Thyroid Research and Practice

: 2017  |  Volume : 14  |  Issue : 2  |  Page : 71--74

Clinicopathologic profile of glomerular diseases associated with autoimmune thyroiditis

Kunal Gandhi, Karamvir Godara, Dhananjai Agrawal, Vinay Malhotra, Pankaj Beniwal, Amith Dsouza 
 Department of Nephrology, Sawai Man Singh Hospital, Jaipur, Rajasthan, India

Correspondence Address:
Kunal Gandhi
Department of Nephrology, Sawai Man Singh Hospital, Jaipur, Rajasthan


Introduction: Thyroid hormones are known to influence renal function, development, and renal hemodynamics. In this study, we aimed to de ne the frequency and characteristics of various glomerular diseases associated with autoimmune thyroiditis. Methods: We reviewed retrospectively 36 patients with autoimmune thyroiditis referred for evaluation of proteinuria, hematuria, and/or renal impairment. Renal biopsy was performed in 32 patients and was examined with light microscopy and immunofluorescence. Six months follow-up data of 22 patients was reviewed. Results: The mean age of study population was 43.6 years. Most of them were females (n = 28). Mean duration of hypothyroidism (HT) was 1.5 years. Hypertension was seen in 16 patients and deranged renal function (estimated glomerular filtration rate <60 ml/min/1.73 m2) in 18 with a mean serum creatinine of 1.28 mg/dl at time of biopsy. 10 patients presented with nephrotic syndrome, 33 presented with isolated proteinuria and 22 presented with hematuria with or without significant proteinuria The most common histopathologic finding was membranous nephropathy (MGN) (n = 16), followed by minimal-change nephropathy (n = 5), focal segmental glomerulosclerosis (n = 5), immunoglobulin A nephropathy (n = 3), amyloidosis (n = 2), and membranoproliferative glomerulonephritis (n = 1). Membranous nephropathy was the most common finding inn patients with the nephrotic syndrome. Conclusion: Glomerular pathologies associated with HT are diverse and similar to those found in the general population; therefore, renal biopsy should be performed in cases with progressive renal failure or urinary abnormalities.

How to cite this article:
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;14:71-74

How to cite this URL:
Gandhi K, Godara K, Agrawal D, Malhotra V, Beniwal P, Dsouza A. Clinicopathologic profile of glomerular diseases associated with autoimmune thyroiditis. Thyroid Res Pract [serial online] 2017 [cited 2021 Mar 3 ];14:71-74
Available from:

Full Text


Autoimmune thyroiditis is a common cause of hypothyroidism (HT) in iodine sufficient adult population, especially in females. The prevalence has been reported to be 5–10% in young Indian females,[1] with Hashimoto's thyroiditis as the most common etiology. The association of glomerular diseases with autoimmune thyroid disease was recognized few years ago, with isolated cases of proteinuria and nephrotic syndrome reported in children as well as adults. Membranous nephropathy was the most common histopathological finding in renal biopsy series. Other findings include membranoproliferative, immunoglobulin A nephropathy (IgAN), and renal amyloidosis.[2],[3],[4] However, the frequency of such association is still largely unknown. Although debatable, a common immunological mechanism has been postulated for the development of glomerulonephritis in autoimmune thyroiditis.[4]

To the best of knowledge, there is no study analyzing the frequency and characteristics of glomerular diseases in patients with autoimmune thyroiditis in Indian population.


A retrospective study analyzing clinical data of 36 diagnosed patients with autoimmune HT referred to Department of Nephrology of our Tertiary Hospital from January 2014 to December 2014 were conducted. These patients were referred for evaluation of hematuria, proteinuria and/or renal impairment. Patients who had clinical manifestations of systemic diseases such as autoimmune disorders, connective tissue diseases, diabetes mellitus, vasculitis, or renal stones were excluded. Baseline clinical and laboratory data of all patients, namely complete blood count, renal function test, serum total protein, serum albumin, fasting lipid profile, urinalysis, 24 h urine protein, and ultrasound of abdomen were noted. Based on the duration of HT, patients were divided into two groups. Group 1 included patients with HT <12 months and Group 2 included those with HT >12 months. Renal biopsy was available for 32 patients and specimen was examined by light microscopy and immunofluorescence. All statistics were done using SPSS software application (version 20: SPSS, Chicago, IL, USA). The results are expressed in frequencies and percentages (categorical variables), and mean ± standard deviation. The mean were compared using Student's t-test. Variables with P< 0.05 were considered significant.


Hematuria was defined as the presence of >5 red blood cells/hpf. Significant proteinuria was 24 h protein excretion of more than 500 mg/day. Nephrotic range proteinuria was defined as urine protein >3.5 g/day. Nephrotic syndrome is defined by the association of a proteinuria higher than 3.5 g/24 h, hypoalbuminemia, edema, and dyslipidemia. Renal impairment was defined as a glomerular filtration rate (GFR) <60 mL/min/1.73 m 2.


A total of 36 patients were included in the study, with a female preponderance in both the groups. The mean age of Group 1 was 44.3 ± 11.9 while Group 2 was 42.8 ± 11.3, which was statistically not significant. 22 patients had hematuria during their disease. Proteinuria was present in 32 patients, with a 100% association in patients with a longer duration of HT (P < 0.05). Nephrotic range proteinuria was seen in 15 patients while 10 fulfilled the criteria for nephrotic syndrome. 18 patients had renal impairment, and 16 were hypertensive. The group wise distribution of clinical features is illustrated in [Table 1].{Table 1}

The serum creatinine was significantly raised with duration of disease (1.09 ± 0.21 vs. 1.38 ± 0.31, P = 0.003), along with a significant decrease in GFR (P = 0.04). There was no difference between the groups in terms of age, 24 h urine protein, serum albumin, or thyroid hormone levels. The laboratory investigations have been shown in [Table 1]. There was no significant correlation between thyroid antibody titers and laboratory parameter mainly GFR and 24 h urine protein.

The histopathology findings are shown in [Table 2]. The most common pathology observed was membranous nephropathy (MGN) observed in 50% of the patients followed by focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD) in 15%. 3 cases of IgAN and 2 cases of amyloidosis were also noted. One patient had membranoproliferative glomerulonephritis (MPGN). MGN was the most common finding in patients with the nephrotic syndrome, whereas 60% of patients with hematuria and proteinuria had FSGS.{Table 2}

Six months follow-up data was available for 22 patients (12 patients with MGN, 4 with FSGS, 3 with MCD, 1 with amyloidosis, MPGN, and IgAN). Patients with 24 h protein more than 1 g were started on the highest tolerated doses of angiotensin-converting enzymes inhibitors (ACE-I) or angiotensin receptor blocking (ARB) agents. Thyroid supplementation was modified in all patients to keep thyroid-stimulating hormone within normal limits. Nine patients were initiated on immunosuppressive therapy. At 6 months, half of the patients with MGN had a decrease in proteinuria to <1 g/24 h, while the other half had some decrease in their baseline proteinuria. Two of three patients with MCD were initiated on steroids had complete remission by 6 months. Only one of the patients with FSGS had had a decrease in proteinuria to <1 g/day. Patients with amyloidosis continued to remain proteinuric despite maximum measures. A patient with MPGN was initiated on mycophenolate sodium and prednisone and maintained stable renal functions with a decrease in proteinuria over a period of 6 months.


Thyroid and kidney are affected in a mutual way – embryologically, physiologically, and pathologically.[5] Both hyper, as well as HT, can affect the kidneys in some way. HT causes a reduction in renal blood flow and a decrease in GFR. The mechanisms postulated include a decreased cardiac output, increased peripheral vascular resistance, intrarenal vasoconstriction, reduced renal response to vasodilators, and a reduced expression of renal vasodilators such as vascular endothelial growth factor and insulin like growth factor-1.[6] Whether this effect is solely due to deficiency of thyroid hormones, is still unknown. Most series have reported a serum creatinine in the range from 1.5 to 2.5 mg/dl which tends to normalize following thyroid supplementation.[7] Increased creatinine release from muscle due to rhabdomyolysis has also been associated with the risk of acute kidney injury. In our series, increased duration of HT was associated with a lower GFR. Various studies have failed to show a significant correlation between the levels of thyroid hormones or thyroid antibodies with the decrease in GFR.[4],[8]

HT, regardless of the autoimmunity, is known to coexist with glomerulonephritis. The findings may range from an isolated proteinuria to a full-blown nephrotic syndrome. The underlying mechanism postulated mediating proteinuria in HT is supposed to be increased transcapillary leakage of plasma proteins, as is seen in generalized edema.[2] A literature search on PubMed resulted in a handful of case reports associating glomerular disease with HT, mostly autoimmune thyroiditis. The most common of these was membranous glomerulopathy. The heavy proteinuria in these patients responded to conservative treatment with angiotensin 1 receptor antagonist (ACE-I) and ARB's and thyroid supplementation. Only a few patient required immunosuppression, especially those with a superimposed crescentic glomerulonephritis.[2],[4],[8] However, none of them progressed to end-stage renal disease. The other pathology seen was IgAN, MCD, FSGS, MPGN, amyloidosis, and chronic sclerosing glomerulonephritis.[4],[7],[9],[10],[11],[12] However, these were isolated case reports, and frequency of such association is largely unknown. Even in our study population, membranous was the most common pathology, followed by FSGS and MCD. Most of our patients with nephrotic syndrome had membranous nephropathy and MCD, a finding similar to those in the general population. Koçak et al. in their study reported an equal incidence of MGN and FSGS on renal biopsy.[4] Most of our patient responded to conservative treatment with full dose ACE-I/ARB's with a reduction in their proteinuria. We continued thyroid supplementation in all patients to achieve a euthyroid state.

The simultaneous occurrence of immune complex glomerulonephritis especially MGN and MPGN in patients with autoimmune thyroiditis could be explained secondary to a common immunological mechanism, although no correlation between the thyroid antibody levels and proteinuria and GFR has been found.[4] However, it may not be possible to explain all cases entirely due to immunological abnormalities as was seen in a postthyroidectomy patient who developed IgAN.[2] Therefore, a causal relationship between glomerulonephritis and autoimmune thyroiditis is at present an unproven hypothesis. Of note, the glomerulus architecture is reversibly altered during hypothyroid status. Patients with early HT had changes in their glomerular basement membrane, which improved within 2 months of starting thyroid supplementation.[13]


Co-existing glomerulonephritis is not uncommon in patients with autoimmune thyroiditis. The physician should be aware of this possibility and should consider repeated urine analysis for early detection.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Marwaha RK, Tandon N, Karak AK, Gupta N, Verma K, Kochupillai N. Hashimoto's thyroiditis: Countrywide screening of goitrous healthy young girls in postiodization phase in India. J Clin Endocrinol Metab 2000;85:3798-802.
2Men-Tai W, Shun-Chen H, Yung-Lung C, Chien-Te L. Concurrent hypothyroidism and IgA nephropathy presenting with acute heart and oliguric renal failure. Acta Nephrol 2012;26:100-3.
3Saha A, Bagri N, Mehera N, Dubey NK, Batra V. Membranoproliferative glomerulonephritis associated with autoimmune thyroiditis. J Pediatr Endocrinol Metab 2011;24:789-92.
4Koçak G, Huddam B, Azak A, Ortabozkoyun L, Duranay M. Coexistent findings of renal glomerular disease with Hashimoto's thyroiditis. Clin Endocrinol (Oxf) 2012;76:759-62.
5Kumar 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.
6Basu G, Mohapatra A. Interactions between thyroid disorders and kidney disease. Indian J Endocrinol Metab 2012;16:204-13.
7Gurkan S, Dikman S, Saland MJ. A case of autoimmune thyroiditis and membranoproliferative glomerulonephritis. Pediatr Nephrol 2009;24:193-7.
8Mariani LH, Berns JS. The renal manifestations of thyroid disease. J Am Soc Nephrol 2012;23:22-6.
9Iwaoka T, Umeda T, Nakayama M, Shimada T, Fujii Y, Miura F, et al. A case of membranous nephropathy associated with thyroid antigens. Jpn J Med 1982;21:29-34.
10Akikusa 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.
11Grcevska L, Polenakovic M, Petrusevska G. Membranous nephropathy associated with thyroid disorders. Nephron 2000;86:534-5.
12Illies F, Wingen AM, Bald M, Hoyer PF. Autoimmune thyroiditis in association with membranous nephropathy. J Pediatr Endocrinol Metab 2004;17:99-104.
13Salomon MI, Di Scala V, Grishman E, Brener J, Churg J. Renal lesions in hypothyroidism: A study based on kidney biopsies. Metabolism 1967;16:846-52.