To the Editor,
Thyroid pathology has a high prevalence in the general population, although autoimmune aetiology is rare. It is associated with a variety of glomerulonephritis types in very few cases, the most frequent being membranous glomerulonephritis.1,2 We present a case of membranous glomerulonephritis secondary to Hashimoto's thyroiditis.
We present the case of a woman aged 66, admitted to our department with proteinuria, generalised oedemas and new-onset hypertension, resistant to prescribed treatment. Analytical tests showed: urea 78mg/dl, creatinine 1.1mg/dl; MDRD-4 formula creatinine clearance 48ml/min; total proteins 4.6g/dl; albumin 1.2g/dl. Protein profile compatible with nephrotic syndrome. Cholesterol: 484mg/dl. Triglycerides: 180mg/dl. LDL: 386mg/dl. Autoimmunity and complement within normal ranges. Negative circulating immune complexes. TSH: 10.17mU/l, T4: 0.78mg/dl. Anti-microsomal antibodies: 84U/ml. Antithyroglobulin antibodies: 4U/ml. Anti-TSH receptor antibodies: 1.6U/l. Proteinuria to 10g/24 hours. An ultrasound-guided renal biopsy was performed with an anatomopathological result of membranous glomerulonephritis. The gynaecological study was normal, as was the abdominal ultrasound and the thoracic-abdominal-pelvic CT scan. Membranous glomerulonephritis probably secondary to Hashimoto's thyroiditis was diagnosed and treatment with levothyroxine, statin and dual blockade of the renin-angiotensin system was commenced.
During follow-up, treatment had to be suspended with ACE inhibitors due to intolerance, despite which there was a progressive decline in proteinuria up to values of 1.5g/24 hours after 6 months of hormonal treatment, and TSH, T3 and T4 figures normalised.
Hashimoto's thyroiditis treatment is not clear; hormone substitution therapy is recommended in cases of thyroiditis with clinical repercussion, although there is no clear consensus in the subclinical cases.3 Our case shows how normalisation of the thyroid hormone values by administering levothyroxine has a linear repercussion in relation to the proteinuria detected. Even so, not all the cases described present this relationship.4
Lastly, we deem it necessary, as other authors have stated, to perform an analysis of the thyroid hormones in every patient with nephrotic syndrome as part of an aetiological screening process.5
