Hypothyroidism a reversible cause of renal dysfunction
Correspondence Address: Source of Support: None, Conflict of Interest: None DOI: 10.4103/0975-2870.148845
Hypothyroidism is a systemic disorder characterized by low circulating thyroxine levels. Of late there was some western and sporadic literature from India on the association of hypothyroidism and reversible renal impairment. We here report this association from two of our patients, who presented to us with simultaneously elevated serum thyroid-stimulating hormone and creatinine levels. Keywords: Glomerular filtration rate, hypothyroidism, renal dysfunction
Hypothyroidism is a systemic disorder characterized by low circulating free thyroxine levels. Of late, there are some reports on the association of renal impairment and primary hypothyroidism. We herein present two cases of this association, who was referred to us with altered thyroid function tests along with elevated renal parameters. Then we review the literature systematically about this association.
Case 1 A health conscious 50-year-old man presented to our out-patient department (OPD) with the reports of master health checkup done routinely. On questioning, he had complaints of weakness and indigestion. He was hypertensive using telmisartan 40 mg with good control. On examination, he had grade II diffuse goiter. His vitals and systemic examination was normal. Investigations: Hemoglobin 10 g% (11-15) with normocytic normochromic anemia, total leukocyte count was 5,100/(4-11,000), erythrocyte sedimentation rate 25 (9-14), complete urine examination and urine analysis was normal, fasting blood sugar 79 mg% (80-110), serum creatinine-2.08 mg/dl (0.8-1.5), corrected serum calcium-9.0 mg/dl (8.4-10.4), T3-0.5 ng/ml (0.6-2.00), T4-4.4 mcg/ml (5-12), thyroid stimulating hormone 86 miU/ml (0.3-5.5), anti-thyroid peroxidase (TPO) antibody (Ab) more than 1,200, electrocardiogram was normal and ultra-sonogram-kidney size was normal with normal echotexture. The patient was diagnosed to have primary hypothyroidism with renal dysfunction and advised to start L-thyroxine initially with 25 mcg then gradually increased to 100 mcg over a period of 5 days and referred to nephrologist, who advised conservative therapy and follow up. On review after 2 months patient came with T3-1.0 ng/ml (0.6-2.00), T4-6.4 mcg/ml (5-12), thyroid-stimulating hormone (TSH) -3.3 miU/ml (0.3-5.5) and his repeated serum creatinine was 1.0 mg/dl. Case 2 The second case is about a 40-year-old female patient who attended nephrology OPD with a history of facial puffiness and myalgias for the past 2 months. These complaints were gradually progressive in nature and associated with loss of appetite. Her past medical history was not significant and she has regular menstrual cycles. Examination revealed peri-orbital edema and her blood pressure was 130/100 mmHg, pulse rate was 60 beats/min. Investigations Hemoglobin-10.0 g% (11-15) with hypochromic, microcytic picture, total leukocyte count-5,800/cmm (4-11,000), erythrocyte sedimentation rate-28 (9-14), complete urine examination was normal with few casts, FBS-90 mg% (80-110), serum creatinine-1.96 mg/dl (0.8-1.4), corrected serum calcium-9.4 mg/dl (8.4-10.4), TSH-98 miU/ml (0.3-5.5), anti TPO Ab more than 1,200 and ultra-sonogram-kidney size was normal with normal echotexture. Creatine kinase was elevated to 1200 IU/l, but urinary myoglobin was not detected. Renal biopsy was normal. She was referred to an endocrinologist as there was no obvious etiology for her renal dysfunction. She was started on levothyroxine 100 mcg. Her blood pressure 120/70 mmHg, serum creatinine 1.0 mg/dl, creatine kinase all normalized after 6 weeks of treatment.
Above description refers to two cases with initial diagnosis of primary hypothyroidism and increased renal parameters and on both occasions thyroid hormone replacement therapy brought about complete recovery of renal function. This association is distinctly uncommon as most of the literature is available on rapid worsening of pre-existing renal disease with the onset of hypothyroidism. Thyroid hormones influence renal development, kidney structure, renal hemodynamics, glomerular filtration rate (GFR), the function of many transport systems along the nephron and sodium and water homeostasis. These effects of thyroid hormone are due to direct renal actions and in part are mediated by cardiovascular and systemic hemodynamic effects that influence kidney function. As a consequence, both hypothyroidism and hyperthyroidism are associated with clinically important alterations in kidney function and have relevance to its assessment. Disorders of thyroid function have also been linked to development of immune-mediated glomerular injury and alterations in thyroid hormones and thyroid hormone testing occur in patients with kidney disease. Many case reports and small case series document increased levels of serum creatinine with hypothyroidism in humans. [1],[2],[3],[4] Recent studies are indicating subclinical and clinical hypothyroidism is common in patients with estimated GFR <60 ml/min per 1.73 m 2 , suggesting the possibility of hypothyroidism might be contributing to the low GFR in some of these individuals. [5] Although the pathophysiology of impaired renal function in hypothyroidism is multi factorial, the reduction in GFR due to the decreased effective blood volume resulting from decreased cardiac output and renal blood flow is likely to be the predominant mechanism. [6] Other mechanisms include thyroxine mediated tubular secretion of creatinine [7] and hypothyroidism may also increase creatinine release from muscle. [8] Rarely, hypothyroidism can cause rhabdomyolysis leading to acute elevation of serum creatinine, [8] where treatment with thyroxine usually sufficient in this form of acute kidney injury (AKI). As in our second case where CPK levels were increased secondary to severe hypothyroidism without any other features of rhabdomyolysis. Hypothyroidism and renal impairment share some common features in between them like symptoms of peri-orbital edema, generalized edema, gastrointestinal manifestations of loss of appetite; signs such as anemia, hypertension and pleural, pericardial effusions as in our second case, so clinicians may err one to another. On contrary hypothyroidism can also be entirely asymptomatic as observed in our first case. Hence a knowledge of this association and high index of suspicion is needed, as there are subtle or no features of hypothyroidism in some patients. We suggest thyroid function tests to be ordered routinely in all patients with renal disease to recognise this association (especially when no other risk factors are found). As this is easily treatable and obviates the need of invasive renal biopsy.
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