Idiopathic nephrotic syndrome

Cause pathogenesis nephrotic syndrome is a combination of causes cited in a large number of proteinuria, hypoproteinemia, edema, Hyperlipidemia their clinical characteristics of a group syndrome. Can be divided into primary and secondary nephrotic syndrome. Idiopathic nephrotic syndrome, the etiology and pathogenesis is not fully understood. Basic pathological defects glomerular basement membrane permeability increase, According to the different clinical manifestations can be divided into primary nephrotic type I and type II. Etiology and pathophysiology etiology remains unknown and may be related to immunization. Type I, type II common pathophysiological changes of glomerular filtration membrane permeability of the plasma albumin, a lot of proteinuria, hypoproteinemia, edema and hyperlipidemia. Edema formation mechanism, the traditional view is that because of the influx of proteinuria, plasma albumin concentration, Colloid osmotic pressure in plasma decreased intravascular water and electrolyte leakage to the tissues. Secondary effectively reduce blood circulation, thus stimulating the atrium, artery and vein pressures, capacity sensors, Reflex Sympathetic to the excitement, renin-angiotensin-aldosterone and antidiuretic hormone secretion, etc., kidney to promote re-absorption of sodium and water, caused edema. But in recent years the nephrotic syndrome hemorrhagic study through the 125 I-labeled human serum albumin in the blood volume for nephrotic edema and remission period compared their results; Nephrotic syndrome decline in blood volume accounted for 30%, mostly normal or elevated, Research shows that when nephropathy sodium regulatory function of the kidney disorder. Nephrotic syndrome of hypoproteinemia was mainly due to urinary protein loss, liver albumin synthesis and in vivo distribution of albumin abnormal increase in the catabolism. Through micro - puncture renal biopsy found that the renal proximal convoluted. distal convoluted tubule cells which contains large amounts of albumin and r-globulin micro-droplets, tubule cells involved in protein degradation of lysosomal activity, Note nephropathy in renal tubules of albumin increased catabolism. Hypoproteinemia body will have a variety of effects. Nephropathy with hypoproteinemia, total cholesterol, free cholesterol and cholesteryl ester were increased, Triglyceride only when serious diseases increased. Have hyperlipidemia was mainly due to hypoproteinemia and colloid osmotic pressure in plasma low, stimulate the liver lipoprotein synthesis, but also that when nephropathy and lipoprotein lipase activity reduction. LDL deposition in the glomerular mesangial, a great number of proteinuria can glomerular filtration excessive thickening of the basement membrane. Mesangial load increased, resulting in glomerulosclerosis. Nephropathy when there hypercoagulable state, the main reason for liver synthetic clotting factor V, VIII and fibrinogen, antithrombin (AT III) activity and hyperlipidemia, endothelial cell injury, through the platelet collection, so that blood flow in the hypercoagulable state. Besides, there is a low r-globulin, high β1α2 globulin, This is due to urinary immunoglobulin synthesis loss and liver increased. There nephropathy cellular immune defects. Total volume decreased T cells, T-cell subtypes, such as abnormal, vulnerable to infection. Pathological pathological types mainly small lesions nephropathy, mesangial proliferative glomerulonephritis, membranous nephropathy, Focal segmental glomerulosclerosis, membrane-proliferative glomerulonephritis, and so on. A clinical performance, general edema almost all developed varying degrees of swelling, puffiness in the face, lower extremities, the most obvious of the scrotum. Can be associated with serious chest, ascites and pericardial effusion, high incidence of heart palpitations and breathing difficulties. Edema sustainable few weeks or a few months, or in the course of disease when swollen when consumers. In infections (especially streptococcal infection), swelling often relapse or aggravated or there will be azotemia. 2, gastrointestinal symptoms because of gastrointestinal edema, often do not think of eating, nausea, vomiting, abdominal distension, and other symptoms of gastrointestinal dysfunction. With azotemia, the above symptoms increase. 3, hypertension non-nephrotic syndrome important clinical performance, but with water, sodium pool fond of increased blood volume, there will be 1:00 hypertension. And II-type primary renal syndrome can be intercalated with hypertension. 4, proteinuria proteinuria diagnosis is the most important conditions for the levy. Urinary protein "3.5g/24h. 5, hypoproteinemia was mainly plasma protein decreased, and the degree of proteinuria in a significant relationship, General plasma albumin "30 g / L, the majority of 15-26g / L. 6, hyperlipemia blood triglyceride significantly increased plasma was available milky white. Hypercholesterolemia is more in the 3 g / L and above. Hyperlipemia can lead to atherosclerosis, thrombosis or embolism occurred.