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   Abstract
  Introduction
  Case Report
  Discussion
  Conclusion
   References
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  Table of Contents  
CASE REPORT
Year : 2015  |  Volume : 25  |  Issue : 4  |  Page : 248-250
 

Grave's disease associated with immunoglobulin A nephropathy: A rare association


1 Department of Internal Medicine, Sher-i-Kashmir Institute of Medical Sciences, Jammu , Jammu and Kashmir, India
2 Department of Pathology, Government Medical College, Jammu , Jammu and Kashmir, India
3 Department of Immunology, Sher-i-Kashmir Institute of Medical Sciences, Jammu , Jammu and Kashmir, India

Date of Web Publication26-Jun-2015

Correspondence Address:
R A Bhat
Flat F-18, Doctors Hostel, Sher i Kashmir Institute of Medical Sciences, Soura Srinagar Kashmir, Jammu and Kashmir
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-4065.147373

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  Abstract 

Immunoglobulin A (Ig A) nephropathy is the most common form of primary glomerulonephritis. The association of Ig A nephropathy with Grave's disease has not been reported so far. We report a case of 20-year-old female with Grave's disease who presented with edema, facial puffiness, and decreased urine output. She was found to be hypertensive with renal failure and nephrotic range proteinuria. Renal biopsy revealed features of Ig A nephropathy. The patient was treated with oral corticosteroids (1 mg/kg/day). To our knowledge, this is the first case showing association of Grave's disease with Ig A nephropathy.


Keywords: Autoimmunity, grave′s disease, immunoglobulin A nephropathy


How to cite this article:
Khan I, Bhat R A, Khan I, Hameed I. Grave's disease associated with immunoglobulin A nephropathy: A rare association. Indian J Nephrol 2015;25:248-50

How to cite this URL:
Khan I, Bhat R A, Khan I, Hameed I. Grave's disease associated with immunoglobulin A nephropathy: A rare association. Indian J Nephrol [serial online] 2015 [cited 2019 May 26];25:248-50. Available from: http://www.indianjnephrol.org/text.asp?2015/25/4/248/147373



  Introduction Top


Thyroid diseases have been shown to have association with various immunological diseases involving kidneys like immunoglobulin A (Ig A) nephropathy, [1] membranoproliferative glomerulonephritis [2] and minimal change disease. [3] Hyperthyroid state exerts various non-immunological effects on kidneys functionally and structurally. [4],[5]

This report is being presented as a first case report to show the association between Grave's disease and Ig A nephropathy, which to the best of our knowledge has not been shown so far.


  Case Report Top


A 22-year-old unmarried female was diagnosed as a case of Grave's disease and was put on methamizole 10 mg twice daily. Her investigations done in previous 1 month showed serum free thyroxine level of 1.05 ng/dl (normal range 0.95-1.74 ng/dl), thyroid-stimulating hormone level of <0.001 μU/mL (0.34-3.88 μU/mL), and anti-thyroid-peroxidase antibody titer of 1738 units/ml (<100 units/ml). Ultrasonography neck revealed diffuse enlargement of thyroid gland. Thyroid scan showed 42% uptake in thyroid gland. She presented to our department with complaints of periorbital puffiness, swelling of feet, and decreased urine output. Her examination revealed blood pressure (BP) of 180/100 mmHg, pulse rate of 100 beats/m in and temperature of 98.8°F. She had periorbital puffiness, pedal edema, and diffuse midline neck swelling. Her hands were warm and moist, and there were no tremors or skin changes. Rest of the systemic examination was normal. Patient was continued on methamizol as the disease was in remission. Her investigations showed hemoglobin 10.3 g/dl, total leukocyte count 6500/mm3, serum creatinine 2.4 mg/dl, bilirubin 0.4 mg/dl, normal AST, ALT and alkaline phosphatase, albumin 2.8 g/dl, uric acid 6.8 mg/dl, blood sugar 89 mg/dl, calcium 8.7 mg/dl and phosphate 4.6 g/dl.

Urine exam ination revealed 6-8 pus cells/HPF; red blood cells of 10-12/hpf; protein - +++, sugar-nil. 24 h urinary protein estimation revealed protein of 13 g/day. Hepatitis B surface antigen/hepatitis C virus serology was negative. Anti-nuclear antibodies and anti-double-stranded DNA were negative. Serum and urine electrophoresis was also negative.

Renal biopsy revealed 23 glomeruli, 12 (52.1%) of which were globally sclerosed. Among the remaining glomeruli, 7 (30.4%) revealed segmental tuft sclerosis and three glomeruli (13%) revealed segmental endocapillary cellularity. Extracapillary proliferation and partial fibrocellular crescents were seen in 2 (8.69%) glomeruli. Tubular atrophy and interstitial fibrosis involved 40-45% of the sample. Viable tubules showed prominent cytoplasmic vacuolar changes and evidence of patchy acute injury with epithelial simplification and loss of brush borders. Arteries showed medial thickening and fibrointimal sclerosis with duplication of internal elastic lamina and focal mucoid degeneration while arterioles revealed variably thickened walls with subendothelial transmural hyalinosis 1 [Figure 1].
Figure 1: Microphotograph showing histopathological examination showing globally sclerosed glomeruli tuft sclerosis with segmental endocapillary cellularity. Tubular atrophy with loss of brush borders is evident

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Differential immunofluorescence study revealed Ig A-3 + mesangial deposits, IgG negative, Ig M 1 + , C3 2 + , C1q negative, kappa 2 + , lambda 3 + mesangial deposits. Biopsy was suggestive of focal endocapillary proliferative Ig A nephropathy with M0E1S1T1 Oxford score [Figure 2].
Figure 2: Microphotograph showing immunofluorescence examination depicting Ig A-3+ mesangial deposits granular as well as confluent, Ig G negative, Ig M 1+, C3 2+, C1q negative, Kappa 2+, lambda 3+ mesangial deposits

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The patient was treated with oral corticosteroids 1 mg/kg and amlodipine. Angiotensin converting enzyme inhibitors were not given initially. Her repeat investigations on follow-up showed improvement in disease course clinically and biochemically with 24 h urinary protein of 2 g/day and serum creatinine level of 1.6 mg/dl. The patient is on amlodipine 10 mg/day and continues on tapering doses of steroid.


  Discussion Top


Hyperthyroidism results in increased renal blood flow and glomerular filtration rate (GFR). [6] The reason is increased renal blood flow and activation of renin-angiotensin-aldosterone system. [7] Furthermore on treating the hyperthyroidism, these effects are reversed and the GFR returns to normal. [6] Serum creatinine is significantly decreased in hyperthyroid patients due to an increase in GFR and due to the reduction in overall muscle mass. Also urinary protein excretion in hyperthyroidism is increased due to increase in GFR. [4]

Hyperthyroidism also affects tubular function. It causes direct down-regulation of aquaporin 1 and 2 channels. This along with increased BP, cardiac output, and renal blood flow results in polyuria. [5] Thyroid diseases are associated with several glomerulonephritides. The most commonly observed association is with membranous nephropathy [8],[9] followed by Ig A nephropathy, [1] membranoproliferative glomerulonephritis [2] and minimal change disease. [3] So for no report of Grave's disease associated with Ig A nephropathy has been reported.

The association of Hashimoto's thyroiditis and membranous nephropathy with immune complex deposition in the glomerular as well as thyroid epithelial basement membrane has been reported. [10] The likely mechanism for association of Grave's disease with Ig A nephropathy beyond chance being the presence of circulating immune complexes can only be speculated. [11] Similarly, the occurrence of thyroid and renal disease in association with other autoimmune diseases such as type 1 diabetes mellitus has been suggested as an autoimmune etiology. [12] Given the fact that hyperthyroid state influences a lot of functional and structural changes in kidneys both at glomerular and tubular levels, pathophysiological mechanisms beyond autoimmunity need to be studied further.


  Conclusion Top


This case report is the first in the literature, which shows association of two autoimmune diseases with different pathophysiological mechanisms with no clear-cut explanation. Further studies are needed to study this association and possible mechanisms. Also non-immune mechanisms in this association need elucidation.

 
  References Top

1.
Enríquez R, Sirvent AE, Amorós F, Andrada E, Cabezuelo JB, Reyes A. IgA nephropathy and autoimmune thyroiditis. Clin Nephrol 2002;57:406-7.  Back to cited text no. 1
    
2.
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. 2
    
3.
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. 3
    
4.
Vargas F, Moreno JM, Rodríguez-Gómez 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. 4
    
5.
Wang W, Li C, Summer SN, Falk S, Schrier RW. Polyuria of thyrotoxicosis: Down regulation of aquaporin water channels and increased solute excretion. Kidney Int 2007;72:1088-94.  Back to cited text no. 5
    
6.
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. 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.
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. 8
    
9.
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. 9
    
10.
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. 10
    
11.
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. 11
    
12.
Dizdar O, Kahraman S, Gençtoy 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. 12
    


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  [Figure 1], [Figure 2]



 

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