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Table of Contents
Year : 2012  |  Volume : 16  |  Issue : 2  |  Page : 204-213

Interactions between thyroid disorders and kidney disease

Department of Nephrology, Christian Medical College, Vellore, Tamil Nadu, India

Date of Web Publication13-Mar-2012

Correspondence Address:
Gopal Basu
Department of Nephrology, Christian Medical College, Vellore - 632004, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2230-8210.93737

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There are several interactions between thyroid and kidney functions in each other organ's disease states. Thyroid hormones affect renal development and physiology. Thyroid hormones have pre-renal and intrinsic renal effects by which they increase the renal blood flow and the glomerular filtration rate (GFR). Hypothyroidism is associated with reduced GFR and hyperthyroidism results in increased GFR as well as increased renin - angiotensin - aldosterone activation. Chronic kidney disease (CKD) is characterized by a low T3 syndrome which is now considered a part of an atypical nonthyroidal illness. CKD patients also have increased incidence of primary hypothyroidism and subclinical hypothyroidism. The physiological benefits of a hypothyroid state in CKD, and the risk of CKD progression with hyperthyroidism emphasize on a conservative approach in the treatment of thyroid hormone abnormalities in CKD. Thyroid dysfunction is also associated with glomerulonephritis often by a common autoimmune etiology. Several drugs could affect both thyroid and kidney functions. There are few described interactions between thyroid and renal malignancies. A detailed knowledge of all these interactions is important for both the nephrologists and endocrinologists for optimal management of the patient.

Keywords: Chronic kidney disease, hyperthyroidism, hypothyroidism, kidney disease, renal function, thyroid disorder

How to cite this article:
Basu G, Mohapatra A. Interactions between thyroid disorders and kidney disease. Indian J Endocr Metab 2012;16:204-13

How to cite this URL:
Basu G, Mohapatra A. Interactions between thyroid disorders and kidney disease. Indian J Endocr Metab [serial online] 2012 [cited 2021 Jun 14];16:204-13. Available from: https://www.ijem.in/text.asp?2012/16/2/204/93737

   Introduction Top

The interplay between thyroid and the kidney in each other's functions is known for many years. [1] Thyroid dysfunction affects renal physiology and development, whereas kidney disease could result in thyroid dysfunction. Disorders of the thyroid and kidney may co-exist with common etiological factors. In addition, treatment strategies of one disease may affect those of the other organ. This review focuses on the important and clinically relevant interactions between thyroid function and renal function, which are essential for the clinician to optimally manage the patient.

   Materials and Methods Top

A search for articles using PubMed search with terms thyroid, hypothyroidism, hyperthyroidism, and renal function, glomerular filtration rate, glomerulonephritis, chronic kidney disease, hemodialysis, peritoneal dialysis, kidney transplantation, and renal carcinoma was performed. The most relevant and current articles were selected, retrieved in their original form or abstracts, as available. The data were collated and analyzed to represent information from the best and current available form of evidence in the particular area. Several classical papers describing certain earlier developments were also cited.

   Effects of Thyroid Hormones on Renal Development Top

Thyroid hormones influence protein synthesis and cell growth. Studies in neonatal rats have demonstrated the accelerating effect of thyroid hormones on renal development. [2] Thyroid hormone status affects the functioning renal mass (measured as the kidney to body mass ratio), with hypothyroidism reducing this ratio and hyperthyroidism increasing it. [3] However, severe hyperthyroidism results in protein breakdown and eventual renal atrophy. In addition, children with congenital hypothyroidism have a high incidence of congenital renal anomalies. [4] Thyroid hormones also influence the neonatal renal function. Perinatal thyroid hormone status affects the mitochondrial energy metabolism enzymes in the cells of the proximal convoluted tubules (PCT). [5] There is an increase in the activity of the Na - P co-transporter (NaPi), [6] Na - H exchanger (NHE), [7] as well as the Na/K ATPase [8] in the PCT. Thus, thyroid hormones play an important role in renal development and early renal function.

   Effects of Thyroid Hormones on Renal Physiology Top

Thyroid hormones affect renal function by both pre-renal and direct renal effects.

1. Pre-renal effects are mediated by the influence of thyroid hormones on the cardiovascular system and the renal blood flow (RBF).

2. The direct renal effects are mediated by the effect of thyroid hormones on

  1. glomerular filtration rate (GFR),
  2. tubular secretory and re-absorptive processes, as well as the
  3. hormonal influences on renal tubular physiology.

Thyroid hormones affect renal clearance of water load by their effects on the GFR. [9] The primacy of Na/K ATPase in solute transport of the PCT is well known. Thyroid hormones influence Na reabsorption at the PCT primarily by increasing the activity of the Na/K ATPase [10] and tubular potassium permeability. [11] Tubular reabsorption of calcium is affected in a similar manner, but not that of magnesium. [12] Thyroid hormones also regulate the adrenergic receptors and dopaminergic activation of the renal tubular cells. [13] They have been shown to affect the renin - angiotensin - aldosterone axis by adrenergic regulation, [14] renin release, [15] as well as influencing the angiotensinase activity. [16]

   Effects of Thyroid Dysfunction on the Kidney Top

Thyroid dysfunction affects RBF, GFR, tubular function, electrolyte homeostasis, and kidney structure. The various effects of hypothyroidism and hyperthyroidism on renal function have been summarized in [Figure 1]. The effects on renal function tests are listed in [Table 1].
Figure 1: Effects of hyperthyroidism and hypothyroidism on renal physiology and function

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Table 1: Clinical effects of hypothyroidism and hyperthyroidism on renal function tests

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   Hyperthyroidism and Renal Function Top

Hyperthyroidism results in increased RBF and GFR. [17] The effect of thyroid hormones on RBF and GFR occurs at multiple levels. Among the pre-renal factors, thyroid hormones increase the cardiac output by positive chronotropic [18] and inotropic effects [19] as well as a reduction in systemic vascular resistance. [20] This indirectly contributes to an increase in RBF. There is an increased endothelial production of nitric oxide (NO) in the renal cortex and medulla by induction of nitric oxide synthase (NOS), [21] directly by the thyroid hormones and indirectly by high arterial pressure related endothelial shear stress. [22] This is accompanied by a reduction in renal vasoconstrictor endothelin. [23] Thus, an increased intrarenal vasodilatation and decreased vasoconstriction ensues, contributing to a net increase in RBF.

The GFR increases by about 18-25% among hyperthyroid patients. [17] This improvement in GFR is not solely due to an increased RBF. The activation of renin - angiotensin - aldosterone system (RAAS) also contributes to the increase in GFR. Thyroid hormones stimulate the RAAS in a multifactorial manner. In hyperthyroidism, there is increased β-adrenergic activity, accompanied by increased density of β-adrenergic receptors in the renal cortex, resulting in increased stimulation of RAAS. [24] T3 increases the renin gene expression. Thyroid hormones increase the plasma renin, angiotensin II, and serum angiotensin converting enzyme levels. In addition, there is an increase in angiotensinogen synthesis by liver and increased density of angiotensin receptors. [25] Thus, there is a net increase in the RAAS activity. This results in afferent arteriolar vasodilatation and efferent arteriolar vasoconstriction and a consequent increased filtration pressure. This adds to the magnitude of increase in GFR over and above that contributed by an increase in RBF. Efferent arteriolar vasoconstriction could result in hypoperfusion of the PCT and consequent avid sodium and chloride reabsorption in PCT. In addition, there is an increased activity of the basolateral NA/K ATPase, [5] apical Na - H exchanger (NHE), [7] and the Na - Pi co-transporter. [6] Activation of these transporters increases the proximal sodium reabsorption. There is a simultaneous increase in the tubular mass, renal mass, and tubular reabsorptive capacity in hyperthyroidism. [26] The increase in basolateral sodium concentration feeds the basolateral sodium calcium exchanger. [27] The avid Cl reabsorption along with its transport through the basolateral chloride channel indirectly increases the calcium reabsorption, especially at the loop of Henle. Thus, there is a decreased Cl delivery to distal nephron. This is sensed by the macula densa which in turn increases the RAAS activity. Hyperthyroidism results in an increase in the sensitivity of macula densa, and therefore further RAAS activation. [28] On treating the hyperthyroidism, these effects are reversed and the GFR returns to normal. [17]

Serum creatinine, an inverse marker of GFR, is significantly decreased in hyperthyroid patients, not only due to an increase in GFR but also due to the reduction in overall muscle mass. [29] Cystatin C, a cysteine protease inhibitor constitutively secreted by all nucleated cells, is a new marker of renal function and indicator of future cardiovascular risk. In hyperthyroidism, increased cell metabolism and production of cystatin C results in increase in serum cystatin C levels despite an increase in GFR. [30] Serum cystatin C levels do not correlate well with GFR in hyperthyroidism. Treatment of hyperthyroidism results in a rebound increase in serum creatinine and decrease in serum cystatin C levels. [30] Urinary neutrophil gelatinase associated lipocalin (NGAL), a promising biomarker of reduced renal function, seems unchanged by the thyroid status.

The 24-hour urine protein increase in hyperthyroidism is probably related to glomerular hyperfiltration, [3] which resolves on treating hyperthyroidism. Urinary N-acetyl-β- D-glucosaminidase (NAG) is increased in hyperthyroidism consequent to glomerular basement membrane disruption and tubular damage due to hyperfiltration, hypertrophy, and hyperplasia. [31] There is a decreased ability to concentrate urine, probably due to increased RBF and osmotic diuresis, rather than vasopressin insensitivity. [32] Hyperthyroidism is associated with a decrease in total body water and exchangeable potassium but not sodium. However, for most part, the serum concentrations of sodium and potassium remain normal. Occasionally, hyperthyroidism is associated with hypokalemia (thyrotoxic hypokalemic periodic paralysis of channelopathies) due to genetic mutation in either L-type calcium channel α1-subunit or potassium inward rectifier 2.6.[33]

   Hypothyroidism and Renal Function Top

The effects of hypothyroidism on the kidney are usually opposite to the effects of hyperthyroidism. The RBF is reduced in hypothyroidism by decreased cardiac output (negative chronotropic and inotropic effects), [34] increased peripheral vascular resistance, [35] intrarenal vasoconstriction, [36] reduced renal response to vasodilators, [37] and a reduced expression of renal vasodilators such as vascular endothelial growth factor (VEGF) and insulin like growth factor-1 (IGF-1). [38] In addition, pathologic changes in the glomerular structure in hypothyroidism, such as glomerular basement membrane thickening and mesangial matrix expansion, may also contribute to reduced RBF. [39]

The GFR is reversibly reduced (by about 40%) in more than 55% of adults with hypothyroidism [40] due to several reasons. There is decreased sensitivity to β-adrenergic stimulus and decreased renin release,[3] along with decreased angiotensin II and impaired RAAS activity, resulting in loss of GFR. [25] There is a structural constraint imposed by limited glomerular surface area for filtration due to renal parenchymal growth retardation in hypothyroidism. [39] There is a reduced proximal tubular absorption of sodium, chloride, and water. [41] In addition, the renal basolateral chloride channel expression is reduced. Thus, reduced chloride reabsorption increases the distal chloride delivery, triggering the macula densa mediated tubuloglomerular feedback which reduces the RAAS activity. Consequently, the GFR falls.

The tubular transport capacity is reduced and the activity of Na/K ATPase is reduced initially in the proximal tubules and later in almost all segments of the nephron. [42] In addition, the NHE activity is also reduced in hypothyroidism. [43] Thus, there is a net reduction in sodium and bicarbonate reabsorption. An increase in sodium and bicarbonate loss in urine results in defective urinary acidification. Decreased tubular reabsorptive capacity also results in inability to maintain the medullary hypertonicity. Medullary hypertonicity is primary the driving force behind urinary concentration. Loss of medullary hypertonicity in hypothyroidism results in impaired urinary concentrating ability of the kidney. [44] However, hypothyroidism causes a reversible increase in vasopressin (antidiuretic hormone or ADH) sensitivity of the collecting ducts, thus increasing free water reabsorption. The increased fluid retention, however, is unable to maximally suppress ADH in hypothyroidism. [45] The resistance of pituitary response to increased fluid retention leads to continued ADH activity and further free water retention. Hypothyroidism results in low cardiac output which triggers the carotid baroreceptors and consequently increases the non-osmotic ADH secretion. [46] In some patients, the urine sodium is not as low as would be expected with reduced cardiac output. In these patients, it is possible that the ADH secretion could be considered as inappropriate. The reduced GFR, reduced sodium reabsorption, and relatively increased ADH secretion and renal ADH supersensitivity mediated impaired free water clearance, all contribute to hyponatremia in hypothyroidism. [40] Hyponatremia is twice as common among hypothyroid patients with raised serum creatinine as among those with normal serum creatinine.

There is a reversible reduction in the kidney to body weight ratio in hypothyroidism, where the renal mass almost doubles with treatment. Hypothyroidism results in a reversible elevation in serum creatinine due to the reduction in GFR as well as possible myopathy and rhabdomyolysis. There is a reduction in serum cystatin C levels in hypothyroidism due to reduced production, consequent to reduced cellular metabolism. [30] Both these changes are reversible with treatment of hypothyroidism. Hypothyroidism also results in increased glomerular capillary permeability to proteins. [47] The consequent proteinuria often precedes the reduction in GFR in hypothyroidism. [48]

   Chronic Kidney Disease and Thyroid Dysfunction Top

Hyperthyroidism can result in/accelerate chronic kidney disease (CKD) by several mechanisms. Firstly, hyperthyroidism results in intra-glomerular hypertension (increased filtration pressure) and consequent hyperfiltration. Secondly, hyperthyroidism predisposes to proteinuria, which is known to cause direct renal injury. Thirdly, hyperthyroidism-induced increased mitochondrial energy metabolism along with down-regulation of superoxide dismutase contributes to the increased free radical generation and consequent renal injury. [49] Oxidative stress also contributes to hypertension in hyperthyroidism, which contributes to CKD progression. [3] The increased RAAS activity can accelerate renal fibrosis. In addition, hyperthyroidism contributes to anemia in CKD patients and is considered one of the causes of resistance to recombinant human erythropoietin (EPO). [50] For the abovementioned reasons, hypothyroidism does not contribute to progression of CKD except by the mild to moderate reduction in GFR. Treatment of hypothyroidism can result in improvement of GFR in CKD patients. [51]

Primary hypothyroidism (non-autoimmune) is commonly observed in CKD patients. Especially, the prevalence of subclinical hypothyroidism increases consistently with decline in GFR. [52] The earliest and the most common thyroid function abnormality in CKD patients is a low T3 level (especially total T3 than free T3). [53] This "low T3 syndrome" occurs in CKD due to several reasons. Fasting, chronic metabolic acidosis and chronic protein malnutrition affect iodothyronine deiodination, as well as protein binding of T3, reducing the peripheral conversion of T4 to T3 and its protein binding. In addition, inflammatory cytokines such as tumor necrosis factor (TNF)-α and interleukin (IL)-1 inhibit the expression of type 1 5′-deiodinase, which is responsible for peripheral conversion of T4 to T3. [54] In addition, impaired renal handling of iodine increases serum iodine levels, causing a prolonged Wolff - Chaikoff effect. [55] The clinical importance of this low T3 syndrome is controversial. The low T3 levels (especially total T3 and not free T3) in CKD patients have been correlated with higher levels of markers of inflammation [highly sensitive C-reactive protein (hsCRP), IL-6, etc.], malnutrition (lower prealbumin, IGF-1), increased endothelial dysfunction, poorer cardiac function, poor survival, and higher all-cause as well as cardiovascular mortality in some studies. [54],[56] Some of these studies were underpowered to detect these associations or did not exclude confounders appropriately. [57] In some other studies, the low free T3 and not the total T3 level is associated with increased mortality. [58] However, recent studies have demonstrated that this association is not invariable, and the free T3 levels may not be associated with long-term mortality in CKD and dialysis patients. [59]

Subsequent studies also demonstrated a low T4 level in many CKD patients. However, the free T4 levels vary from being low to normal in CKD. This is primarily because of an impaired protein binding of T4 in CKD. The thyroid profile is similar to that observed in several non-thyroidal illnesses (NTIs) such as severe infections, heart failure, malignancies, and in several hospitalized patients without renal disease. This led to the consideration of a "sick euthyroid state" in CKD, which is now called "non-thyroidal illness." However, unlike other NTI states, there is no increase in total rT3 levels in CKD. [60] This is due to an increased redistribution of rT3 into extravascular and intracellular spaces. In some patients, due to an impaired renal clearance, free rT3 levels may be mildly elevated. Another difference from other NTIs is that the thyroid stimulating hormone (TSH) levels are elevated in CKD. However, TSH is released in response to thyrotropin releasing hormone (TRH) in CKD patients, indicating pituitary disturbances in uremia. [61] In addition, the circadian rhythm of TSH and its glycosylation is altered in CKD, compromising its activity. Thus, CKD patients have low T3 and normal or reduced T4 levels, and consequently elevated TSH and attendant increase in thyroid gland volume. [62],[63],[64] These mechanisms are probably reflective of the physiological adaptation of the body to CKD to reduce the protein nitrogen turnover, reduce the protein catabolism and nitrogenous waste load. The reduced T3 levels and associated complications without increase in rT3, the reduced free T4 levels along with an elevated TSH, and hyporesponsiveness of TSH to TRH question the "euthyroid" state and raise the possibility of benefit from thyroid supplementation CKD. However, three decades of research in this area have not been able to clarify the need for thyroid hormone replacement in CKD. Attempts at T3 replacement have often resulted in negative nitrogen balance by increased muscle catabolism, implying the prudence in not correcting the low T3 state in CKD. Though it is clear that hypothyroidism would threaten the patient's well-being, it is not clear as to what level of thyroid dysfunction forms the threshold necessary for treatment by thyroxine replacement in CKD. In general, mild elevations of TSH (less than 20 IU/ml) with or without low T3/T4generally do not warrant thyroid hormone supplementation. One has to consider the dangers of hyperthyroidism as well as the teleological benefits of a hypothyroid state in CKD and the lack of clearly evident benefits of thyroid hormone replacement in the literature before deciding on therapy. A clinical decision of the treating nephrologists and endocrinologists should be made on an individual patient basis, after carefully considering the clinical features, possible hypothyroid manifestations, putative benefits, and possible risks of thyroid hormone therapy or the lack of it.

CKD results in reduced iodide excretion, which results in increased serum inorganic iodide level and the thyroid gland iodine content and consequent thyroid gland enlargement. Structural changes in thyroid among CKD patients include an increased prevalence of goiter (especially among women), thyroid nodules, and thyroid carcinoma, compared to general population. [65]

There is no increase in the incidence of autoimmune thyroid disease in CKD patients. In fact, the incidence of positive thyroglobulin and thyroid microsomal antibodies is low in CKD patients. However, autoimmune thyroid disease may occur along with other autoimmune diseases associated with CKD, such as lupus nephritis, type 1 diabetes mellitus, etc. When elevated TSH is detected in association with other autoimmune disease, it is important to screen for antithyroid antibodies. Management strategy for autoimmune thyroid disease remains unaltered by the presence of CKD.

The various effects of CKD on thyroid profile are depicted in [Figure 2].
Figure 2: Effects of chronic kidney disease on thyroid profile

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   Thyroid Dysfunction in Dialysis and Kidney Transplantation Top

Patients on hemodialysis (HD) due to CKD have low thyroid hormone levels and elevated TSH. The minor increases in TSH levels (5 - 20 mU/l), observed in about 20% of uremic patients, are usually not considered to be reflecting "hypothyroidism" in this select group of patients. Though the total T4 levels are low, heparin inhibits T4 binding to protein, thereby increasing free T4 fraction in CKD patients after heparin dialysis. [66] Among the CKD patients on HD, there is a compensatory influence on cellular transport of thyroid hormones, which helps maintain the euthyroid state despite low serum thyroid hormone levels. [67] For all these reasons, despite low serum thyroid hormone profile, thyroid hormone supplementation should not be initiated without substantial elevation in TSH level and careful consideration.

Among patients on peritoneal dialysis (PD), there is a significant increase in prevalence of hypothyroidism (especially subclinical) and low T3 levels. [68] Thyroxine-binding globulin (TBG), T4, and T3 are lost in the PD effluent. Despite continuous and substantial protein loss, TBG levels are normal. The T4 and T3 losses are minor (10% and 1%, respectively) and easily compensated for. Thus, thyroid hormone replacement is not necessary in CKD patients on PD.

Kidney transplantation reverses the CKD syndrome and thus has an effect of CKD-mediated thyroid profile abnormalities. The low T3 and T4 levels recover after transplantation, although gradually, over the first 3-4 months. During the initial few months after transplantation, kidney transplant patients predominantly exhibit a reduction in T4 levels lower than the pre-transplant level, before it gradually rises back to normal. [69] In general, post-transplant thyroid volume and free T3 levels correlate well with graft function. [70] Pre-transplant low T3 levels are associated with future risk of graft loss. [71] But therapy with T3 supplementation does not improve graft survival, negating the possibility of a causal association. [72] Thus, there is no need to supplement thyroid hormones for the low T3 levels noted in the first few months of renal transplantation. Thyroid carcinoma is the fifth most common malignancy among kidney transplant patients. [73]

   Other Kidney Diseases Associated with Thyroid Dysfunction Top

Several glomerulonephritides may occur in association with thyroid diseases. The most commonly observed association is with membranous nephropathy, [74],[75] followed by IgA nephropathy, [76] membranoproliferative glomerulonephritis, [77] and minimal change disease. [78] There are several mechanisms for these associations. The presence of circulating immune complexes among patients with thyroid disease, [79] the association of Hashimoto's thyroiditis and membranous nephropathy with immune complex deposition in the glomerular as well as thyroid epithelial basement membrane, [80] and the common occurrence of thyroid and renal disease in association with other autoimmune diseases such as type 1 diabetes mellitus [81] suggest a common autoimmune pathogenesis or an autoimmune disorder (such as lupus or vasculitis) with associated thyroid and renal disease. Hypothyroidism could result in obstructive sleep apnea which is associated independently with minimal change disease.

Proteinuria, especially in nephrotic syndrome, often results in urinary loss of thyroid hormones bound to the various binding proteins such as TBG, albumin, prealbumin, and transthyretin. [82] This results in a reduction in the serum total thyroid hormone levels. Thyroid compensates for this by increasing the free fraction of the hormones and maintaining euthyroid state. However, patients with low thyroid reserve may develop hypothyroidism consequent to this urinary loss. In patients on supplemental thyroxine, proteinuria can increase the dose requirement to maintain euthyroid state. [83] Primary hypothyroidism has also been described in congenital nephrotic syndrome, with urinary loss of thyroid hormones resulting in increased TSH level in utero. [84]

In addition to the glomerulonephritides mentioned above, isolated cases of hyperthyroidism have been associated with tubulointerstitial nephritis and uveitis (TINU) syndrome. [85] The disease responds well to steroid therapy.

Patients with acute kidney injury may develop an NTI (euthyroid sick syndrome), but without elevation of reverse T3 levels. [86] Hypothyroidism can result in rhabdomyolysis related acute kidney injury. [87]

   Thyroid and Renal Malignancy Top

There is an increased predisposition of patients with thyroid cancer to develop renal cell carcinoma (RCC) [88] due to genetic predisposition or treatment of disease. In addition, thyroid malignancy could metastasize to the kidney [89] and RCC is one of the common tumors metastasizing to the thyroid. [90] While clear cell carcinoma of thyroid, morphologically resembling the RCC, is described, some RCC may morphologically resemble thyroid follicular carcinoma. [91] Thyroid malignancies expressing EPO receptors have favorable prognosis, [92] while RCC expressing aberrant thyroid hormone receptors may contribute to carcinogenesis. [93]

   Drugs in Thyroid and Renal Disease Top

Drugs used in thyroid or kidney disease may have adverse effects on the other organ's functions. Thionamides such as methimazole, carbimazole, propylthiouracil cause hypothyroidism as well as renal dysfunction by immune mechanisms resulting in various glomerular disease such as vasculitis, [94] lupus nephritis, [95] or necrotizing glomerulonephritis with pulmonary hemorrhage. [96]

Alemtuzumab, used in renal transplantation, has been reported to result in autoimmune thyroid disease. [97] Interferon-α, used again in renal cell carcinoma as well as for treatment of hepatitis B and C virus infection pre-transplant causes hyperthyroidism. [98] Lenalidomide, used in renal cell carcinoma for its antitumor and antiangiogenic properties, results in a subacute thyroiditis and transient thyrotoxicosis. [99] Sunitinib, a new therapeutic agent against RCC, results in hypothyroidism, which some authors believe to be associated with better prognosis. [100]

Lithium use causes hypothyroidism as well as nephrogenic diabetes insipidus and CKD. Amiodarone is associated with both hypothyroidism and hyperthyroidism as well as acute renal damage. [101] Rifampicin causes both a tubulointerstitial nephritis as well as hyperthyroidism. [102]

An important consideration is the therapy of hyperthyroid patients with CKD. In general, CKD patients require lower doses of 131 I for treatment of Grave's disease. Hyperthyroid patients on HD, due to 131 I clearance by dialysis, require the usual therapeutic dose of 131 I for treatment. [103] Patients on PD require a fivefold reduction in the 131 I dose for treatment of thyroid carcinoma, to avoid excessive radiation. [104] The interactions of various drugs in thyroid and kidney disease are given in [Table 2].
Table 2: Drugs in thyroid and kidney diseases

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   Conclusion Top

There are various mechanisms of interaction between kidney and thyroid functions in the disease states of each other organ. There are not only functional alterations but also structural correlates of these interactions. TSH elevations are common in CKD and do not always reflect hypothyroidism. In addition, therapeutic measures of CKD such as HD, PD, and kidney transplantation have profound effects on thyroid function. Drugs used in thyroid dysfunction may result in renal dysfunction or require dose reduction in CKD. The variable association of low T3 to inflammation, endothelial dysfunction, and poor survival in CKD and transplant patients is of importance. A detailed knowledge of these interactions is important for both the nephrologists and endocrinologists for optimal diagnosis and management of the patient.

   References Top

1.Kaptein EM. Thyroid function in renal failure. Contrib Nephrol 1986;50:64-72.  Back to cited text no. 1
2.Braunlich H. Postnatal development of kidney function in rats receiving thyroid hormones. Exp Clin Endocrinol 1984;83:243-50.  Back to cited text no. 2
3.Vargas F, Moreno JM, Rodriguez-Gomez I, Wangensteen R, Osuna A, Alvarez-Guerra M, et al. Vascular and renal function in experimental thyroid disorders. Eur J Endocrinol 2006;154:197-212.  Back to cited text no. 3
4.Kumar J, Gordillo R, Kaskel FJ, Druschel CM, Woroniecki RP. Increased prevalence of renal and urinary tract anomalies in children with congenital hypothyroidism. J Pediatr 2009;154:263-6.  Back to cited text no. 4
5.Wijkhuisen A, Djouadi F, Vilar J, Merlet-Benichou C, Bastin J. Thyroid hormones regulate development of energy metabolism enzymes in rat proximal convoluted tubule. Am J Physiol 1995;268: F634-42.  Back to cited text no. 5
6.Alcalde AI, Sarasa M, Raldua D, Aramayona J, Morales R, Biber J, et al. Role of thyroid hormone in regulation of renal phosphate transport in young and aged rats. Endocrinology 1999;140:1544-51.  Back to cited text no. 6
7.Baum M, Dwarakanath V, Alpern RJ, Moe OW. Effects of thyroid hormone on the neonatal renal cortical Na+/H+ antiporter. Kidney Int 1998;53:1254-8.  Back to cited text no. 7
8.Nakhoul F, Thompson CB, McDonough AA. Developmental change in Na,K-ATPase alpha1 and beta1 expression in normal and hypothyroid rat renal cortex. Am J Nephrol 2000;20:225-31.  Back to cited text no. 8
9.Emmanouel DS, Lindheimer MD, Katz AI. Mechanism of impaired water excretion in the hypothyroid rat. J Clin Invest 1974;54:926-34.  Back to cited text no. 9
10.Lin HH, Tang MJ. Thyroid hormone upregulates Na,K-ATPase alpha and beta mRNA in primary cultures of proximal tubule cells. Life Sci 1997;60:375-82.  Back to cited text no. 10
11.Katz AI, Lindheimer MD. Renal sodium- and potassium-activated adenosine triphosphatase and sodium reabsorption in the hypothyroid rat. J Clin Invest 1973;52:796-804.  Back to cited text no. 11
12.McCaffrey C, Quamme GA. Effects of thyroid status on renal calcium and magnesium handling. Can J Comp Med 1984;48:51-7.  Back to cited text no. 12
13.Del Compare JA, Aguirre JA, Ibarra FR, Barontini M, Armando I. Effects of thyroid hormone on the renal dopaminergic system. Endocrine 2001;15:297-303.  Back to cited text no. 13
14.Pracyk JB, Slotkin TA. Thyroid hormone differentially regulates development of beta-adrenergic receptors, adenylatecyclase and ornithine decarboxylase in rat heart and kidney. J Dev Physiol 1991;16:251-61.  Back to cited text no. 14
15.Vaamonde CA, Sebastianelli MJ, Vaamonde LS, Pellegrini EL, Watts RS, Klingler EL Jr, et al. Impaired renal tubular reabsorption of sodium in hypothyroid man. J Lab Clin Med 1975;85:451-66.  Back to cited text no. 15
16.Segarra AB, Ramirez M, Banegas I, Hermoso F, Vargas F, Vives F, et al. Influence of thyroid disorders on kidney angiotensinase activity. Horm Metab Res 2006;38:48-52.  Back to cited text no. 16
17.Den Hollander JG, Wulkan RW, Mantel MJ, Berghout A. Correlation between severity of thyroid dysfunction and renal function. Clin Endocrinol (Oxf) 2005;62:423-7.  Back to cited text no. 17
18.Hammond HK, White FC, Buxton IL, Saltzstein P, Brunton LL, Longhurst JC. Increased myocardial beta-receptors and adrenergic responses in hyperthyroid pigs. Am J Physiol 1987;252: H283-90.  Back to cited text no. 18
19.Walker JD, Crawford FA, Kato S, Spinale FG. The novel effects of 3,5,3¢-triiodo-L-thyronine on myocyte contractile function and beta-adrenergic responsiveness in dilated cardiomyopathy. J Thorac Cardiovasc Surg 1994;108:672-9.  Back to cited text no. 19
20.Celsing F, Blomstrand E, Melichna J, Terrados N, Clausen N, Lins PE, et al. Effect of hyperthyroidism on fibre-type composition, fibre area, glycogen content and enzyme activity in human skeletal muscle. Clin Physiol 1986;6:171-81.  Back to cited text no. 20
21.Quesada A, Sainz J, Wangensteen R, Rodriguez-Gomez I, Vargas F, Osuna A. Nitric oxide synthase activity in hyperthyroid and hypothyroid rats. Eur J Endocrinol 2002;147:117-22.  Back to cited text no. 21
22.Xiao Z, Zhang Z, Ranjan V, Diamond SL. Shear stress induction of the endothelial nitric oxide synthase gene is calcium-dependent but not calcium-activated. J Cell Physiol 1997;171:205-11.  Back to cited text no. 22
23.Singh G, Sharma AC, Thompson EB, Gulati A. Renal endothelin mechanism in altered thyroid states. Life Sci 1994;54:1901-8.  Back to cited text no. 23
24.Haro JM, Sabio JM, Vargas F. Renal beta-adrenoceptors in thyroxine-treated rats. J Endocrinol Invest 1992;15:605-8.  Back to cited text no. 24
25.Asmah BJ, Wan Nazaimoon WM, Norazmi K, Tan TT, Khalid BA. Plasma renin and aldosterone in thyroid diseases. Horm Metab Res 1997;29:580-3.  Back to cited text no. 25
26.Kobori H, Ichihara A, Miyashita Y, Hayashi M, Saruta T. Mechanism of hyperthyroidism-induced renal hypertrophy in rats. J Endocrinol 1998;159:9-14.  Back to cited text no. 26
27.Kumar V, Prasad R. Molecular basis of renal handling of calcium in response to thyroid hormone status of rat. Biochim Biophys Acta 2002;1586:331-43.  Back to cited text no. 27
28.Graves TK, Olivier NB, Nachreiner RF, Kruger JM, Walshaw R, Stickle RL. Changes in renal function associated with treatment of hyperthyroidism in cats. Am J Vet Res 1994;55:1745-9.  Back to cited text no. 28
29.Manetti L, Pardini E, Genovesi M, Campomori A, Grasso L, Morselli LL, et al. Thyroid function differently affects serum cystatin C and creatinine concentrations. J Endocrinol Invest 2005;28:346-9.  Back to cited text no. 29
30.Kimmel M, Braun N, Alscher M. Influence of thyroid function on different kidney function tests. Kidney Blood Press Res 2012;35:9-17.  Back to cited text no. 30
31.Nakamura S, Ishiyama M, Kosaka J, Mutoh J, Umemura N, Harase C. Urinary N-acetyl-beta-D-glucosaminidase (NAG) activity in patients with Graves' disease, subacute thyroiditis, and silent thyroiditis: A longitudinal study. Endocrinol Jpn 1991;38:303-8.  Back to cited text no. 31
32.Katz AI, Emmanouel DS, Lindheimer MD. Thyroid hormone and the kidney. Nephron 1975;15:223-49.  Back to cited text no. 32
33.Pothiwala P, Levine SN. Analytic review: Thyrotoxicperiodic paralysis: A review. J Intensive Care Med 2010;25:71-7.  Back to cited text no. 33
34.Crowley WF Jr, Ridgway EC, Bough EW, Francis GS, Daniels GH, Kourides IA, et al. Noninvasive evaluation of cardiac function in hypothyroidism. Response to gradual thyroxine replacement. N Engl J Med 1977;296:1-6.  Back to cited text no. 34
35.Diekman MJ, Harms MP, Endert E, Wieling W, Wiersinga WM. Endocrine factors related to changes in total peripheral vascular resistance after treatment of thyrotoxic and hypothyroid patients. Eur J Endocrinol 2001;144:339-46.  Back to cited text no. 35
36.Singer MA. Of mice and men and elephants: Metabolic rate sets glomerular filtration rate. Am J Kidney Dis 2001;37:164-78.  Back to cited text no. 36
37.Klein I, Ojamaa K. Thyroid hormone and the cardiovascular system. N Engl J Med 2001;344:501-9.  Back to cited text no. 37
38.Schmid C, Brandle M, Zwimpfer C, Zapf J, Wiesli P. Effect of thyroxine replacement on creatinine, insulin-like growth factor 1, acid-labile subunit, and vascular endothelial growth factor. Clin Chem 2004;50:228-31.  Back to cited text no. 38
39.Bradley SE, Coelho JB, Sealey JE, Edwards KD, Stephan F. Changes in glomerulotubular dimensions, single nephron glomerular filtration rates and the renin-angiotensin system in hypothyroid rats. Life Sci 1982;30:633-9.  Back to cited text no. 39
40.Montenegro J, Gonzalez O, Saracho R, Aguirre R, Martinez I. Changes in renal function in primary hypothyroidism. Am J Kidney Dis 1996;27:195-8.  Back to cited text no. 40
41.Zimmerman RS, Ryan J, Edwards BS, Klee G, Zimmerman D, Scott N, et al. Cardiorenal endocrine dynamics during volume expansion in hypothyroid dogs. Am J Physiol 1988;255: R61-6.  Back to cited text no. 41
42.Garg LC, Tisher CC. Effects of thyroid hormone on Na-K-adenosine triphosphatase activity along the rat nephron. J Lab Clin Med 1985;106:568-72.  Back to cited text no. 42
43.Marcos Morales M, PurchioBrucoli HC, Malnic G, Gil Lopes A. Role of thyroid hormones in renal tubule acidification. Mol Cell Biochem 1996;154:17-21.  Back to cited text no. 43
44.Michael UF, Barenberg RL, Chavez R, Vaamonde CA, Papper S. Renal handling of sodium and water in the hypothyroid rat. Clearance and micropuncture studies. J Clin Invest 1972;51:1405-12.  Back to cited text no. 44
45.Derubertis FR Jr, Michelis MF, Bloom ME, Mintz DH, Field JB, Davis BB. Impaired water excretion in myxedema. Am J Med 1971;51:41-53.  Back to cited text no. 45
46.Hanna FW, Scanlon MF. Hyponatraemia, hypothyroidism, and role of arginine-vasopressin. Lancet 1997;350:755-6.  Back to cited text no. 46
47.Wheatley T, Edwards OM. Mild hypothyroidism and oedema: Evidence for increased capillary permeability to protein. Clin Endocrinol (Oxf) 1983;18:627-35.  Back to cited text no. 47
48.Suher M, Koc E, Ata N, Ensari C. Relation of thyroid disfunction, thyroid autoantibodies, and renal function. Ren Fail 2005;27:739-42.  Back to cited text no. 48
49.Mori T, Cowley AW Jr. Renal oxidative stress in medullary thick ascending limbs produced by elevated NaCl and glucose. Hypertension 2004;43:341-6.  Back to cited text no. 49
50.Kaynar K, Ozkan G, Erem C, Gul S, Yilmaz M, Sonmez B, et al. An unusual etiology of erythropoietin resistance: Hyperthyroidism. Ren Fail 2007;29:759-61.  Back to cited text no. 50
51.Van Welsem ME, Lobatto S. Treatment of severe hypothyroidism in a patient with progressive renal failure leads to significant improvement of renal function. Clin Nephrol 2007;67:391-3.  Back to cited text no. 51
52.Lo JC, Chertow GM, Go AS, Hsu CY. Increased prevalence of subclinical and clinical hypothyroidism in persons with chronic kidney disease. Kidney Int 2005;67:1047-52.  Back to cited text no. 52
53.Wiederkehr MR, Kalogiros J, Krapf R. Correction of metabolic acidosis improves thyroid and growth hormone axes in haemodialysis patients. Nephrol Dial Transplant 2004;19:1190-7.  Back to cited text no. 53
54.Zoccali C, Tripepi G, Cutrupi S, Pizzini P, Mallamaci F. Low triiodothyronine: A new facet of inflammation in end-stage renal disease. J Am Soc Nephrol 2005;16:2789-95.  Back to cited text no. 54
55.Bando Y, Ushiogi Y, Okafuji K, Toya D, Tanaka N, Miura S. Non-autoimmune primary hypothyroidism in diabetic and non-diabetic chronic renal dysfunction. Exp Clin Endocrinol Diabetes 2002;110:408-15.  Back to cited text no. 55
56.Carrero JJ, Qureshi AR, Axelsson J, Yilmaz MI, Rehnmark S, Witt MR, et al. Clinical and biochemical implications of low thyroid hormone levels (total and free forms) in euthyroid patients with chronic kidney disease. J Intern Med 2007;262:690-701.  Back to cited text no. 56
57.Tripepi G, Zoccali C. Low triiodothyronine and cardiovascular disease. Circulation 2003;108: e29-30; author reply e29-30.  Back to cited text no. 57
58.Ozen KP, Asci G, Gungor O, Carrero JJ, Kircelli F, Tatar E, et al. Nutritional state alters the association between free triiodothyronine levels and mortality in hemodialysis patients. Am J Nephrol 2011;33:305-12.  Back to cited text no. 58
59.Fernandez-Reyes MJ, Diez JJ, Collado A, Iglesias P, Bajo MA, Estrada P, et al. Are low concentrations of serum triiodothyronine a good marker for long-term mortality in hemodialysis patients? Clin Nephrol 2010;73:238-40.  Back to cited text no. 59
60.Kaptein EM, Feinstein EI, Nicoloff JT, Massry SG. Serum reverse triiodothyronine and thyroxine kinetics in patients with chronic renal failure. J Clin Endocrinol Metab 1983;57:181-9.  Back to cited text no. 60
61.Ramirez G, O'Neill W Jr, Jubiz W, Bloomer HA. Thyroid dysfunction in uremia: Evidence for thyroid and hypophyseal abnormalities. Ann Intern Med 1976;84:672-6.  Back to cited text no. 61
62.Singh PA, Bobby Z, Selvaraj N, Vinayagamoorthi R. An evaluation of thyroid hormone status and oxidative stress in undialyzed chronic renal failure patients. Indian J Physiol Pharmacol 2006;50:279-84.  Back to cited text no. 62
63.Lim VS. Thyroid function in patients with chronic renal failure. Am J Kidney Dis 2001;38Suppl 1: S80-4.  Back to cited text no. 63
64.Hegedus L, Andersen JR, Poulsen LR, Perrild H, Holm B, Gundtoft E, et al. Thyroid gland volume and serum concentrations of thyroid hormones in chronic renal failure. Nephron 1985;40:171-4.  Back to cited text no. 64
65.Miki H, Oshimo K, Inoue H, Kawano M, Morimoto T, Monden Y, et al. Thyroid carcinoma in patients with secondary hyperparathyroidism. J Surg Oncol 1992;49:168-71.  Back to cited text no. 65
66.Silverberg DS, Ulan RA, Fawcett DM, Dossetor JB, Grace M, Bettcher K. Effects of chronic hemodialysis on thyroid function in chronic renal failure. Can Med Assoc J 1973;109:282-6.  Back to cited text no. 66
67.Rodrigues MC, Santos GM, da Silva CA, Baxter JD, Webb P, Lomri N, et al. Thyroid hormone transport is disturbed in erythrocytes from patients with chronic renal failure on hemodialysis. Ren Fail 2004;26:461-6.  Back to cited text no. 67
68.Kang EW, Nam JY, Yoo TH, Shin SK, Kang SW, Han DS, et al. Clinical implications of subclinical hypothyroidism in continuous ambulatory peritoneal dialysis patients. Am J Nephrol 2008;28:908-13.  Back to cited text no. 68
69.Junik R, Wlodarczyk Z, Masztalerz M, Odrowaz-Sypniewska G, Jendryczka E, Manitius J. Function, structure, and volume of thyroid gland following allogenic kidney transplantation. Transplant Proc 2003;35:2224-6.  Back to cited text no. 69
70.Reinhardt W, Misch C, Jockenhovel F, Wu SY, Chopra I, Philipp T, et al. Triiodothyronine (T3) reflects renal graft function after renal transplantation. Clin Endocrinol (Oxf) 1997;46:563-9.  Back to cited text no. 70
71.Rotondi M, Netti GS, Rosati A, Mazzinghi B, Magri F, Ronconi E, et al. Pretransplant serum FT3 levels in kidney graft recipients are useful for identifying patients with higher risk for graft failure. Clin Endocrinol (Oxf) 2008;68:220-5.  Back to cited text no. 71
72.Acker CG, Flick R, Shapiro R, Scantlebury VP, Jordan ML, Vivas C, et al. Thyroid hormone in the treatment of post-transplant acute tubular necrosis (ATN). Am J Transplant 2002;2:57-61.  Back to cited text no. 72
73.Wang CX, Liu LS, Chen LZ, Chen SY, Wu PG, Fei JG, et al. Characteristics of neoplasm occurrence and the therapeutic effect of sirolimus in South Chinese kidney transplant recipients. Transplant Proc 2006;38:3536-9.  Back to cited text no. 73
74.Weetman AP, Pinching AJ, Pussel BA, Evans DJ, Sweny P, Rees AJ. Membranous glomerulonephritis and autoimmune thyroid disease. Clin Nephrol 1981;15:50-1.  Back to cited text no. 74
75.Illies F, Wingen AM, Bald M, Hoyer PF. Autoimmune thyroiditis in association with membranous nephropathy. J Pediatr Endocrinol Metab 2004;17:99-104.  Back to cited text no. 75
76.Enriquez R, Sirvent AE, Amoros F, Andrada E, Cabezuelo JB, Reyes A. IgA nephropathy and autoimmune thyroiditis. Clin Nephrol 2002;57:406-7.  Back to cited text no. 76
77.Gurkan S, Dikman S, Saland MJ. A case of autoimmune thyroiditis and membranoproliferative glomerulonephritis. Pediatr Nephrol 2009;24:193-7.  Back to cited text no. 77
78.Tanwani LK, Lohano V, Broadstone VL, Mokshagundam SP. Minimal change nephropathy and Graves' disease: Report of a case and review of the literature. Endocr Pract 2002;8:40-3.  Back to cited text no. 78
79.Brohee D, Delespesse G, Debisschop MJ, Bonnyns M. Circulating immune complexes in various thyroid diseases. Clin Exp Immunol 1979;36:379-83.  Back to cited text no. 79
80.Akikusa B, Kondo Y, Iemoto Y, Iesato K, Wakashin M. Hashimoto's thyroiditis and membranous nephropathy developed in progressive systemic sclerosis (PSS). Am J Clin Pathol 1984;81:260-3.  Back to cited text no. 80
81.Dizdar O, Kahraman S, Genctoy G, Ertoy D, Arici M, Altun B, et al. Membranoproliferative glomerulonephritis associated with type 1 diabetes mellitus and Hashimoto's thyroiditis. Nephrol Dial Transplant 2004;19:988-9.  Back to cited text no. 81
82.Feinstein EI, Kaptein EM, Nicoloff JT, Massry SG. Thyroid function in patients with nephrotic syndrome and normal renal function. Am J Nephrol 1982;2:70-6.  Back to cited text no. 82
83.Junglee NA, Scanlon MF, Rees DA. Increasing thyroxine requirements in primary hypothyroidism: Don't forget the urinalysis! J Postgrad Med 2006;52:201-3.  Back to cited text no. 83
84.Chadha V, Alon US. Bilateral nephrectomy reverses hypothyroidism in congenital nephrotic syndrome. Pediatr Nephrol 1999;13:209-11.  Back to cited text no. 84
85.Ebihara I, Hirayama K, Usui J, Seki M, Higuchi F, Oteki T, et al. Tubulointerstitial nephritis and uveitis syndrome associated with hyperthyroidism. Clin Exp Nephrol 2006;10:216-21.  Back to cited text no. 85
86.Bernet VJ. Reversible renal insufficiency attributable to thyroid hormone withdrawal in a patient with type 2 diabetes mellitus. Endocr Pract 2004;10:339-44.  Back to cited text no. 86
87.Kursat S, Alici T, Colak HB. A case of rhabdomyolysis induced acute renal failure secondary to statin-fibrate-derivative combination and occult hypothyroidism. Clin Nephrol 2005;64:391-3.  Back to cited text no. 87
88.Berthe E, Henry-Amar M, Michels JJ, Rame JP, Berthet P, Babin E, et al. Risk of second primary cancer following differentiated thyroid cancer. Eur J Nucl Med Mol Imaging 2004;31:685-91.  Back to cited text no. 88
89.Kumar A, Nadig M, Patra V, Srivastava DN, Verma K, Bal CS. Adrenal and renal metastases from follicular thyroid cancer. Br J Radiol 2005;78:1038-41.  Back to cited text no. 89
90.Papi G, Fadda G, Corsello SM, Corrado S, Rossi ED, Radighieri E, et al. Metastases to the thyroid gland: Prevalence, clinicopathological aspects and prognosis: A 10-year experience. Clin Endocrinol (Oxf) 2007;66:565-71.  Back to cited text no. 90
91.Jung SJ, Chung JI, Park SH, Ayala AG, Ro JY. Thyroid follicular carcinoma-like tumor of kidney: A case report with morphologic, immunohistochemical, and genetic analysis. Am J Surg Pathol 2006;30:411-5.  Back to cited text no. 91
92.Eccles TG, Patel A, Verma A, Nicholson D, Lukes Y, Tuttle RM, et al. Erythropoietin and the erythropoietin receptor are expressed by papillary thyroid carcinoma from children and adolescents. Expression of erythropoietin receptor might be a favorable prognostic indicator. Ann Clin Lab Sci 2003;33:411-22.  Back to cited text no. 92
93.Kamiya Y, Puzianowska-Kuznicka M, McPhie P, Nauman J, Cheng SY, Nauman A. Expression of mutant thyroid hormone nuclear receptors is associated with human renal clear cell carcinoma. Carcinogenesis 2002;23:25-33.  Back to cited text no. 93
94.Yu F, Chen M, Gao Y, Wang SX, Zou WZ, Zhao MH, et al. Clinical and pathological features of renal involvement in propylthiouracil-associated ANCA-positive vasculitis. Am J Kidney Dis 2007;49:607-14.  Back to cited text no. 94
95.Wang LC, Tsai WY, Yang YH, Chiang BL. Methimazole-induced lupus erythematosus: A case report. J Microbiol Immunol Infect 2003;36:278-81.  Back to cited text no. 95
96.Calanas-Continente A, Espinosa M, Manzano-Garcia G, Santamaria R, Lopez-Rubio F, Aljama P. Necrotizing glomerulonephritis and pulmonary hemorrhage associated with carbimazole therapy. Thyroid 2005;15:286-8.  Back to cited text no. 96
97.Kirk AD, Hale DA, Swanson SJ, Mannon RB. Autoimmune thyroid disease after renal transplantation using depletional induction with alemtuzumab. Am J Transplant 2006;6:1084-5.  Back to cited text no. 97
98.Umemoto S, Izumi K, Kanno H. [Two cases of hyperthyroidism induced by interferon-alpha therapy for renal cell carcinoma]. Hinyokika Kiyo 2007;53:225-9.  Back to cited text no. 98
99.Stein EM, Rivera C. Transient thyroiditis after treatment with lenalidomide in a patient with metastatic renal cell carcinoma. Thyroid 2007;17:681-3.  Back to cited text no. 99
100.Feldman DR, Martorella AJ, Robbins RJ, Motzer RJ. Re: Hypothyroidism in patients with metastatic renal cell carcinoma treated with sunitinib. J Natl Cancer Inst 2007;99:974-5; author reply 976-7.  Back to cited text no. 100
101.Morales AI, Barata JD, Bruges M, Arevalo MA, Gonzalez de Buitrago JM, Palma P, et al. Acute renal toxic effect of amiodarone in rats. Pharmacol Toxicol 2003;92:39-42.  Back to cited text no. 101
102.Paydas S, Balal M, Karayaylali I, Seyrek N. Severe acute renal failure due to tubulointerstitial nephritis, pancreatitis, and hyperthyroidism in a patient during rifampicin therapy. Adv Ther 2005;22:241-3.  Back to cited text no. 102
103.Holst JP, Burman KD, Atkins F, Umans JG, Jonklaas J. Radioiodine therapy for thyroid cancer and hyperthyroidism in patients with end-stage renal disease on hemodialysis. Thyroid 2005;15:1321-31.  Back to cited text no. 103
104.Kaptein EM, Levenson H, Siegel ME, Gadallah M, Akmal M. Radioiodine dosimetry in patients with end-stage renal disease receiving continuous ambulatory peritoneal dialysis therapy. J Clin Endocrinol Metab 2000;85:3058-64.  Back to cited text no. 104


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Müge Keskin,Esra Ademoglu,Arzu Or Koca,Derun Taner Ertugrul
Ankara Medical Journal. 2019;
[Pubmed] | [DOI]
36 Thyroid hormones and diabetic nephropathy: An essential relationship to recognize
Qianqian Han,Junlin Zhang,Yiting Wang,Hanyu Li,Rui Zhang,Ruikun Guo,Li Li,Geer Teng,Jiali Wang,Tingli Wang,Fang Liu
Nephrology. 2019; 24(2): 160
[Pubmed] | [DOI]
37 The relationship between thyroid dysfunction and nephrotic syndrome: a clinicopathological study
Ling-Zhi Li,Yao Hu,Shuang-Lan Ai,Lu Cheng,Jing Liu,Emily Morris,Yi Li,Shen-Ju Gou,Ping Fu
Scientific Reports. 2019; 9(1)
[Pubmed] | [DOI]
38 Shear Wave Elastography in Diagnosing Secondary Hyperparathyroidism
Laura Cotoi,Florin Borcan,Ioan Sporea,Dana Amzar,Oana Schiller,Adalbert Schiller,Cristina Adriana Dehelean,Gheorghe Nicusor Pop,Dana Stoian
Diagnostics. 2019; 9(4): 213
[Pubmed] | [DOI]
39 Vitamin C improves liver and renal functions in hypothyroid rats by reducing tissue oxidative injury
Mahdi Esmaeilizadeh,Mahmoud Hosseini,Farimah Beheshti,Vajihe Alikhani,Zakieh Keshavarzi,Mohsen Shoja,Mozhgan Mansoorian,Hamid Reza Sadeghnia
International Journal for Vitamin and Nutrition Research. 2019; : 1
[Pubmed] | [DOI]
40 Thyroid disease in end-stage renal disease
Connie M. Rhee
Current Opinion in Nephrology and Hypertension. 2019; 28(6): 621
[Pubmed] | [DOI]
41 Perfluoroalkyl acids and thyroid hormones across stages of kidney function
Ram B. Jain,Alan Ducatman
Science of The Total Environment. 2019; 696: 133994
[Pubmed] | [DOI]
42 Prevalence of hypothyroidism among chronic kidney disease patients in security force hospital (SFH) in Saudi Arabia
Faisal Alshammari,Sultan Alhazaa,Abdullah Althemery,Fahad Alsabaan,Abdulelah AlGosaibi,Manal Alshammari,Ali Aldabies,Mohammad Alfifi
Journal of Family Medicine and Primary Care. 2019; 8(10): 3313
[Pubmed] | [DOI]
Simo Liu,Jing Ke,Baoyu Zhang,Caiguo Yu,Yingmei Feng,Dong Zhao
Endocrine Practice. 2018; 24(10): 889
[Pubmed] | [DOI]
44 Thyroid hormone: a resurgent treatment for an emergent concern
Mason T. Breitzig,Matthew D. Alleyn,Richard F. Lockey,Narasaiah Kolliputi
American Journal of Physiology-Lung Cellular and Molecular Physiology. 2018; 315(6): L945
[Pubmed] | [DOI]
45 Associations between longitudinal serum perfluoroalkyl substance (PFAS) levels and measures of thyroid hormone, kidney function, and body mass index in the Fernald Community Cohort
Bevin E. Blake,Susan M. Pinney,Erin P. Hines,Suzanne E. Fenton,Kelly K. Ferguson
Environmental Pollution. 2018;
[Pubmed] | [DOI]
46 Evaluation of Serum Symmetric Dimethylarginine Concentration as a Marker for Masked Chronic Kidney Disease in Cats With Hyperthyroidism
M.E. Peterson,F.V. Varela,M. Rishniw,D.J. Polzin
Journal of Veterinary Internal Medicine. 2018; 32(1): 295
[Pubmed] | [DOI]
47 A Study on Renal Function Status of Patients with Hypothyroidism attending a Tertiary Care Hospital in North Bengal
Shubhrajit Saha,Indrajit Nath,Mita S Das,Samarpita Mukherjee
Indian journal of Medical Biochemistry. 2018; 22(1): 10
[Pubmed] | [DOI]
48 Iodine in excess in the alterations of carbohydrate and lipid metabolic pattern as well as histomorphometric changes in associated organs
Deotima Sarkar,Arijit Chakraborty,Adipa Saha,Amar K Chandra
Journal of Basic and Clinical Physiology and Pharmacology. 2018; 29(6): 631
[Pubmed] | [DOI]
49 Auto-immune Thyroiditis in an Infant Masquerading as Congenital Nephrotic Syndrome
Sunil N. Jondhale,Sushma U. Save,Rahul G. Koppikar,Sandeep B. Bavdekar
The Indian Journal of Pediatrics. 2018;
[Pubmed] | [DOI]
50 Spontaneous primary hypothyroidism in 7 adult cats
Mark E. Peterson,Marcia A. Carothers,David A. Gamble,Mark Rishniw
Journal of Veterinary Internal Medicine. 2018;
[Pubmed] | [DOI]
51 The relationship between subclinical hypothyroidism and serum levels of uric acid and creatinine in children aged 2–14 years
Saba Sayari,Ziba Molaei,Zohre Torabi
Annals of Pediatric Endocrinology & Metabolism. 2018; 23(1): 38
[Pubmed] | [DOI]
52 Clinical feasibility of monitoring resting heart rate using a wearable activity tracker in patients with thyrotoxicosis: prospective longitudinal observational study (Preprint)
Jie-Eun Lee,Dong Hwa Lee,Tae Jung Oh,Kyoung Min Kim,Sung Hee Choi,Soo Lim,Young Joo Park,Do Joon Park,Hak Chul Jang,Jae Hoon Moon
JMIR mHealth and uHealth. 2018;
[Pubmed] | [DOI]
53 Amla (Emblica officinalis) improves hepatic and renal oxidative stress and the inflammatory response in hypothyroid female wistar rats fed with a high-fat diet
P. Rajaa Muthu,Zachariah Bobby,P. Sankar,V. Vickneshwaran,Sajini Elizabeth Jacob
Journal of Basic and Clinical Physiology and Pharmacology. 2017; 0(0)
[Pubmed] | [DOI]
54 Prevalence of malnutrition-inflammation complex syndrome and its correlation with thyroid hormones in chronic haemodialysis patients
Venice Chávez Valencia,Oliva Mejía Rodríguez,Martha Eva Viveros Sandoval,Juan Abraham Bermúdez,Sergio Gutiérrez Castellanos,Citlalli Orizaga de la Cruz,Martha Alicia Roa Córdova
Nefrología (English Edition). 2017;
[Pubmed] | [DOI]
55 Moderate-to-high normal levels of thyrotropin is a risk factor for urinary incontinence and an unsuitable quality of life in women over 65 years
Estela Cuevas-Romero,Angélica Sánchez-Cardiel,Angélica M. Zamora-Gallegos,Rosalía Cruz-Lumbreras,Dora L. Corona-Quintanilla,Francisco Castelán,Margarita Martínez-Gómez
Clinical and Experimental Pharmacology and Physiology. 2017;
[Pubmed] | [DOI]
56 Prevalencia del síndrome complejo de malnutrición e inflamación y su correlación con las hormonas tiroideas en pacientes en hemodiálisis crónica
Venice Chávez Valencia,Oliva Mejía Rodríguez,Martha Eva Viveros Sandoval,Juan Abraham Bermúdez,Sergio Gutiérrez Castellanos,Citlalli Orizaga de la Cruz,Martha Alicia Roa Córdova
Nefrología. 2017;
[Pubmed] | [DOI]
57 Correlation between Thyroid Stimulating Hormone and Renal Function in Euthyroid Residents of Japan: Results from the Kyushu and Okinawa Population Study (KOPS)
Yuki Tanaka,Norihiro Furusyo,Yoshifumi Kato,Takatsugu Ueyama,Sho Yamasaki,Hiroaki Ikezaki,Masayuki Murata,Jun Hayashi
Journal of Atherosclerosis and Thrombosis. 2017;
[Pubmed] | [DOI]
Modesta Petraviciute,Lina Zabuliene,Birute Pauliukiene,Jurgita Urboniene,Migle Gudynaite,Marius Miglinas
Medicinos teorija ir praktika. 2017; 22(3): 243
[Pubmed] | [DOI]
59 Indoxyl sulfate – the uremic toxin linking hemostatic system disturbances with the prevalence of cardiovascular disease in patients with chronic kidney disease
Tomasz W. Kaminski,Krystyna Pawlak,Malgorzata Karbowska,Michal Mysliwiec,Dariusz Pawlak
BMC Nephrology. 2017; 18(1)
[Pubmed] | [DOI]
60 Effects of hyper- and hypothyroidism on the development and proliferation of testicular cells in prepubertal rats
Mohamed Babo Fadlalla,Quanwei Wei,Jaafar Sulieman Fedail,Asif Mehfooz,Dagan Mao,Fangxiong Shi
Animal Science Journal. 2017;
[Pubmed] | [DOI]
61 Increased risk for hypothyroidism after anticholinesterase pesticide poisoning: a nationwide population-based study
Hung-Sheng Huang,Keng-Wei Lee,Chung-Han Ho,Chien-Chin Hsu,Shih-Bin Su,Jhi-Joung Wang,Hung-Jung Lin,Chien-Cheng Huang
Endocrine. 2017;
[Pubmed] | [DOI]
S. I. Dolomatov,V. G. Sipovski,N. Y. Novikov,I. N. Kasich,I. V. Myshko,?. Deri,A. N. Lytvinenko
Nephrology (Saint-Petersburg). 2017; 21(1): 57
[Pubmed] | [DOI]
63 Metabolic blood profile of beef heifers during oestrous and non-oestrous states
EM Crane,JC Munro,SL Bourgon,M Diel de Amorim,R Ventura,AH Fredeen,YR Montanholi
Reproduction in Domestic Animals. 2016; 51(5): 819
[Pubmed] | [DOI]
64 Metabolite profiling study on the toxicological effects of polybrominated diphenyl ether in a rat model
Young-Sang Jung,Jueun Lee,Jungju Seo,Geum-Sook Hwang
Environmental Toxicology. 2016;
[Pubmed] | [DOI]
65 The interaction between thyroid and kidney disease
Connie M. Rhee
Current Opinion in Endocrinology & Diabetes and Obesity. 2016; 23(5): 407
[Pubmed] | [DOI]
66 A rare cause of acute kidney injury: hypothyroidism / Akut böbrek hasarinin nadir bir nedeni: Hipotiroidizm
Simal Köksal Cevher,Ezgi Çoskun Yenigün,Ramazan Öztürk,Fatih Dede
Turkish Journal of Biochemistry. 2016; 41(4)
[Pubmed] | [DOI]
67 Multinodular Goiter Spontaneous Hemorrhage in ESRD Patients Result in Acute Respiratory Failure
Wen-Hui Lei,Chu-Xiao Shao,Jun Xin,Jie Li,Ming-Feng Mao,Xue-Ping Yu,Lie Jin
Medicine. 2016; 95(6): e2777
[Pubmed] | [DOI]
68 Incidence and risk factors for severe renal impairment after first diagnosis of heart failure: A cohort and nested case–control study in UK general practice
Alexander Michel,Mar Martín-Pérez,Ana Ruigómez,Luis A. García Rodríguez
International Journal of Cardiology. 2016; 207: 252
[Pubmed] | [DOI]
69 High prevalence of subclinical hypothyroidism and nodular thyroid disease in patients on hemodialysis
Ana Beatriz B.A. Da Costa,Caio Pellizzari,Gisah A. Carvalho,Beatriz C. SantćAnna,Rafaela L. Montenegro,Roberto G. Zammar Filho,Cleo O. Mesa Junior,Patrícia R. Hauck Prante,Marcia Olandoski,Mauricio Carvalho
Hemodialysis International. 2016; 20(1): 31
[Pubmed] | [DOI]
70 Treatment for non-thyroidal illness syndrome in advanced chronic kidney disease: a single-blind controlled study
Wenjun Yan,Lijuan Wang,Tianlun Huang,Gaosi Xu
Journal of Nephrology. 2016;
[Pubmed] | [DOI]
71 Thyroid function, reduced kidney function and incident chronic kidney disease in a community-based population: the Atherosclerosis Risk in Communities study
Ulla T. Schultheiss,Natalie Daya,Morgan E. Grams,Jochen Seufert,Michael Steffes,Josef Coresh,Elizabeth Selvin,Anna Köttgen
Nephrology Dialysis Transplantation. 2016; : gfw301
[Pubmed] | [DOI]
72 Triiodothyronine regulates cell growth and survival in renal cell cancer
Anna M. Czarnecka,Damian Matak,Lukasz Szymanski,Karolina H. Czarnecka,Slawomir Lewicki,Robert Zdanowski,Ewa Brzezianska-Lasota,Cezary Szczylik
International Journal of Oncology. 2016; 49(4): 1666
[Pubmed] | [DOI]
73 Thyroid dysfunction and kidney disease: An update
Pedro Iglesias,María Auxiliadora Bajo,Rafael Selgas,Juan José Díez
Reviews in Endocrine and Metabolic Disorders. 2016;
[Pubmed] | [DOI]
74 The effect of TSH change per year on the risk of incident chronic kidney disease in euthyroid subjects
Da Young Lee,Jae Hwan Jee,Ji Eun Jun,Tae Hyuk Kim,Sang-Man Jin,Kyu Yeon Hur,Sun Wook Kim,Jae Hoon Chung,Moon-Kyu Lee,Jae Hyeon Kim
Endocrine. 2016;
[Pubmed] | [DOI]
75 Thyroid hormones associate with risk of incident chronic kidney disease and rapid decline in renal function: a prospective investigation
Xiaolin Huang,Lin Ding,Kui Peng,Lin Lin,Tiange Wang,Zhiyun Zhao,Yu Xu,Jieli Lu,Yuhong Chen,Weiqing Wang,Yufang Bi,Guang Ning,Min Xu
Journal of Translational Medicine. 2016; 14(1)
[Pubmed] | [DOI]
76 Abnormal Thyroid-Stimulating Hormone and Chronic Kidney Disease in Elderly Adults in Taipei City
Mei-hsing Chuang,Kuo-Meng Liao,Yao-Min Hung,Paul Yung-Pou Wang,Yi-Chang Chou,Pesus Chou
Journal of the American Geriatrics Society. 2016; 64(6): 1267
[Pubmed] | [DOI]
77 Prevalence and Clinical Significance of Low T3 Syndrome in Non-Dialysis Patients with Chronic Kidney Disease
Jingxian Fan,Peng Yan,Yingdeng Wang,Bo Shen,Feng Ding,Yingli Liu
Medical Science Monitor. 2016; 22: 1171
[Pubmed] | [DOI]
78 Endocrine Abnormalities in Patients with Chronic Kidney Disease
Piotr Kuczera,Marcin Adamczak,Andrzej Wiecek
PRILOZI. 2015; 36(2)
[Pubmed] | [DOI]
79 Subclinical hypothyroidism as a rare cofactor in chronic kidney disease (CKD) – related anemia
Agnieszka Bargenda,Kinga Musial,Danuta Zwolinska
Journal of Pediatric Endocrinology and Metabolism. 2015; 28(7-8)
[Pubmed] | [DOI]
80 The correct renal function evaluation in patients with thyroid dysfunction
Mariadelina Simeoni,Annamaria Cerantonio,Ida Pastore,Rossella Liguori,Marta Greco,Daniela Foti,Elio Gulletta,Antonio Brunetti,Giorgio Fuiano
Journal of Endocrinological Investigation. 2015;
[Pubmed] | [DOI]
81 Thyroid dysfunction and dyslipidemia in chronic kidney disease patients
Saroj Khatiwada,Rajendra KC,Sharad Gautam,Madhab Lamsal,Nirmal Baral
BMC Endocrine Disorders. 2015; 15(1)
[Pubmed] | [DOI]
82 Effects of dietary creatine supplementation on systemic microvascular density and reactivity in healthy young adults
Roger de Moraes,Diogo Van Bavel,Beatriz de Moraes,Eduardo Tibiriçá
Nutrition Journal. 2014; 13(1): 115
[Pubmed] | [DOI]
83 Thyroid Function Tests in End-Stage Renal Disease
Dhananjay P. Kulkarni,Jean L. Holley
Seminars in Dialysis. 2014; : n/a
[Pubmed] | [DOI]
84 The relationship between thyroid function and estimated glomerular filtration rate in patients with chronic kidney disease
C. M. Rhee,K. Kalantar-Zadeh,E. Streja,J.-J. Carrero,J. Z. Ma,J. L. Lu,C. P. Kovesdy
Nephrology Dialysis Transplantation. 2014;
[Pubmed] | [DOI]
85 Thyroid functional disease: an under-recognized cardiovascular risk factor in kidney disease patients
C. M. Rhee,G. A. Brent,C. P. Kovesdy,O. P. Soldin,D. Nguyen,M. J. Budoff,S. M. Brunelli,K. Kalantar-Zadeh
Nephrology Dialysis Transplantation. 2014;
[Pubmed] | [DOI]
86 Thyroid Disorders and Chronic Kidney Disease
Mohamed Mohamedali,Srikanth Reddy Maddika,Anix Vyas,Viswanathan Iyer,Pramil Cheriyath
International Journal of Nephrology. 2014; 2014: 1
[Pubmed] | [DOI]
87 An update for the controversies and hypotheses of regulating nonthyroidal illness syndrome in chronic kidney diseases
Gaosi Xu,Wenjun Yan,Jingzhen Li
Clinical and Experimental Nephrology. 2014;
[Pubmed] | [DOI]
88 Effect on Renal Function of Restoration of Euthyroidism in Hyperthyroid Cats with Iatrogenic Hypothyroidism
T.L. Williams,J. Elliott,H.M. Syme
Journal of Veterinary Internal Medicine. 2014; : n/a
[Pubmed] | [DOI]
89 Thyroid hormone replacement for nephrotic syndrome patients with euthyroid sick syndrome: a meta-analysis
Huixin Liu,Wenjun Yan,Gaosi Xu
Renal Failure. 2014; : 1
[Pubmed] | [DOI]
90 The Thyroid and the Kidney: A Complex Interplay in Health and Disease
Periklis Dousdampanis,Konstantina Trigka,Georgios A. Vagenakis,Costas Fourtounas
The International Journal of Artificial Organs. 2014; 37(1): 1
[Pubmed] | [DOI]
91 Hypothyroidism and Reversible Kidney Dysfunction: An Essential Relationship to Recognize
Mireille El Ters,Sandeep M. Patel,Suzanne M. Norby
Endocrine Practice. 2013; 1(-1): 1
[Pubmed] | [DOI]
92 Antithyroid drug or hypothyroidism causes cellular damage in the renal cortex of adult male albino rats
Maha A. Gazia
The Egyptian Journal of Histology. 2013; 36(3): 636
[Pubmed] | [DOI]
93 Pathophysiology and treatment of kidney disease in cats
Amy Breton
The Veterinary Nurse. 2012; 3(10): 600
[Pubmed] | [DOI]


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