Primary hypothyroidism (hypothyroidism) due to systemic low metabolism caused by thyroid gland disease itself hypothyroxinemic or thyroid hormone resistance syndrome caused by thyroid hormone. The main function is to promote the material and energy metabolism, promote the growth and development process. When Hypothyroidism Thyroid hormone deficiency when the body. The thermal effect of sugar, fat and protein, slow metabolism caused by anemia, cardiovascular disease, hyperlipidemia, myocardial enzyme change, mucous edema. The clinical manifestation is chills, fatigue, dry, rough skin, high cholesterol, myxedema, hoarseness, bradycardia and other symptoms.
For FT3, FT4, TSH and its relationship with renal function, rarely reported in domestic literature. Recent reports of renal function in patients with primary hypothyroidism decreased. Many studies showed that patients with primary hypothyroidism BUN, Scr, UA, the positive rate of urinary protein was significantly higher than the normal control group, CCr, GFR (glomerular filtration rate) is lower than the normal control group, but the decline in renal function has nothing to do with TSH and FT4, FT3 decline is the main cause of renal dysfunction, including FT3 and CCr, GFR changes were positively correlated, and UA changes were negatively correlated.
Thyroid hormone is one of the main factors of GFR. FT3 is the activated form of thyroid hormones play a physiological role in the cell, but also affect the renal function of primary thyroid hormone, hypothyroidism associated renal damage is TSH first increased, followed by FT4, TT4, FT3 and TT3 decreased, there is a visible change the sequence and different features.
Hypothyroidism mechanisms leading to renal damage: because thyroid hormone deficiency leads to low metabolism in the body, organ dysfunction, reduced protein synthesis, muscle weakness, mucin tissue increased, with a positive ion and a large number of water molecules, caused by mucous edema, interstitial water and sodium retention, increased capillary permeability, blood capacity is reduced. The patients with hypothyroidism due to mucopolysaccharide deposition and (or) autoimmune factors in renal glomerulus, renal tubular basement membrane thickening, proliferation of endothelial cells, renal tubular epithelial cell cytoplasm and increase the content of the reduced blood flow, renal vasoconstriction, GFR and RPF (effective renal plasma flow) decreased. The glomerular functional lesion renal tubular damage is more obvious. The hypothyroidism. Reduced blood volume, plasma ANP release decreased, GFR decreased. The hypothyroidism due to myocardial myxedema caused by myocardial contractility of heart injury. Bradycardia, cardiac output decreased. The hypothyroidism associated with elevated blood lipids, vascular atherosclerosis prone to resulting in systemic vascular resistance increased.
The pathological types of hypothyroid renal damage including membranous nephropathy, mesangial proliferative nephropathy, focal segmental glomerulosclerosis, minimalchange nephropathy, the most common membranous nephropathy. Some scholars reported deposition of visible thyroid microsomal antibody in the glomerulus, show that immune mechanism may play a role in autoimmune thyroiditis associated nephropathy, need a large sample of cases confirmed.
Clinical hypothyroidism often because the performance of non specificity was misdiagnosed, and renal dysfunction is rarely reported. Patients with hypothyroidism, glomerular capillary pressure and glomerular filtration membrane leads to plasma protein leakage injury and proteinuria. Both hypothyroidism and chronic renal failure patients with EPO (erythropoietin) normocytic normochromic anemia associated with hypothyroidism. Body basal metabolic rate is low, the use of reduced oxygen, oxygen saturation increased, to reduce the production of EPO kidney; anemia of chronic renal failure is the kidney itself produces EPO reduced. Therefore, hypothyroidism patients often appear blood Cr, UA increased, CCr decreased, abnormal renal function, urinary protein, edema, anemia. Clinically misdiagnosed as nephritis. Therefore, patients with clinical edema, renal dysfunction, urinary protein positive without nephropathy and normal renal ultrasound for the thyroid should pay attention to Gland function checks to avoid some unnecessary examinations, especially traumatic examination such as renal biopsy. According to the dynamic changes of renal function and serum TSH, FT3, FT4 levels can be found in patients with primary hypothyroidism, to avoid misdiagnosis and has important clinical significance for the prevention of medical risk. Other patients with hypothyroidism the disease should pay attention to the monitoring of renal function to the medication guide.
Hypothyroidism Thyroid hormone deficiency, can promote kidney damage from many aspects, and increased with increasing degree of hypothyroidism, resulting in renal fibrosis, renal failure. Severe primary hypothyroidism appeared late, swelling and kidney damage, clinical manifestations resembling primary chronic glomerular nephritis end-stage. Hypothyroidism can cause kidney function decline, but the functional impairment of renal function, can be reversed by thyroid hormone therapy, correction of hypothyroidism, renal function can be restored.