HELIOS Klinikum-Berlin, Franz Volhard Clinic, Medical Faculty of the Charité, Germany
Correspondence and offprint requests to: Ralph Kettritz, Franz Volhard Clinic, Wiltbergstrasse 50, D-13125 Berlin, Germany. Email: kettritz{at}fvk-berlin.de
Keywords: renal function; thyroid disease
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Introduction |
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Cases |
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Hormonal studies quickly verified Graves' disease. We were interested to find a serum creatinine concentration of 27 µmol/l with a 24 h measured creatinine clearance of 254 ml/min. Of greater concern was a cystatin C concentration of 1.31 mg/l. The normal concentration is <1 mg/l. Treatment of her hyperthyroidism resulted in restoration of both values towards normal.
A 26-year-old male was referred due to an elevated creatine phosphokinase (CPK) value measured by his family doctor. He had gone to the doctor because of a tick bite 2 days earlier. The patient recalled having fallen on his back during a judo match 1 week earlier and had some vague aches but denied chronic pain. He was employed as a heating and air conditioning specialist and had no other complaints. In retrospect, he admitted to cold intolerance but could give no details. The physical examination, including neurological examination and Achilles muscle stretch reflex, were unremarkable. The patient weighed 70 kg.
The patient's serum creatinine concentration was 140 µmol/l. His 24 h measured creatinine clearance was 70 ml/min. The urinary sediment was normal; there was no proteinuria. CPK was 3910 U. Total cholesterol was 365 mg/dl, with a low-density lipoprotein cholesterol concentration of 281 mg/dl. The thyroid-stimulating hormone value was >100 U, while free T3 and free T4 were remarkably low. Autoantibodies consistent with Hashimoto's thyroiditis were detected in high titres, and scintigraphy was consistent with that diagnosis.
Questions
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Discussion |
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Jayagopal et al. studied the effects of the hyperthyroid and hypothyroid state on changes in cystatin C and serum creatinine in 17 patients with hypothyroidism and 19 patients with hyperthyrodism [1]. All patients were newly diagnosed. The hypothyroid patients had a mean serum creatinine of 91 µmol/l while the hyperthyroid patients had a mean serum creatinine of 59 µmol/l. Creatinine fell by 13% in the hypothyroid patients after treatment, similar to our patient. The value increased in the hyperthyroid patients after treatment so that the groups were similar (78 µmol/l compared with 72 µmol/l). Cystatin C was lower in untreated hypothyroid patients than in those with untreated hyperthyroidism (0.76 mg/l compared with 1.12 mg/l). Treatment caused cystatin C to increase by 14% in the hypothyroid patients, compared with a 21% decrease in the hyperthyroid patients. The authors suggested that hyperthyroidism is associated with a reversible increase in cystatin C production, whereas in hypothyroidism the reverse is the case. Cystatins are endogenous cysteine protease inhibitors that modulate the turnover of intracellular and extracellular proteins. Cystatin C belongs to the type 2 cystatin superfamily and consists of 120 amino acid residues. Almost 99% of the protein is cleared from the circulation by glomerular filtration and tubular reabsorption followed by metabolization. In any event, cystatin C is not a reliable marker of the glomerular filtration rate in this common endocrine condition. Wiesli et al. made similar observations and drew the same conclusions [2]. Schmitt and Bachmann have raised the same caveat for the rat [3]. We measured creatinine clearence in our patient with hyperthyroidism and found increased values indicating an increased GFR. Increased glomerular filtration is characteristic of hyperthyroidism and is attributed to an enhanced cardiac output, decreased renal vascular resistance and elevated renal blood flow.
Hypothyroidism is associated with reversible acute renal failure [4]. In our patient, the effect on renal function was modest and disappeared with treatment. Hypothyroid myopathy is associated with proximal weakness and myalgias, muscle enlargement, slow relaxation of the reflexes and marked (up to 100-fold) increase in the creatine kinase level, as was the case in our patient. Elevated creatine kinase is regularly reported in hypothyroid patients. The mechanisms are most probably related to impaired glycogenolysis and impaired mitochondrial oxidative metabolism. Hypothyroidism can rarely cause rhabdomyolysis, precipitating parenchymal acute renal failure [5,6]
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Teaching points |
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Conflict of interest statement. None declared.
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References |
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