http://informahealthcare.com/rnf ISSN: 0886-022X (print), 1525-6049 (electronic) Ren Fail, 2014; 36(3): 441–443 ! 2014 Informa Healthcare USA, Inc. DOI: 10.3109/0886022X.2013.868162
CASE REPORT
Coexistence of chronic renal failure, hashimoto thyroiditis and idiopathic hypoparathyroidism: a rare case report Saliha Yildiz1, Yasemin Soyoral2, Davut Demirkiran3, and Mustafa Ozturk1 1
Medical Faculty, Department of Internal Medicine, Division of Endocrinology, Yuzuncu Yil University, Van, Turkey, 2Medical Faculty, Department of Internal Medicine, Division of Nephrology, Yuzuncu Yil University, Van, Turkey, and 3Medical Faculty, Department of Internal Medicine, Yuzuncu Yil University, Van, Turkey Abstract
Keywords
Hypoparathyroidism is an uncommon disease and its coexistence with chronic renal failure is quite rare. Hypocalcemia and hyperphosphatemia are seen in both diseases. Diagnosis of hypoparathyroidism may be overlooked when parathormone response is not evaluated in patients with chronic renal failure. A 19-year-old female patient who had been receiving hemodialysis for 3 years because of chronic renal failure was diagnosed as idiopathic hypoparathyroidism and hashimoto thyroiditis. When her medical records on the first admission and medical history were evaluated, hypoparathyroidism and hashimoto thyroiditis were seen to be present also when she was started hemodialysis. Idiopathic hypoparathyroidism should be suspected in case as absence of parathormone response to hypocalcemia in patients with chronic renal failure. It should be taken into consideration that hashimoto thyroiditis may accompany and required analysis should be done.
Chronic renal failure, hemodialysis, hypocalcemia, hyperphosphatemia, idiopathic hypoparathyroidism
Hypoparathyroidism is a rare disease and secondary hyperparathyroidism is frequently seen in chronic renal failure (CRF). It has been known that respectively the most important activation factor and inhibitory factor are calcium (Ca) and calcitriol [1,25 (OH)D] in the pathogenesis of the secondary hyperparathyroidism.1–3 Hypoparathyroidism may be surgical, autoimmune, familial or idiopathic. Biochemical features of hypoparathyroidism are hypocalcemia, hyperphosphatemia and extremely low or undetectable parathormone (PTH) level. Idiopathic hypoparathyroidism is an uncommon disease and coexistence with CRF is extremely rare. As hypocalcemia and hyperphosphatemia are present in both diseases, diagnosis of hypoparathyroidism may be overlooked in a patient with CRF.1,2 Hashimoto thyroiditis is an immunologic disease characterized with presence of antithyroid antibodies. It is familiar and may be seen together with other autoimmune diseases like idiopathic hypoparathyroidism, pernicious anemia, adrenocortical insufficiency, myasthenia gravis and vitiligo. Female/male ratio is 4:1. Circulating thyroid hormone level is frequently found normal or low.4 To the best of our knowledge, there is not a case of chronic renal failure, hypoparathyroidism and hashimoto thyroiditis
Address correspondence to Yasemin Soyoral, MD, Medical Faculty, Department of Internal Medicine, Division of Nephrology, Yuzuncu Yil University, Van, Turkey. Tel: +90 432-2150474; Fax: +90 432 2168352; E-mail: [email protected]
Received 24 July 2013 Revised 31 October 2013 Accepted 10 November 2013 Published online 27 January 2014
coexistence in literature published in English. Herein we reported a rare coexistence of end-stage renal disease, idiopathic hypoparathyroidism and hashimoto thyroiditis.
Case report A 19-year-old female patient who had been receiving hemodialysis in another institution for 3 years because of end-stage renal failure with unknown etiology was hospitalized for further evaluation as she was detected to have hypocalcemia and disproportionately low PTH level on examination during her admission to nephrology outpatient clinic for control. On her family history, her parents have consanguinity, the patient’s twin sister is healthy and her father is hypertensive. The patient had been using Ca carbonate 3 500 mg/day, folic acid 5 mg/day, metoprolol 25 mg/day, darbepoetin 40 mcg/week and carnitine 3 g/week. Her blood pressure was 135/90 mmHg, heart rate was 90/ min, height was 148 cm, weight was 45.5 kg and body mass index was 20.8 kg/m2. Trousseau finding was positive. Her cognitive and mental functions were normal. She did not have any phenotypic findings except for urochromia. Laboratory findings were as follows during hospitalization in our clinic: Blood urea nitrogen: 42 mg/dL (normal range: 0–50 mg/dL), urea: 91 mg/dL (normal range: 0–50 mg/ dL), creatinine (Cr): 7.5 mg/dL (normal range: 0.7–1.3 mg/ dL), corrected Ca: 6.9 mg/dL (normal range: 8.8–10.2 mg/dL), phosphorus (P): 4.4 mg/dL (normal range: 2.7–4.5 mg/dL), albumin: 3.81 g/dL (normal range: 3.5–5.2 g/dL), PTH: 29.8 pg/mL (normal range: 15–68.3 pg/mL), iron (Fe): 38 mcg/dL
20 14
Introduction
History
442
S. Yildiz et al.
(normal range: 37–145 mcg/dL), total iron binding capacity: 228 mcg/dL (normal range: 112–346 mcg/dL), ferritin: 572 ng/mL (normal range: 12–150 ng/mL), vitamin B12: 500 pg/mL (normal range: 150–980 pg/mL), luteinizing hormone: 3.1 mIU/mL (normal range: 2.39–6.60 mIU/mL), follicle stimulating hormone: 5.7 mIU/mL (normal range: 3.03–8.08 mIU/mL), estradiol: 43 pg/mL (normal range: 21–251 pg/mL), prolactin: 23 ng/mL (normal range: 3.4– 19.4 ng/mL), dehydroepiandrosterone sulfate: 25 mg/dL (normal range: 61–493 mg/dL), cortisol: 9.9 mg/dL, (normal range: 3.7–19.4 mg/dL), free T4: 1.22 ng/dL (normal range: 0.7–1.8 ng/dL), thyroid stimulating hormone (TSH): 3.67 mIU/ mL (normal range: 0.35–4.94 mIU/mL), thyroid antimicrosomal antibody: 19 IU/mL (0–5.6 IU/mL), antithyroglobulin antibody: 19 IU/mL (0–4.11 IU/mL). Thyroid was detected to be heterogeneous on thyroid ultrasonography. The patient was examined in terms of autoimmune polyglandular syndrome as she was decided to have hypoparathyroidism because of disproportionately low PTH response to hypocalcemia. Candida was negative on oral smear. Blood Extractable Nuclear Antigen Antibodies panel and tissue transglutaminase IgA studied for polyglandular endocrinopathy were found negative. Adrenal insufficiency was not detected in adrenocorticotropic hormone test. Audiogram that was performed for prediagnosis of HDR syndrome composed of hypoparathyroidism, deafness and renal disorder was normal in the patient whose mental functions were normal. The 3 years earlier medical records of the patient were reevaluated. It was found that she had applied to emergency with complaints of swelling in hands and feet, contraction and paresthesia in the hands and dyspnea, to be hospitalized with diagnosis of renal failure and her complaints were learned to begin 2–3 months before hospitalization. In her first hospitalization, laboratory findings were as follows: hemoglobin: 5.1 g/dL (normal range: 8.5–11.0 g/dL), MCV: 73 fl (normal range: 80–100 fl), blood cell count: 9.7 103/dL (normal range: 3.5–11.0 103/dL), urea: 215 mg/dL, Cr: 6.4 mg/dL, corrected Ca: 3.8 mg/dL, P: 10.2 mg/dL, magnesium (Mg): 3.8 mg/dL (normal range: 1.58–2.55 mg/dL), albumin: 2.3 g/ dL, PTH: 127 pg/mL, TSH: 5.3 mIU/mL, fT4: 0.8 ng/dL, venous blood gas pH: 7.30, pCO2: 32 and HCO3: 15.4. The patient’s renal ultrasonography was detected to be consistent with CRF and she had immediately undergone hemodialysis. When her electrocardiogram taken in that period was re-evaluated, corrected QT time was 0.59 s and supported hypocalcemia. The patient had been administered IV Ca and phosphate binding treatment including oral Ca and antihypertensive treatment besides hemodialysis performed using dialysate including 1.75 mmol/L Ca. The patient whose general condition improved had been discharged and recommended to receive hemodialysis three times a week. After evaluating her first admission at emergency and her 3 years later hospitalization, she had been diagnosed as idiopathic hypoparathyroidism and hashimoto thyroiditis. She was discharged with treatment of phosphate binding treatment including Ca and calcitriol. The patient who came
Ren Fail, 2014; 36(3): 441–443
for control did not have any complaints, her physical examination was normal and Ca: 8.4 mg/dL, albumin: 4.1 g/ dL, P: 3.95 mg/dL, PTH: 33.4 pg/mL, fT4: 1.2 ng/dL and TSH: 3.6 mIU/mL.
Discussion Hypoparathyroidism may be surgical, autoimmune, familial or idiopathic. The most characteristic biochemical features of hypoparathyroidism are hypocalcemia, hyperphosphatemia and extremely low or undetectable PTH level. The most common cause of hypoparathyroidism is operations of cervical region leading to removal or injury of parathyroid glands.1 She did not have any cervical operations. Hypoparathyroidism has familial forms with autosomal recessive or dominant inheritance.1 She does not have a history suggesting familial hypoparathyroidism and her clinical findings are not consistent with these diagnosis. Hypoparathyroidism may be seen in Kearns–Sayre syndrome characterized with ophthalmoplegia, mitochondrial dysfunction, myopathy and pigmentary retinopathy or MELAS syndrome characterized with mitochondrial encephalopathy, lactic acidosis in stroke like episodes.5 In addition, hypoparathyroidism may be seen because of Fe or copper deposition in parathyroid.1 No findings suggestive for these diagnosis were detected in our patient according to medical history, clinical and laboratory findings. Severe Mg deprivation hinders PTH release paralyzing parathyroid glands.1 Mg levels of our patient were normal. Acquired hypoparathyroidism sometimes is seen in polyglandular endocrinopathies. Type 1 polyglandular autoimmune syndrome is frequently related with primary adrenal insufficiency and mucocutaneous candidiasis and is an autosomal recessive disease. It typically emerges at ages of 5–9.1 It emerged at the age of 16 in the subject patient and neither adrenal insufficiency nor mucocutaneous candidiasis was detected. A similar form of acquired hypoparathyroidism may appear as an isolated finding. In many of patients with isolated hypoparathyroidism, there are antibodies recognizing parathyroid Ca receptor. Idiopathic (isolated) hypoparathyroidism begins at ages of 2–10, however it may be seen later also and is more common among girls.1,5 The emergence of disease in our patient occurred at the age of 16. Autoimmune hypoparathyroidism has been reported in patients who have anti Ca receptor antibodies (CaR). These antibodies suppress PTH by functionally activating CaR. These rare cases have been seen together with Addison’s disease or other autoimmune diseases like hashimoto thyroiditis as in our patient.1 Hashimoto thyroiditis is the major cause of goiter in children and young adults. It is an immunologic disease. In early stages, thyroglobulin antibody is detected to markedly elevate and TPO (thyroid peroxidase) is detected to mildly elevate. Afterwards while anti thyroglobulin decreases and disappears, anti TPO remains positive for years. Injury of the gland leads to a reduction in serum T3 (tri-iodothyronine) and free T4 levels and an increase in TSH level. Circulating thyroid hormone level is frequently detected normal or low.4 Although thyroid function tests were
DOI: 10.3109/0886022X.2013.868162
Chronic renal failure and idiopathic hypoparathyroidism
normal in our patient, the thyroid autoantibody was detected as positive. The thyroid gland was normal in size but it was ultrasonographically heterogenous that’s why she was diagnosed as Hashimoto thyroiditis. Secondary hyperparathyroidism characterized with elevated parathyroid hormone and bone disease is frequent in end-stage renal disease. In advanced chronic renal failure, parathormone levels typically increases to 5–10 times bigger than normal size, even may reach to 20–40 times a bigger size.6 The most common cause of secondary hypoparathyroidism in CRF is hyperphosphatemia and hypocalcemia. Our patient had low PTH levels (PTH: 127 pg/mL) despite very low Ca levels (corrected Ca: 3.8 mg/dL) on her first admission. Presence of hypocalcemia and hyperphosphatemia was probably attributed to CRF by overlooking inadequate elevation of PTH. Idiopathic hypoparathyroidism is a rare disease and case reports of its coexistence with CRF except HDR syndrome are quite rare. In 2005, Bednarek-Tupikowska et al.7 reported a 24-year-old male patient with hypoparathyroidism, hypothyroidism and CRF. Our patient was younger than this patient despite similarity in terms of coincidence. She had hypoparathyroidism and hashimoto thyroiditis when she began to receive dialysis and these diagnoses were overlooked as she was a dialysis patient. In conclusion, Idiopathic hypoparathyroidism should be suspected in case as absence of parathormone response to hypocalcemia in patients with chronic renal failure. It should be taken into consideration that hashimoto thyroiditis may accompany and required analysis should be done.
Declaration of interest
443
There are no conflicts of interest among all authors regarding this article.
References 1. Shoback D, Sellmeyer D, Bikle DD. Causes of hypocalcemia, hypoparathyroidism, metabolic bone disease. In: Gardner DG, Shoback D, eds. Greenspan’s Basic and Clinical Endocrinology. 9th ed. New York: McGraw Hill; 2011:254–255. 2. Sherman SS, Hollis BW, Tobin JD. Vitamin D status and related parameters in a healthy population: the effects of age, sex, and season. J Clin Endocrinol Metab. 1990;71:405–413. 3. Walker AT, Stewart AF, Korn EA, Shiratori T, Mitnick MA, Carpenter TO. Effect of parathyroid hormone-like peptides on 25-hydroxyvitamin D-1 alpha-hydroxylase activity in rodents. Am J Physiol. 1990;258:297–303. 4. Cooper DS, Ladenson PW. Thyroiditis, chronic thyroiditis, the thyroid gland. In: Gardner DG, Shoback D, eds. Greenspan’s Basic and Clinical Endocrinology. 9th ed. New York: McGraw Hill; 2011:212–213. 5. Bringhurst FR, Demay MB, Krane SM, Kronenberg HM. 331Bone and mineral metabolism in health and disease; Disorders of Bone and mineral Metabolism, Part XIV; Endocrinology and Metabolism. In: Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 16th ed. New York: McGraw Hill; 2008:2264. 6. Goodman WG. Renal osteodystrophy; Chronic renal failure. In: Lerma EV, Berns JS, Nissenson AR, eds. Current Diagnosis Treatment: Nephrology Hypertension. New York: McGraw Hill; 2009;3:171. 7. Bednarek-Tupikowska G, Kuliczkowska J, Filus A. A case of primary hypoparathyroidism and hypothyroidism co-existing with chronic renal failure. Pol Merkur Lekarski. 2005;18:433–435.
Copyright of Renal Failure is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
CASE REPORT
Coexistence of chronic renal failure, hashimoto thyroiditis and idiopathic hypoparathyroidism: a rare case report Saliha Yildiz1, Yasemin Soyoral2, Davut Demirkiran3, and Mustafa Ozturk1 1
Medical Faculty, Department of Internal Medicine, Division of Endocrinology, Yuzuncu Yil University, Van, Turkey, 2Medical Faculty, Department of Internal Medicine, Division of Nephrology, Yuzuncu Yil University, Van, Turkey, and 3Medical Faculty, Department of Internal Medicine, Yuzuncu Yil University, Van, Turkey Abstract
Keywords
Hypoparathyroidism is an uncommon disease and its coexistence with chronic renal failure is quite rare. Hypocalcemia and hyperphosphatemia are seen in both diseases. Diagnosis of hypoparathyroidism may be overlooked when parathormone response is not evaluated in patients with chronic renal failure. A 19-year-old female patient who had been receiving hemodialysis for 3 years because of chronic renal failure was diagnosed as idiopathic hypoparathyroidism and hashimoto thyroiditis. When her medical records on the first admission and medical history were evaluated, hypoparathyroidism and hashimoto thyroiditis were seen to be present also when she was started hemodialysis. Idiopathic hypoparathyroidism should be suspected in case as absence of parathormone response to hypocalcemia in patients with chronic renal failure. It should be taken into consideration that hashimoto thyroiditis may accompany and required analysis should be done.
Chronic renal failure, hemodialysis, hypocalcemia, hyperphosphatemia, idiopathic hypoparathyroidism
Hypoparathyroidism is a rare disease and secondary hyperparathyroidism is frequently seen in chronic renal failure (CRF). It has been known that respectively the most important activation factor and inhibitory factor are calcium (Ca) and calcitriol [1,25 (OH)D] in the pathogenesis of the secondary hyperparathyroidism.1–3 Hypoparathyroidism may be surgical, autoimmune, familial or idiopathic. Biochemical features of hypoparathyroidism are hypocalcemia, hyperphosphatemia and extremely low or undetectable parathormone (PTH) level. Idiopathic hypoparathyroidism is an uncommon disease and coexistence with CRF is extremely rare. As hypocalcemia and hyperphosphatemia are present in both diseases, diagnosis of hypoparathyroidism may be overlooked in a patient with CRF.1,2 Hashimoto thyroiditis is an immunologic disease characterized with presence of antithyroid antibodies. It is familiar and may be seen together with other autoimmune diseases like idiopathic hypoparathyroidism, pernicious anemia, adrenocortical insufficiency, myasthenia gravis and vitiligo. Female/male ratio is 4:1. Circulating thyroid hormone level is frequently found normal or low.4 To the best of our knowledge, there is not a case of chronic renal failure, hypoparathyroidism and hashimoto thyroiditis
Address correspondence to Yasemin Soyoral, MD, Medical Faculty, Department of Internal Medicine, Division of Nephrology, Yuzuncu Yil University, Van, Turkey. Tel: +90 432-2150474; Fax: +90 432 2168352; E-mail: [email protected]
Received 24 July 2013 Revised 31 October 2013 Accepted 10 November 2013 Published online 27 January 2014
coexistence in literature published in English. Herein we reported a rare coexistence of end-stage renal disease, idiopathic hypoparathyroidism and hashimoto thyroiditis.
Case report A 19-year-old female patient who had been receiving hemodialysis in another institution for 3 years because of end-stage renal failure with unknown etiology was hospitalized for further evaluation as she was detected to have hypocalcemia and disproportionately low PTH level on examination during her admission to nephrology outpatient clinic for control. On her family history, her parents have consanguinity, the patient’s twin sister is healthy and her father is hypertensive. The patient had been using Ca carbonate 3 500 mg/day, folic acid 5 mg/day, metoprolol 25 mg/day, darbepoetin 40 mcg/week and carnitine 3 g/week. Her blood pressure was 135/90 mmHg, heart rate was 90/ min, height was 148 cm, weight was 45.5 kg and body mass index was 20.8 kg/m2. Trousseau finding was positive. Her cognitive and mental functions were normal. She did not have any phenotypic findings except for urochromia. Laboratory findings were as follows during hospitalization in our clinic: Blood urea nitrogen: 42 mg/dL (normal range: 0–50 mg/dL), urea: 91 mg/dL (normal range: 0–50 mg/ dL), creatinine (Cr): 7.5 mg/dL (normal range: 0.7–1.3 mg/ dL), corrected Ca: 6.9 mg/dL (normal range: 8.8–10.2 mg/dL), phosphorus (P): 4.4 mg/dL (normal range: 2.7–4.5 mg/dL), albumin: 3.81 g/dL (normal range: 3.5–5.2 g/dL), PTH: 29.8 pg/mL (normal range: 15–68.3 pg/mL), iron (Fe): 38 mcg/dL
20 14
Introduction
History
442
S. Yildiz et al.
(normal range: 37–145 mcg/dL), total iron binding capacity: 228 mcg/dL (normal range: 112–346 mcg/dL), ferritin: 572 ng/mL (normal range: 12–150 ng/mL), vitamin B12: 500 pg/mL (normal range: 150–980 pg/mL), luteinizing hormone: 3.1 mIU/mL (normal range: 2.39–6.60 mIU/mL), follicle stimulating hormone: 5.7 mIU/mL (normal range: 3.03–8.08 mIU/mL), estradiol: 43 pg/mL (normal range: 21–251 pg/mL), prolactin: 23 ng/mL (normal range: 3.4– 19.4 ng/mL), dehydroepiandrosterone sulfate: 25 mg/dL (normal range: 61–493 mg/dL), cortisol: 9.9 mg/dL, (normal range: 3.7–19.4 mg/dL), free T4: 1.22 ng/dL (normal range: 0.7–1.8 ng/dL), thyroid stimulating hormone (TSH): 3.67 mIU/ mL (normal range: 0.35–4.94 mIU/mL), thyroid antimicrosomal antibody: 19 IU/mL (0–5.6 IU/mL), antithyroglobulin antibody: 19 IU/mL (0–4.11 IU/mL). Thyroid was detected to be heterogeneous on thyroid ultrasonography. The patient was examined in terms of autoimmune polyglandular syndrome as she was decided to have hypoparathyroidism because of disproportionately low PTH response to hypocalcemia. Candida was negative on oral smear. Blood Extractable Nuclear Antigen Antibodies panel and tissue transglutaminase IgA studied for polyglandular endocrinopathy were found negative. Adrenal insufficiency was not detected in adrenocorticotropic hormone test. Audiogram that was performed for prediagnosis of HDR syndrome composed of hypoparathyroidism, deafness and renal disorder was normal in the patient whose mental functions were normal. The 3 years earlier medical records of the patient were reevaluated. It was found that she had applied to emergency with complaints of swelling in hands and feet, contraction and paresthesia in the hands and dyspnea, to be hospitalized with diagnosis of renal failure and her complaints were learned to begin 2–3 months before hospitalization. In her first hospitalization, laboratory findings were as follows: hemoglobin: 5.1 g/dL (normal range: 8.5–11.0 g/dL), MCV: 73 fl (normal range: 80–100 fl), blood cell count: 9.7 103/dL (normal range: 3.5–11.0 103/dL), urea: 215 mg/dL, Cr: 6.4 mg/dL, corrected Ca: 3.8 mg/dL, P: 10.2 mg/dL, magnesium (Mg): 3.8 mg/dL (normal range: 1.58–2.55 mg/dL), albumin: 2.3 g/ dL, PTH: 127 pg/mL, TSH: 5.3 mIU/mL, fT4: 0.8 ng/dL, venous blood gas pH: 7.30, pCO2: 32 and HCO3: 15.4. The patient’s renal ultrasonography was detected to be consistent with CRF and she had immediately undergone hemodialysis. When her electrocardiogram taken in that period was re-evaluated, corrected QT time was 0.59 s and supported hypocalcemia. The patient had been administered IV Ca and phosphate binding treatment including oral Ca and antihypertensive treatment besides hemodialysis performed using dialysate including 1.75 mmol/L Ca. The patient whose general condition improved had been discharged and recommended to receive hemodialysis three times a week. After evaluating her first admission at emergency and her 3 years later hospitalization, she had been diagnosed as idiopathic hypoparathyroidism and hashimoto thyroiditis. She was discharged with treatment of phosphate binding treatment including Ca and calcitriol. The patient who came
Ren Fail, 2014; 36(3): 441–443
for control did not have any complaints, her physical examination was normal and Ca: 8.4 mg/dL, albumin: 4.1 g/ dL, P: 3.95 mg/dL, PTH: 33.4 pg/mL, fT4: 1.2 ng/dL and TSH: 3.6 mIU/mL.
Discussion Hypoparathyroidism may be surgical, autoimmune, familial or idiopathic. The most characteristic biochemical features of hypoparathyroidism are hypocalcemia, hyperphosphatemia and extremely low or undetectable PTH level. The most common cause of hypoparathyroidism is operations of cervical region leading to removal or injury of parathyroid glands.1 She did not have any cervical operations. Hypoparathyroidism has familial forms with autosomal recessive or dominant inheritance.1 She does not have a history suggesting familial hypoparathyroidism and her clinical findings are not consistent with these diagnosis. Hypoparathyroidism may be seen in Kearns–Sayre syndrome characterized with ophthalmoplegia, mitochondrial dysfunction, myopathy and pigmentary retinopathy or MELAS syndrome characterized with mitochondrial encephalopathy, lactic acidosis in stroke like episodes.5 In addition, hypoparathyroidism may be seen because of Fe or copper deposition in parathyroid.1 No findings suggestive for these diagnosis were detected in our patient according to medical history, clinical and laboratory findings. Severe Mg deprivation hinders PTH release paralyzing parathyroid glands.1 Mg levels of our patient were normal. Acquired hypoparathyroidism sometimes is seen in polyglandular endocrinopathies. Type 1 polyglandular autoimmune syndrome is frequently related with primary adrenal insufficiency and mucocutaneous candidiasis and is an autosomal recessive disease. It typically emerges at ages of 5–9.1 It emerged at the age of 16 in the subject patient and neither adrenal insufficiency nor mucocutaneous candidiasis was detected. A similar form of acquired hypoparathyroidism may appear as an isolated finding. In many of patients with isolated hypoparathyroidism, there are antibodies recognizing parathyroid Ca receptor. Idiopathic (isolated) hypoparathyroidism begins at ages of 2–10, however it may be seen later also and is more common among girls.1,5 The emergence of disease in our patient occurred at the age of 16. Autoimmune hypoparathyroidism has been reported in patients who have anti Ca receptor antibodies (CaR). These antibodies suppress PTH by functionally activating CaR. These rare cases have been seen together with Addison’s disease or other autoimmune diseases like hashimoto thyroiditis as in our patient.1 Hashimoto thyroiditis is the major cause of goiter in children and young adults. It is an immunologic disease. In early stages, thyroglobulin antibody is detected to markedly elevate and TPO (thyroid peroxidase) is detected to mildly elevate. Afterwards while anti thyroglobulin decreases and disappears, anti TPO remains positive for years. Injury of the gland leads to a reduction in serum T3 (tri-iodothyronine) and free T4 levels and an increase in TSH level. Circulating thyroid hormone level is frequently detected normal or low.4 Although thyroid function tests were
DOI: 10.3109/0886022X.2013.868162
Chronic renal failure and idiopathic hypoparathyroidism
normal in our patient, the thyroid autoantibody was detected as positive. The thyroid gland was normal in size but it was ultrasonographically heterogenous that’s why she was diagnosed as Hashimoto thyroiditis. Secondary hyperparathyroidism characterized with elevated parathyroid hormone and bone disease is frequent in end-stage renal disease. In advanced chronic renal failure, parathormone levels typically increases to 5–10 times bigger than normal size, even may reach to 20–40 times a bigger size.6 The most common cause of secondary hypoparathyroidism in CRF is hyperphosphatemia and hypocalcemia. Our patient had low PTH levels (PTH: 127 pg/mL) despite very low Ca levels (corrected Ca: 3.8 mg/dL) on her first admission. Presence of hypocalcemia and hyperphosphatemia was probably attributed to CRF by overlooking inadequate elevation of PTH. Idiopathic hypoparathyroidism is a rare disease and case reports of its coexistence with CRF except HDR syndrome are quite rare. In 2005, Bednarek-Tupikowska et al.7 reported a 24-year-old male patient with hypoparathyroidism, hypothyroidism and CRF. Our patient was younger than this patient despite similarity in terms of coincidence. She had hypoparathyroidism and hashimoto thyroiditis when she began to receive dialysis and these diagnoses were overlooked as she was a dialysis patient. In conclusion, Idiopathic hypoparathyroidism should be suspected in case as absence of parathormone response to hypocalcemia in patients with chronic renal failure. It should be taken into consideration that hashimoto thyroiditis may accompany and required analysis should be done.
Declaration of interest
443
There are no conflicts of interest among all authors regarding this article.
References 1. Shoback D, Sellmeyer D, Bikle DD. Causes of hypocalcemia, hypoparathyroidism, metabolic bone disease. In: Gardner DG, Shoback D, eds. Greenspan’s Basic and Clinical Endocrinology. 9th ed. New York: McGraw Hill; 2011:254–255. 2. Sherman SS, Hollis BW, Tobin JD. Vitamin D status and related parameters in a healthy population: the effects of age, sex, and season. J Clin Endocrinol Metab. 1990;71:405–413. 3. Walker AT, Stewart AF, Korn EA, Shiratori T, Mitnick MA, Carpenter TO. Effect of parathyroid hormone-like peptides on 25-hydroxyvitamin D-1 alpha-hydroxylase activity in rodents. Am J Physiol. 1990;258:297–303. 4. Cooper DS, Ladenson PW. Thyroiditis, chronic thyroiditis, the thyroid gland. In: Gardner DG, Shoback D, eds. Greenspan’s Basic and Clinical Endocrinology. 9th ed. New York: McGraw Hill; 2011:212–213. 5. Bringhurst FR, Demay MB, Krane SM, Kronenberg HM. 331Bone and mineral metabolism in health and disease; Disorders of Bone and mineral Metabolism, Part XIV; Endocrinology and Metabolism. In: Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 16th ed. New York: McGraw Hill; 2008:2264. 6. Goodman WG. Renal osteodystrophy; Chronic renal failure. In: Lerma EV, Berns JS, Nissenson AR, eds. Current Diagnosis Treatment: Nephrology Hypertension. New York: McGraw Hill; 2009;3:171. 7. Bednarek-Tupikowska G, Kuliczkowska J, Filus A. A case of primary hypoparathyroidism and hypothyroidism co-existing with chronic renal failure. Pol Merkur Lekarski. 2005;18:433–435.
Copyright of Renal Failure is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
