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Thyroid function in chronic kidney disease

Biff F Palmer, MD
William L Henrich, MD, MACP
Section Editor
Jeffrey S Berns, MD
Deputy Editor
Alice M Sheridan, MD


The kidney normally plays an important role in the metabolism, degradation, and excretion of several thyroid hormones. It is not surprising, therefore, that impairment in kidney function leads to disturbed thyroid physiology. All levels of the hypothalamic-pituitary-thyroid axis may be involved, including alterations in hormone production, distribution, and excretion. (See "Thyroid hormone synthesis and physiology".)

As a result, abnormalities in thyroid function tests are frequently encountered in uremia. However, the overlap in symptomatology between the uremic syndrome and hypothyroidism requires a cautious interpretation of these tests. Nevertheless, it is ordinarily possible in the individual uremic patient to assess thyroid status accurately by physical diagnosis and thyroid function testing.

Epidemiologic data suggest that predialysis patients with chronic kidney disease have an increased risk of hypothyroidism [1,2]. Many cases are subclinical.

The changes in thyroid hormone metabolism that occur in the nephrotic syndrome and the general issue of thyroid function in nonthyroidal illness are discussed elsewhere. (See "Endocrine dysfunction in the nephrotic syndrome" and "Thyroid function in nonthyroidal illness".)


The kidney normally contributes to the clearance of iodide, primarily by glomerular filtration. Thus, iodide excretion is diminished in advanced renal failure, leading sequentially to an elevated plasma inorganic iodide concentration and an initial increment in thyroidal iodide uptake. The ensuing marked increase in the intrathyroidal iodide pool results in diminished uptake of radiolabeled iodide by the thyroid in uremic patients [3]. Increases in total body inorganic iodide can potentially block thyroid hormone production (the Wolff-Chaikoff effect). Such a change may explain the slightly higher frequency of goiter and hypothyroidism in patients with chronic kidney disease [4].

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Literature review current through: Nov 2017. | This topic last updated: Mar 07, 2017.
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  1. 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.
  2. Chonchol M, Lippi G, Salvagno G, et al. Prevalence of subclinical hypothyroidism in patients with chronic kidney disease. Clin J Am Soc Nephrol 2008; 3:1296.
  3. Ramírez G, Jubiz W, Gutch CF, et al. Thyroid abnormalities in renal failure. A study of 53 patients on chronic hemodialysis. Ann Intern Med 1973; 79:500.
  4. Kaptein EM. Thyroid hormone metabolism and thyroid diseases in chronic renal failure. Endocr Rev 1996; 17:45.
  5. Kaptein EM, Quion-Verde H, Chooljian CJ, et al. The thyroid in end-stage renal disease. Medicine (Baltimore) 1988; 67:187.
  6. Medri G, Carella C, Padmanabhan V, et al. Pituitary glycoprotein hormones in chronic renal failure: evidence for an uncontrolled alpha-subunit release. J Endocrinol Invest 1993; 16:169.
  7. Wartofsky L, Burman KD. Alterations in thyroid function in patients with systemic illness: the "euthyroid sick syndrome". Endocr Rev 1982; 3:164.
  8. Santini F, Chiovato L, Bartalena L, et al. Study of serum 3,5,3'-triiodothyronine sulfate concentration in patients with systemic non-thyroidal illness. Eur J Endocrinol 1996; 134:45.
  9. 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.
  10. Spaulding SW, Gregerman RI. Free thyroxine in serum by equilibrium dialysis: effects of dilution, specific ions and inhibitors of binding. J Clin Endocrinol Metab 1972; 34:974.
  11. Hochstetler LA, Flanigan MJ, Lim VS. Abnormal endocrine tests in a hemodialysis patient. J Am Soc Nephrol 1994; 4:1754.
  12. Herschman JM, Jones CM, Bailey AL. Reciprocal changes in serum thyrotropin and free thyroxine produced by heparin. J Clin Endocrinol Metab 1972; 34:574.
  13. Zoccali C, Tripepi G, Cutrupi S, et al. Low triiodothyronine: a new facet of inflammation in end-stage renal disease. J Am Soc Nephrol 2005; 16:2789.
  14. Zoccali C, Mallamaci F, Tripepi G, et al. Low triiodothyronine and survival in end-stage renal disease. Kidney Int 2006; 70:523.
  15. Lim VS, Flanigan MJ, Zavala DC, Freeman RM. Protective adaptation of low serum triiodothyronine in patients with chronic renal failure. Kidney Int 1985; 28:541.
  16. Czernichow P, Dauzet MC, Broyer M, Rappaport R. Abnormal TSH, PRL and GH response to TSH releasing factor in chronic renal failure. J Clin Endocrinol Metab 1976; 43:630.
  17. Duntas L, Wolf CF, Keck FS, Rosenthal J. Thyrotropin-releasing hormone: pharmacokinetic and pharmacodynamic properties in chronic renal failure. Clin Nephrol 1992; 38:214.
  18. Pasqualini T, Zantleifer D, Balzaretti M, et al. Evidence of hypothalamic-pituitary thyroid abnormalities in children with end-stage renal disease. J Pediatr 1991; 118:873.
  19. Wheatley T, Clark PM, Clark JD, et al. Abnormalities of thyrotrophin (TSH) evening rise and pulsatile release in haemodialysis patients: evidence for hypothalamic-pituitary changes in chronic renal failure. Clin Endocrinol (Oxf) 1989; 31:39.
  20. Spector DA, Davis PJ, Helderman JH, et al. Thyroid function and metabolic state in chronic renal failure. Ann Intern Med 1976; 85:724.
  21. Enia G, Panuccio V, Cutrupi S, et al. Subclinical hypothyroidism is linked to micro-inflammation and predicts death in continuous ambulatory peritoneal dialysis. Nephrol Dial Transplant 2007; 22:538.
  22. Meuwese CL, Dekker FW, Lindholm B, et al. Baseline levels and trimestral variation of triiodothyronine and thyroxine and their association with mortality in maintenance hemodialysis patients. Clin J Am Soc Nephrol 2012; 7:131.
  23. Castellano M, Turconi A, Chaler E, et al. Thyroid function and serum thyroid binding proteins in prepubertal and pubertal children with chronic renal insufficiency receiving conservative treatment, undergoing hemodialysis, or receiving care after renal transplantation. J Pediatr 1996; 128:784.
  24. Davis FB, Spector DA, Davis PJ, et al. Comparison of pituitary-thyroid function in patients with endstage renal disease and in age- and sex-matched controls. Kidney Int 1982; 21:362.
  25. Lin CC, Chen TW, Ng YY, et al. Thyroid dysfunction and nodular goiter in hemodialysis and peritoneal dialysis patients. Perit Dial Int 1998; 18:516.
  26. Ramirez G. Abnormalities in the hypothalamic-hypophyseal axes in patients with chronic renal failure. Semin Dial 1994; 7:138.