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EDITORIAL
Year : 2017  |  Volume : 14  |  Issue : 2  |  Page : 43-44

The kidney and the thyroid – Together in function and disease


Editor in Chief, Thyroid Research in Practice, Visiting Professor Endocrinology and Medical Education, Sri Balaji Vidyapeeth, Pondicherry, India

Date of Web Publication26-May-2017

Correspondence Address:
Krishna G Seshadri
Editor in Chief, Thyroid Research in Practice, 175 Brahmputra Street Palaniappa Nagar, Valasaravakkam, Chennai - 600 087, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/trp.trp_19_17

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How to cite this article:
Seshadri KG. The kidney and the thyroid – Together in function and disease. Thyroid Res Pract 2017;14:43-4

How to cite this URL:
Seshadri KG. The kidney and the thyroid – Together in function and disease. Thyroid Res Pract [serial online] 2017 [cited 2017 Nov 18];14:43-4. Available from: http://www.thetrp.net/text.asp?2017/14/2/43/207132



The effects of thyroid hormone (TH) on renal development, structure, and function are well documented.[1] Some of these are direct, others due to the effect of systemic hemodynamic changes. Congenital hypothyroidism (CH) is associated with renal dysmorphogenesis possibly related to mutations encoding the transcription factor PAX8.[2] Reduced renal mass is common in patients with CH. Higher prevalence of renal agenesis, dysplasia, ectopy, and other genitourinary abnormalities has been reported.[3]

Varying levels of creatinine elevation, mostly modest but sometimes significant, have been reported in hypothyroidism which are in the most part reversible on therapy.[4] Studies on patients who have undergone thyroidectomy suggest changes in creatinine in hypothyroid patients reflect changes in glomerular filtration rate (GFR).[5] This is attributable to both direct effects of TH on the kidney and indirect effects through action on the heart and vasculature.

In addition to the above, TH has effects on the expression and function of a number of renal ion channels and transporters. Down regulation of aquaporin 1 and 2 in addition to the known hemodynamic changes described in thyrotoxicosis in addition to cause polyuria.[6] Nonosmotic arginine vasopressin release, decreased concentrating capacity, and reversible reduction in sodium reabsorption in proximal and distal tubules may in part cause hyponatremia seen in hypothyroidism.[7]

In this issue of the journal, Gandhi et al. underline another important association between the kidney and thyroid.[8] A few case reports of reversible proteinuria biopsy-proven glomerulonephritis (GN) have been described in both hypo- and hyper-thyroidism. The renal pathology in these patients has varied from membranous nephropathy, minimal change, membranoproliferative GN, and IgA nephropathy.[9] Glomerular disease has been reported after the treatment for hyperthyroidism both medical and ablative.[10],[11]

In this retrospective analysis of patients referred for the evaluation of proteinuria or hematuria, the authors demonstrated a significant association between hypothyroidism of duration >1 year and proteinuria; nonsignificant associations were seen with nephrotic-range proteinuria and nephrotic syndrome. Serum creatinine elevations (1.09 ± 0.21 vs. 1.38 ± 0.31, P = 0.003) and decreases in GFR (P = 0.04) also correlated with disease duration of >1 year. Biopsy findings were available in 32 of the 36 patients; 50% should membranous nephropathy followed by focal segmental glomerulosclerosis, minimal change disease, and IgA nephropathy in the order of prevalence. Follow-up data were available in 22 patients. Reductions in proteinuria to <1 g/24 h were seen >50% in the membranous GN group who 16 were given standard of care in addition to thyroxine therapy. It is unclear if the improvement seen was due to thyroxine per se.

The coexistence of two autoimmune disorders raises the possibility of autoimmunity as the common thread that explains the association. Indeed, there are reports of thyroid peroxidase (TPO) and thyroglobulin deposits in the kidney.[12] The authors have not reported anti-TPO levels in this study. Despite the numbers and the limitations obvious to the reader, Gandhi et al. provide a timely reminder to the clinician to be vigilant of the important relationship between the thyroid and kidney. The take home would be to consider thyroid dysfunction in unexplained creatinine elevations and electrolyte imbalance. Since it can be reversed. Thyroid dysfunction may be a gratifying find in these circumstances. The relationship between glomerular disease and autoimmune thyroid disease is tenacious but still worth exploring.



 
  References Top

1.
Mariani LH, Berns JS. The renal manifestations of thyroid disease. J Am Soc Nephrol 2012;23:22-6.  Back to cited text no. 1
[PUBMED]    
2.
Park SM, Chatterjee VK. Genetics of congenital hypothyroidism. J Med Genet 2005;42:379-89.  Back to cited text no. 2
[PUBMED]    
3.
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. 3
[PUBMED]    
4.
Kreisman SH, Hennessey JV. Consistent reversible elevations of serum creatinine levels in severe hypothyroidism. Arch Intern Med 1999;159:79-82.  Back to cited text no. 4
[PUBMED]    
5.
Karanikas G, Schütz M, Szabo M, Becherer A, Wiesner K, Dudczak R, et al. Isotopic renal function studies in severe hypothyroidism and after thyroid hormone replacement therapy. Am J Nephrol 2004;24:41-5.  Back to cited text no. 5
    
6.
Wang W, Li C, Summer SN, Falk S, Schrier RW. Polyuria of thyrotoxicosis: Downregulation of aquaporin water channels and increased solute excretion. Kidney Int 2007;72:1088-94.  Back to cited text no. 6
[PUBMED]    
7.
Schmitt R, Klussmann E, Kahl T, Ellison DH, Bachmann S. Renal expression of sodium transporters and aquaporin-2 in hypothyroid rats. Am J Physiol Renal Physiol 2003;284:F1097-104.  Back to cited text no. 7
[PUBMED]    
8.
Gandhi K, Godara K, Agrawal D, Malhotra V, Beniwal P, Dsouza A. Clinicopathologic profile of glomerular diseases associated with autoimmune thyroiditis. Thyroid Res Pract 2017;14:71-4.  Back to cited text no. 8
  [Full text]  
9.
Iglesias P, Díez JJ. Thyroid dysfunction and kidney disease. Eur J Endocrinol 2009;160:503-15.  Back to cited text no. 9
    
10.
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. 10
[PUBMED]    
11.
Becker BA, Fenves AZ, Breslau NA. Membranous glomerulonephritis associated with Graves' disease. Am J Kidney Dis 1999;33:369-73.  Back to cited text no. 11
[PUBMED]    
12.
Shima Y, Nakanishi K, Togawa H, Obana M, Sako M, Miyawaki M, et al. Membranous nephropathy associated with thyroid-peroxidase antigen. Pediatr Nephrol 2009;24:605-8.  Back to cited text no. 12
    




 

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