Nephrotic Syndrome Symptoms

      First, the symptoms:Nephrotic syndrome has four main features, namely, a large number of proteinuria, hypoproteinemia, hypercholesterolemia, and systemic edema.

      A large number of proteinuriaA large number of proteinuria is a sign of nephrotic syndrome. The main ingredient is albumin, also contains other plasma protein components. Glomerular basement membrane permeability changes are the underlying causes of proteinuria, changes in charge barrier and mechanical barrier (glomerular capillary pore barrier), renal tubular epithelial cell reabsorption and catabolic capacity for proteinuria formation Also have an impact. Glomerular filtration rate, plasma protein concentration and protein intake directly affect the degree of proteinuria. Glomerular filtration rate decreased, proteinuria will be reduced; severe hypoproteinemia, urinary protein excretion can increase, high protein diet will increase urinary protein excretion; therefore, only the daily quantitative method of protein, can not be accurate Determine the degree of urinary protein can be further done albumin clearance rate, urinary protein / creatinine (> 3.5 often kidney disease range of proteinuria). Urine protein electrophoresis detection of urinary IgG components increased urinary protein selectivity is low. Urinary protein selectivity has no definite clinical value and is now less used.
Hypoproteinemia

Is the second feature of nephrotic syndrome. Serum albumin is less than 30g / L. Nephrotic syndrome when the liver increased the synthesis of albumin, when the diet to give enough protein and heat card, the patient's liver synthesis of albumin about 22.6g per day, significantly higher than the normal daily 15.6g. When the liver synthesis of albumin compensatory effect is not enough to make up for the loss of urinary protein, it will appear hypoproteinemia. Hypoalbuminemia and urinary protein excretion are not consistent.Nephrotic syndrome patients are usually negative nitrogen balance, in the high protein load, can be converted to positive nitrogen balance, high protein load may be due to increased glomerular filtration protein leaving urinary protein excretion increased, so the plasma protein is not obvious, But at the same time taking the angiotensin converting enzyme inhibitor, can inhibit urinary protein excretion, serum albumin concentration can be significantly increased.

It is noteworthy that hypoglycemia, the drug and albumin binding will be reduced, the blood free drug concentration, may increase the toxicity of drugs.Nephrotic syndrome, a variety of plasma protein composition can change, α2 and β globulin increased, α1 globulin more normal. IgG levels were significantly decreased, and IgA, IgM, IgE levels more normal or elevated fibrinogen, coagulation factor Ⅴ, Ⅶ, Ⅷ, Ⅹ may rise, may be related to increased liver synthesis, with platelet count increased, anticoagulation Blood enzymes Ⅲ (heparin-related factors) decreased, C protein and S protein concentration more normal or increased, but decreased activity. This will help to achieve hypercoagulable state. The increase in fibrin degradation products (FDP) in the urine reflects changes in glomerular permeability. In summary, the various factors of coagulation and agglutination in the blood increased, while the mechanisms of anticoagulation and fibrinolysis were impaired. Due to the combined effect of hypercholesterolemia and hyperfibrinogenemia, plasma viscosity increases, and when the vascular endothelium is damaged, spontaneous thrombosis is likely to occur.In addition, transporters are also reduced, such as proteins that carry important metal ions (copper, iron, and zinc), and proteins that bind to important hormones (thyroxine, cortisol, prostaglandins) and active 25- (OH) D3 Decline, which can lead to secondary hyperparathyroidism, calcium and phosphorus metabolism disorders, causing renal bone disease. Sustained reduction of transferrin, the glucocorticoid in the treated patients free and combined with the hormone ratio changes, resulting in the drug metabolism and efficacy changes.

3. HyperlipidemiaThe total cholesterol, triglyceride significantly increased, low density lipoprotein (LDH), very low density lipoprotein (VLDH) levels increased. Hyperlipidemia is associated with hypoalbuminemia, and LDL / HLDL is elevated only when serum albumin is less than 10-20 g / L. High density lipoprotein (HDL) is normal or decreased. LDL / HDL ratio increased, so that the risk of atherosclerotic complications increased, hyperlipidemia and thrombosis and progressive glomerulosclerosis.Patients may be lipid urine, urine reflexed fat body, may be containing cholesterol-containing epithelial cells or fat body tube type.

4. edemaThe most noticeable symptoms of patients is gradually increased systemic edema, the initial morning eyelids, facial, ankle visible edema; with the development of edema spread to the body, and the emergence of pleural effusion, ascites, pericardial effusion, Scrotum or labia edema, pulmonary edema can also occur. Severe eyes can not open, head and neck thicker, the skin can be waxy pale, coupled with the chest, the presence of ascites, it appears obvious difficulty breathing, can not be supine only sitting position. If there is skin damage, the tissue fluid overflow and difficult to stop. Edema and postural relationship is obvious, such as the emergence of edema unrelated to the position, should be suspected and venous thrombosis. The severity of edema is generally positively correlated with the extent of hypoalbuminemia. It is generally believed that edema is mainly caused by a large number of proteinuria caused by plasma protein (especially albumin) decreased plasma colloid osmotic pressure decreased intravascular water to the tissue gap caused by movement. Another thought that the intrinsic edema and primary renal sodium and water retention, the possible factors are:

① glomerular filtration rate decreased;② increased renal tubular reabsorption;③ distal tubule on plasma atrial peptide (ANP) decreased ability to respond.

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