Kidney damage in hyperthyroidism

Introduction to kidney damage in hyperthyroidism Hyperthyroidism (hyperthyroidism) refers to a clinical syndrome caused by increased levels of thyroid hormones in the blood circulation caused by various causes. Clinically characterized by high metabolic syndrome, thyroid enlargement, exophthalmia, neurological and cardiovascular system disorders, pathologically thyroid gland can be diffuse, nodular or mixed swelling, thyroid hormone levels in the blood circulation Increases can lead to a series of changes in the kidneys. There are mainly renal vasodilation, renal plasma flow, glomerular filtration rate, renal tubular resorption rate and excretion ability. At the same time, due to the increase of renal medullary blood flow, the decrease of medullary solute concentration reduces the osmotic pressure, resulting in impaired renal tubular concentrating function. Hyperthyroidism due to increased bone breakdown, moderate hypercalcemia can occur and kidney disease or even renal insufficiency, a small number of patients with renal tubular acidosis. basic knowledge The proportion of illness: 0.0006% Susceptible people: no special people Mode of infection: non-infectious Complications: nephrotic syndrome, hyperthyroidism, sinus tachycardia, atrial flutter, atrioventricular block, ventricular premature contraction, periodic paralysis, periodic hypospadias, myasthenia gravis, hypokalemia, diarrhea, nausea and vomiting Dehydration pulmonary edema heart failure electrolyte disorder

Causes of renal damage in hyperthyroidism

Immunity factor (35%):

In 1956, Adams et al found that long-acting thyroid stimulating hormone (LATS) acts similarly to TSH. It is an immunoglobulin (IgG) produced by B lymphocytes, an autoantibody against the thyroid gland, and can be associated with thyroid subcellular cells. In combination with ingredients, excitatory thyroid follicles secrete thyroid hormone and cause hyperthyroidism. 60% to 90% of patients with hyperthyroidism have increased LATS. Later, LATS-P substance is also found to be an IgG. It is only excited by human thyroid tissue, also known as human thyroid gland. Stimulating immunoglobulin (HTSI), more than 90% of patients with hyperthyroidism are positive.

Genetic factors (35%):

Clinically, it is not uncommon to find familial Graves disease. The same twins have Graves disease up to 30% to 60%, and ectopic eggs are only 3% to 9%. Family history investigation can be affected by other types of hyperthyroidism. Thyroid diseases such as hypothyroidism, or TSI positive in family members, suggest that Graves disease has a family genetic predisposition, which may be autosomal recessive or autosomal dominant, or polygenic.

Other causes of illness (25%):

(1) hyperactive nodular goiter or adenoma: In the past, it was considered that this disease was not an autoimmune disease. Because no IgG, TSI, IATS and other immune tests were detected in the blood, a single nodule was reported in China in 1988. Serum thyroglobulin antibody and microsomal antibody were detected, the positive rate was 16.9% (62/383), and the multiple nodule positive rate was 54.7% (104/190). The hyperplastic thyroid tissue in these nodules was not regulated by TSI. It has become a hyperactive or hyperactive thyroid nodule or adenoma. Currently, the incidence of thyroid adenoma and cancer is also caused by tumor genes.

(2) increased secretion of TSH in pituitary tumors, causing pituitary hyperthyroidism: such as hyperthyroidism associated with TSH secretory tumor or acromegaly.

(3) subacute thyroiditis, chronic lymphocytic thyroiditis, painless thyroiditis, etc. can be associated with hyperthyroidism.

(4) Hyperthyroidism caused by hyperthyroidism, known as iodine thyroid: such as thyroid gland patients with excessive iodine, taking thyroid tablets or excessive levothyroxine sodium (L-T4) can cause hyperthyroidism, a small number of patients taking amiodarone Ketone drugs can also cause hyperthyroidism.

(5) ectopic endocrine tumors can cause hyperthyroidism: such as ovarian tumors, choriocarcinoma, digestive system tumors, respiratory tumors and breast cancer and other secretory thyroid stimulating hormone can cause clinical hyperthyroidism.

(6) Albright syndrome: clinical manifestations of multiple fibrous dysplasia, skin pigmentation, elevated blood AKP, may be associated with hyperthyroidism.

(7) familial hyperglobulinemia (TBG): can cause hyperthyroidism, the disease may be due to familial genetic defects or related to medication.

Regardless of the cause of hyperthyroidism, any kidney damage caused by elevated thyroid hormone levels that cause kidney disease is hyperthyroidism.

Pathogenesis

Hyperthyroidism (referred to as hyperthyroidism) is caused by a variety of causes of increased thyroid hormones in the blood circulation, and acts on endocrine diseases caused by systemic organs. The pathophysiological effects of excessive secretion of thyroid hormones are multifaceted, and the mechanism of action is not yet complete. To clarify that its main effects on the kidneys are:

1. Glomerular filtration rate and renal tubular resorption rate and excretion ability increased

Thyroid hormone excites myocardial sympathetic nerve, catecholamine action is enhanced; thyroid hormone has a direct effect on myocardial, promotes protein synthesis, increases Na+-K+-ATPase activity in myocardium, increases Ca2-ATPase activity in sarcoplasmic reticulum, and increases myosin ATPase activity, which increases myocardial contraction, increases cardiac output, accelerates heart rate at rest, reduces peripheral vascular resistance, and increases arterial blood pressure. It is characterized by a typical high hemodynamic cycle. Renal plasma flow, increased glomerular filtration rate, increased renal tubular reabsorption rate and excretion ability.

2. Impaired urine concentration

In hyperthyroidism, due to the increase of renal medullary blood flow, the medullary solute concentration decreased, the osmotic pressure decreased, the urine concentration function was impaired, the serum osmotic pressure was higher than normal during hyperthyroidism, and there was high blood calcium and high urinary calcium. Drink more urine, obviously thirst, due to increased heat production in the body, eating, increased water intake and gastrointestinal dysfunction can also affect water discharge, serum sodium and potassium are normal, aldosterone secretion is normal.

3. Calcium, phosphorus metabolism disorders

Thyroid hormone can excite bone and osteoblasts, leading to decalcification of bone, increase of urinary calcium and phosphorus, and normal or slightly higher blood calcium concentration. Blood AKP can be increased. In addition, the cause of elevated blood calcium may be related to Accelerated bone metastasis, enhanced PTH effect, calcitonin deficiency and increased vitamin D activity. Hyperthyroidism promotes the production of highly active vitamin D3 metabolites in the kidney, which stimulates the absorption of calcium in the gastrointestinal tract and reduces renal tubular absorption of calcium and phosphate. Salt promotes the increase of urinary phosphorus excretion. As bone absorption and formation are accelerated and absorption is strengthened, and obvious calcium and phosphorus metabolism disorders, osteoporosis can occur in patients with hyperthyroidism.

4. Renal tubular acidosis

Hyperthyroidism may be associated with distal renal tubular acidosis, which may be related to the influence of calcium deposition on renal tubular function. In addition, due to autoimmune disorders during hyperthyroidism, thyroid and tubular lesions are also caused.

Prevention of kidney damage in hyperthyroidism

In recent years, the incidence of hyperthyroidism has increased. Prevention of hyperthyroidism and disease progression can effectively control the occurrence of renal damage. The main prevention methods are:

1. Coastal areas should pay attention to iodine-containing foods in the diet. It is recommended not to use high iodine diet to prevent iodine.

2. Inland areas, especially in areas with iodine deficiency, there should be restrictions on iodine supplementation. Time should also be taken when taking thyroid tablets.

3. Regular census of physical health should be measured thyroid B ultrasound or thyroid function, to detect hyperthyroidism patients early; passively found hyperthyroidism patients, the condition has been delayed for 2 to 3 years.

4. Prevention of hyperthyroidism crisis, the serious manifestation of the disease, such as delays in treatment can often cause death; the main incentives for mental stimulation, infection, inadequate preparation before surgery, etc., should emphasize active prevention, measures have the following What time is it:

(1) Avoid mental stimulation.

(2) Prevention and control of infection as soon as possible.

(3) Do not arbitrarily stop taking drugs.

(4) Prepare for surgery or radionuclide iodine treatment.

Renal damage complications of hyperthyroidism Complications nephrotic syndrome hyperthyroidism heart disease sinus tachycardia atrial flutter atrioventricular block ventricular premature contraction periodic paralysis periodic hypotension magnesium myasthenia gravis hypokalemia diarrhea nausea and vomiting coma dehydration Pulmonary edema heart failure electrolyte disorder

The clinically relevant complications of hyperthyroidism are mainly renal tubular acidosis. Individual nephrotic syndrome has been reported. Hyperthyroidism itself may involve multiple systems. The common complications are as follows.

Hyperthyroidism

16 to 73 years old can be ill, the incidence rate of 13.4% to 21.8% of patients with hyperthyroidism, often occurs 2 to 3 years after hyperthyroidism, in addition to the typical clinical manifestations of hyperthyroidism, the electrocardiogram often has sinus tachycardia, atrial fibrillation Tremor, atrial flutter, atrioventricular block, ventricular premature contraction, myocardial injury and cardiac hypertrophy, etc., the heart enlargement can be aortic valve type, or left and right heart enlargement, heart disease can be improved after the cure of hyperthyroidism, The disease should often be differentiated from myocarditis, coronary heart disease, rheumatic heart disease and other heart enlargement diseases.

2. Hyperthyroidism periodic paralysis

This disease occurs mostly in male young adults, often mixed with hyperthyroid myopathy, hyperthyroidism with normal potassium, abnormal electromyogram, and periodic paralysis of hyperthyroidism:

(1) Blood potassium <3.5mmol/L, abnormal potassium metabolism.

(2) Abnormal potassium distribution: elevated blood sugar can shift potassium from the outside of the cell to the inside of the cell.

(3) The excitability of the central nervous system is enhanced, and the vagus nerve can promote the abnormal distribution of insulin after the increase of insulin release.

(4) Immune factors can cause IATS, LATS-P, T3 and T4 levels to increase, and thyroid hormones promote potassium levels.

(5) The hyperadrenergic state of hyperthyroidism can promote the decrease of potassium level and the occurrence of hyperthyroidism periodic paralysis. This type should be related to Bartter syndrome, familial periodic paralysis, hypomagnesemia, hyperaldosteronism. , myasthenia gravis and drug-induced hypokalemia.

3. Hyperthyroidism

The incidence accounts for 1% to 2% of hyperthyroidism. The elderly are more common, often associated with infection, trauma, surgery, childbirth, overwork, sudden withdrawal, drug reaction and other complications, resulting in hyperthyroidism, sympathetic activity. The function is strengthened and the crisis is caused. In the early stage of the crisis, the fever can reach above 39 °C, the pulse rate is 120-160 beats/min, restlessness, loss of appetite, nausea, vomiting, diarrhea, mental paralysis, sweating, lethargy, development. To half coma and coma, coma patients indicate that there is a crisis, very dangerous, elevated white blood cells, abnormal liver function, GPT, GOT, bilirubin, etc. can be elevated, may have dehydration, hypotension, electrolyte imbalance, acidosis , heart failure and pulmonary edema, serum T3, T4, FT3, FT4 can be elevated, the mortality rate is high, must be promptly rescued on the spot.

Symptoms of Kidney Damage in Hyperthyroidism Common Symptoms Angina Pectoris Eyeball Elevation Intraocular Pressure Increases Indigestion Tachycardia Heart Expands Diuretic and Inflammatory Hypoproteinemia Paralysis

1. First, there is clinical manifestation of hyperthyroidism itself.

Such as fear of heat, sweating, eating more, losing weight, palpitations, etc., basal metabolic rate (BMR) increased after hyperthyroidism, can be annoying heat, sweating, weight loss, low work efficiency, muscle wasting, fatigue, fatigue, protein metabolism negative Balance, cholesterol decline or normal, subcutaneous fat disappears, fat metabolism accelerates, hepatic glycogen and muscle glycogen decomposition increase, gluconeogenesis increases, blood sugar can increase or postprandial hyperglycemia, abnormal glucose metabolism can occur diabetes.

Thyroid hormone can promote diuretic, excretion of potassium and magnesium, so hyperthyroidism is prone to water and salt metabolism and vitamin metabolism disorders, such as hypokalemia cycle paralysis and hypomagnesemia, due to thyroid hormone excitatory myocardial sympathetic nerve, enhance catecholamine action, patients Can occur tachycardia, arrhythmia, increased heart sounds, increased pulse pressure, even heart enlargement, apical systolic murmur, elderly patients prone to atrial fibrillation, angina or even hyperthyroidism, can occur when co-occurring with coronary heart disease Heart failure.

The spirit and nervous system are prone to mental stress, such as irritability, agitation, insomnia, dizziness, irritability, irritability, multiple words, hand shaking, hyperreflexia, and hyperthyroidism and autonomic dysfunction can occur in severe cases.

Because thyroid hormone can increase bowel movements, digestive system is prone to hunger, appetite hyperactivity, increased stool frequency, dyspepsia diarrhea, nutrition and malabsorption, severe hypoproteinemia and ascites, cachexia, and even bed rest Can not afford, the elderly are more common.

Hyperthyroidism causes dysfunction of the endocrine system, the most common is the involvement of gonadal function, female amenorrhea and irregular menstruation, male impotence, but female pregnancy is not affected, care should be taken to prevent hyperthyroidism and heart failure during childbirth.

In addition, the eyeball is prominent (exceeding 16mm is the protruding eye). In severe cases, the upper and lower jaws can not be closed, the eyeball regulation is poor, the convergence of the radiation is dysregulated, the sympathetic nerve activity is hyperthyroidism, the eyelid is widened and the gaze is widened, and the intraocular pressure is suppressed during the malignant eye. Increased, can cause corneal ulcers, perforation, conjunctival congestion, edema and even blindness.

In severe cases, hyperthyroidism can occur; multiple anemia, stomach disease, high blood pressure, high blood fat, hyperviscosity and immune dysfunction.

2. Clinical manifestations of kidney damage

Hyperthyroidism due to excessive secretion of thyroid hormone caused by hyperthyroidism increased, renal tubular reabsorption rate and excretion capacity increased, renal medullary blood flow increased, medullary solute concentration decreased, osmotic pressure decreased, urine concentration function was affected Loss, patients may appear more polydipsia, obvious thirst, may have mild proteinuria, may be related to increased renal blood flow, there are reports of patients with nephrotic syndrome, renal dysfunction may have corresponding clinical manifestations, a small number Patients can be complicated with renal tubular acidosis.

Examination of renal damage in hyperthyroidism

1. Basal metabolic rate (BMR) determination

Hyperthyroidism increased by >15%, parallel with the onset of hyperthyroidism, can be measured by instrument or calculated by calculation method, the formula: quiet pulse + pulse pressure -111-BMR%.

2. Blood cholesterol is reduced

<150 mg/L (3.9 mmol/L).

3.24h increased muscle uric acid

>100mg/L (760mmol/L), intramuscular creatine phosphokinase (CRK), lactate dehydrogenase (LDH), aspartate aminotransferase (SGOT) increased.

4. Peripheral blood cell elevation

White blood cells should be >4.5×109/L, and neutral polynuclear leukocytes should be >50%. Antithyroid drugs can be used.

5. The rate of thyroid uptake 131I is increased, females are 9% to 55% at 6h, males are 9% to 50%, 24h is 20% to 45%, and 3h is 59, 6% to 25%. This experiment is subject to many drugs and The effect of foods containing iodine, so these factors should be avoided 2 to 3 weeks before the inspection.

6. Plasma protein-bound iodine (PRI) normal value is 0.3 ~ 0.63pmol / L, hyperthyroidism increased, > 0.63pmol / L.

7. Thyroid hormone

T3 normal value is 950 ~ 205ng / L, T4 normal value is 60 ~ 14.8g / L, resin uptake ratio (RUR) is 0.8 ~ 1.1, free T4 index (FT4I) is 9.6 ~ 16.3, FT3I 6.0 ~ 11.4pmol / L, FT4 For (32.5±6.0) pmol/L, hyperthyroidism increased, rT3 normal value was 0.2-0.8 nmol/L, hyperthyroidism also increased, and sometimes changed earlier than T3 and T4.

8.TSH radioimmunoassay

The normal value is 3 to 10 mU/L, and the pituitary hyperthyroidism is elevated. Generally, the hyperthyroidism TSH is at a normal level or decreased.

9.T3 inhibition test

It is used to identify the property of 131I increase in thyroid gland. The method is to measure the 131I value first, then take T3 60g/d (3 times/d) orally, and then measure the 131I rate after 6 days. Compare the results and also take oral thyroxine tablets. 60mg, 3 times / d, after 13 days, the 131I value was measured again. The results showed that in normal people and simple goiter, the 131I inhibition rate of T3 inhibition test was >50%, and the inhibition rate of hyperthyroidism was <50%, or no inhibition. In the experiment, malignant exophthalmos are not inhibited. It is not advisable to treat this patient with arrhythmia in elderly patients with hyperthyroidism and coronary heart disease because it can cause arrhythmia.

10.TRH (thyroid stimulating hormone releasing hormone)

T3, T4 increased in hyperthyroidism, feedback inhibited TRH, stimulated TSH secretion, so after intravenous injection of TRH 300mg, the pituitary still does not secrete TSH or rarely secretes TSH, the TSH of hyperthyroidism patients does not increase, and the level of TSH in patients with hypothyroidism increases.

11. Thyroid antibody test

Clinically, thyroglobulin antibody (TGA), thyroid microsomal antibody (TMA) and other antibodies such as antinuclear antibody (ANA), anti-smooth muscle antibody (SMA), anti-mitochondrial antibody (AMA), anti-myocardial antibody (CMA) are commonly used. >90% of patients with hyperthyroidism, such as anti-parietal cell antibody (PCA), thyroid stimulating antibody (TSAb) or thyroid-stimulated immunoglobulin (TSI), may be positive.

12. Urine check

Conventional urine tests showed proteinuria, increased urinary calcium, phosphorus, decreased urine concentration, and high blood calcium and renal tubular acidosis.

13. Thyroid scanning and radionuclide computed tomography imaging examination

Can understand the thyroid enlargement, single nodules or multiple nodules, thyroid metabolic function, meaningful for differential diagnosis.

14.B-ultrasound

The extent and nature of thyroid enlargement, single nodules or multiple nodules can be found.

15. Tendon reflection relaxation time

Commonly used Achilles tendon reflex, normal person Achilles tendon reflex relaxation time 250 ~ 3380ms, about 40% hyperthyroidism patients < 240ms (measured by instrument), can be used for the auxiliary diagnosis of hyperthyroidism and follow-up observation after treatment.

Diagnosis and diagnosis of renal damage in hyperthyroidism

Diagnostic criteria

The diagnosis of this disease must be based on the diagnosis of hyperthyroidism, such as the clinical manifestations of the above-mentioned kidney damage and clear laboratory tests, should consider the kidney disease caused by hyperthyroidism.

Diagnosis of hyperthyroidism: According to the clinical manifestations of hypermetabolism and the typical signs and laboratory examination of diffuse thyroid enlargement, the serum thyroid stimulating hormone (TSH) is reduced, serum total thyroxine (TT4), total triiodide Thyroprotinin (TT3), serum free triiodothyronine (FT3) and serum free thyroxine (FT4) can be diagnosed, thyroid stimulating antibody (TS-Ab) positive or TSH affected Positive antibody (TR-Ab) can further confirm that the disease is autoimmune thyroid hyperthyroidism (Graves disease). Because Graves disease is a kind of autoimmune thyroid disease, thyroid peroxidase antibody can also occur at the same time. (TPO-Ab) positive, thyroglobulin antibody (TG-Ab) positive.

A small number of patients with TSH decreased, FT4 was normal, but serum free triiodothyronine (FT3) increased, can be diagnosed as T3 type hyperthyroidism, total thyroxine (TT4) and total triiodothyronine (TT3) due to The effect of thyroid hormone-binding globulin levels is second to FT4 and FT3 in the diagnosis of hyperthyroidism.

131I uptake rate: 24h uptake rate increased, peak intake was advanced.

Differential diagnosis

Identify with some of the following diseases:

1. Identification of polyuria caused by other causes, such as diabetes insipidus, diabetes, etc.

2. Renal conditions secondary to hypercalcemia should be differentiated from other causes of hypercalcemia, such as primary hyperparathyroidism, tumors, sarcoidosis.

3. Renal tubular acidosis should also be differentiated from other causes.

4. It should also be differentiated from the disease of the kidney itself.

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