thyrotropin; Thyroxine; Triiodothyronine; Triiodothyronine, Reverse