Journal of Integrative Nephrology and Andrology

: 2015  |  Volume : 2  |  Issue : 3  |  Page : 93--95

Chronic Kidney Disease Caused by Hypothyroidism

Zhenhua Li, Yi Wang 
 Department of Nephrology, Yueyang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China

Correspondence Address:
Yi Wang
Department of Nephrology, Yueyang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai


Primary hypothyroidism refers to a systemic hypometabolic status due to hypothyroxinemia or thyroid hormone resistance caused by pathologic changes to the thyroid gland. The main role of thyroid hormone is to promote energy metabolism and facilitate growth and development processes within the body. In a hypothyroidism state caused by thyroid hormone deficiency, the body«SQ»s thermogenic effect is down-regulated and metabolisms of protein, sugar, and fat were slowed down, which might further lead to cardiovascular disease, hyperlipidemia, myocardial damage and myxedema, as well as other changes. Hypothyroidism tends to be neglected or misdiagnosed due to its trivial and nonspecific clinical manifestations, and a combined renal dysfunction is rarely reported. Herein a case of kidney dysfunction caused by hypothyroidism is reported and relevant literature was reviewed.

How to cite this article:
Li Z, Wang Y. Chronic Kidney Disease Caused by Hypothyroidism.J Integr Nephrol Androl 2015;2:93-95

How to cite this URL:
Li Z, Wang Y. Chronic Kidney Disease Caused by Hypothyroidism. J Integr Nephrol Androl [serial online] 2015 [cited 2020 Jul 5 ];2:93-95
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Full Text

 Patient Introduction

The patient is a 75-year-old female complaining of "swollen eyelids with edema in the lower extremities for 3 months." She came to the outpatient clinic of the authors' unit on October 17, 2014. The patient was found with urinary protein (+) and urine red blood cells (+)/HP during the routine examination on July 2014, after which she experienced gradual swelling of the face, the eyelids, and lower extremities. She was then admitted to a local hospital on September 8 and results of renal function tests were as follows: Creatinine 106 μmol/L, 24 h urine protein 0.18 g, urine β2-microglobulin: 0.08 μg/mL (normal: <0.2 μg/mL), urine glucosaminidase: 2.5 U/L (normal: 0.3-12 U/L), retinol binding protein: 0.24 mg/L (normal: <0.7 mg/L), urinary albumin: 52 mg/L (normal: 0-20 mg/L), urinary transferrin: 3.6 mg/L (normal: <2.2 mg/L); cardiac enzymes: creatine kinase: 220 U/L (normal: 20-140 U/L), CK-MB: 16 U/L (normal: 0-25 U/L), aspartate aminotransferase: 46 U/L (normal: 8-40 U/L), lactate dehydrogenase: 248 U/L (normal: 104-245 U/L), α-hydroxybutyrate dehydrogenase: 211 U/L (normal: 110-220 U/L), BNP: 106 pg/mL. Electrocardiogram showed sinus rhythm (64 beats/min) with ST-T change while echocardiography showed left atrial enlargement, left ventricular wall thickening, mild mitral regurgitation, mild aortic regurgitation, impaired left ventricular diastolic function, and pericardial effusion; kidney emission computed tomography examination revealed filtration rates of left kidney of 41.09 mL/min and right kidney of 45.63 mL/min; renal ultrasound detected calculi in the right kidney; no abnormalities were found in blood test, liver function, electrolytes, coagulation function, viral hepatitis antibodies, tumor markers, and urine immunoprotein electrophoresis, as well as antinuclear antibody, extractable nuclear antigen, anti-neutrophil cytoplasmic antibody titers. The diagnosis of "chronic kidney disease stage 2" was made by local hospital and Shenkang (injection), olmesartan, Shenshuaining, Haikunshenxi, and Bailing capsules were prescribed. The patient continued taking olmesartan, Shenshuaining, and Bailing after discharge for 2 months and experienced no improvements in eyelids and lower extremity swelling, as well as other symptoms. The patient then came to the integrative medicine outpatient clinic of the authors' unit. Since the onset, the patient complained of fever before "catching cold" in January with the temperature between 37.5°C and 37.8°C. No cough, expectoration, abdominal pain, diarrhea, urinary urgency or dysuria was present. The patient also complained of intolerance of cold, edema of the eyelids and lower limbs, lassitude, and lack of appetite, she had normal bowel movements and satisfactory sleep at night.

Past history

The patient had a history of hypertension for more than 10 years with the highest blood pressure of 180/90 mmHg, her current medication was olmesartan (1 # bid) and satisfactory control was not achieved.

Physical examination

Patient had a temperature of 36.8°C, respiratory rate of 16 beats/min, pulse of 62 beats/min and blood pressure of 160/90 mmHg. The patient was mildly lethargic and was oriented to person, place, and time. She appeared pale with mild edema on the face. No enlargement was found in the thyroid gland. Bilateral breath sounds were clear with no rales or rhonchi. The heart beats were regular without pathological murmurs. Abdominal examinations revealed no remarkable findings. Percussion pain was not present on both kidneys and palmar erythema was not seen. Notably, mild nonpitting edema was found in the lower extremities. Neurological examinations revealed no remarkable findings.

The patient had undergone extensive examinations to rule out hematuria and proteinuria secondary to other relevant diseases, and hence we only ordered follow-up tests, including complete blood count (CBC), liver and kidney function, electrolytes, urinalysis, 24 h urine protein excretion and renal ultrasound, as well as thyroid hormone tests to rule out hypothyroidism. Results of these tests were as follows: Urine protein (−), urine RBC (+)/HP, leukocytes 2-4 cells/HP; blood urea nitrogen (BUN): 6.7 mmol/L (normal: 2.5-6.5 mmol/L), creatinine (SCr): 112 μmol/L (normal: 36-125 μmol/L), uric acid (UA) 406 μmol/L (normal: 149-416 μmol/L); 24 h urine protein: 0.15 g/24 h, thyroid hormones: T3: 0.54 nmol/L, FT3: 1.65 pmol/L, T4: 3.80 nmol/L, FT4: 4.74 pmol/L, thyroid-stimulating hormone (TSH):> 150 mIU/L. Liver function, CBC, and electrolyte tests revealed normal findings. Bilateral renal ultrasonography showed that the right kidney was 88 mm × 40 mm in size and the left one was 91 mm × 45 mm in size. The endocrinology department was consulted considering the patient's proteinuria and hematuria might be due to thyroid dysfunction. Patient was recommended to discontinue all other medications except olmesartan. After consultation, oral euthyrox (50 μg, once daily) was given and patient was asked to come back for follow-up 1-month later to recheck the thyroid function and related antibodies.

At the telephone follow-up 2 weeks later, patient reported significantly improved symptoms. The kidney function was re-examined on November 11, 2014 in the other hospital and results were as follows: BUN: 16.43 mg/dL (5.87 mmol/L), SCr: 1.13 mg/dL (99.89 μmol/L), UA: 263 μmol/L, CysC: 1.12 mg/L. Levels of glucose, lipids, liver enzymes and C-reactive protein were normal. During endocrinology follow-up on November 24, 2014 at the authors' unit, the patient reported significant improvements of fatigue and anorexia, the facial and lower extremity edema was completely dissipated. Thyroid functions were re-examined and results were: T3: 1.04 nmol/L, FT3: 3.94 pmol/L, T4: 132.80 nmol/L, FT4: 19.18 pmol/L, TSH: 24.21 mIU/L, thyroid peroxidase-antibody (Ab): 2.3 IU/mL, thyroid receptor-Ab: 21.454 IU/mL and thyroglobulin-Ab: 3.36 IU/mL. Euthyrox was continued at an increased dose of 75 μg for once daily. Review of thyroid function on January 15, 2015 in our hospital showed improved results: T3: 1.0 nmol/L, FT3: 3.47 pmol/L, T4: 168.6 nmol/L, FT4: 25.47 pmol/L and TSH: 4.586 mIU/L. Other tests done on January 26, 2015 at Renji Hospital revealed normal liver function, fasting glucose, lipids, electrolytes, CBC, and urinalysis results. Renal function test results were as follows: BUN: 5.6 mmol/L (normal: 2.9-8.2 mmol/L), SCr: 80.5 μmol/L (normal: 45-105 μmol/L), UA: 425 μmol/L (normal: 155-428 μmol/L) and 24 h urine protein excretion: 59.5 mg/24 h.

Multiple systems, including the kidneys, are often involved in the pathophysiology of thyroid diseases. Thyroid dysfunction, or hypothyroidism could hamper renal functions predominantly in the aspects of hemodynamic changes, tubular dysfunction, and bone metabolism disorders. [1] Possible mechanisms leading to impaired renal function were:

Significantly reduced systemic metabolism due to thyroid hormone deficiency resulting in organ dysfunction, reduced protein synthesis, weakened muscle contraction and myxedema caused by increased interstitial mucin accumulation, and water trapping. Sodium retention and increased capillary permeability would further lead to hypovolemia.Deposition of mucopolysaccharides in patients with hypothyroidism and/or glomerular and tubular basement membrane thickening due to autoimmune injuries. In addition, endothelial cell proliferation and increased tubular epithelial cell cytoplasm content may restrict blood flow and cause renal vasoconstriction, thus reducing glomerular filtration rate (GFR) and renal plasma flow (RPF) (effective RPF). Damage to the glomerulus is more prominent than to the tubules.Hypovolemia in hypothyroidism may reduce plasma atrial natriuretic peptide release and reduce GFR.Myocardial myxedema in hypothyroidism may hamper the contractility of the heart resulting in bradycardia and decreased cardiac output.Patients with hypothyroidism often have elevated blood lipids, which may exacerbate the atherosclerotic change in blood vessels resulting in increased vascular resistance. [2]

Hypothyroidism is sometimes overlooked or misdiagnosed due to its nonspecific manifestations. The increased glomerular capillary pressure and subsequent filtration membrane damage in patients with hypothyroidism may lead to proteinuria due to leakage of plasma proteins; Patients with chronic renal failure or hypothyroidism may have normocytic and normochromic anemia, which is associated with low erythropoietin (EPO) levels. The lower basal metabolic rate in patients with hypothyroidism and subsequently decreased utility of oxygen may result in increased oxygen saturation and decreased EPO level. In addition, chronic renal failure may further impair EPO production. Therefore, patients with hypothyroidism often have elevated SCr and UA, dropped CCr level, kidney dysfunction, proteinuria, edema, and anemia, who are predisposed to be misdiagnosed as nephritis.

Thyroid hormone deficiency during hypothyroidism can lead to kidney damage in various ways, and the damage tend to be aggravated with the increased severity of hypothyroidism, which could eventually progress to renal fibrosis and renal failure. [3] Symptoms such as edema and renal dysfunction in severe primary hypothyroidism resembles closely to those seen in end-stage primary chronic glomerulonephritis. Meanwhile, hypothyroidism usually leads to functional renal failure, which could be reversed by thyroid hormone replacement therapy. [4]

Kidney damage caused by hypothyroidism usually present as proteinuria and microscopic hematuria, although nephrotic syndrome has also been reported, [5] some of which may progress to uncompensated renal dysfunction. In summary, hypothyroidism can lead to renal damage in many forms. Patients with unexplained proteinuria, hematuria, edema, and renal dysfunction should raise the suspicion of physicians to the diagnosis of hypothyroidism, so that appropriate diagnosis and treatment could be achieved.


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