Treatment for Kidney Disease

Treatment for Kidney Disease

White / creatinine (> 3.5 for nephropathy range proteinuria).

1. Urine protein electrophoresis detection of increased urinary IgG components suggest low urinary protein selectivity. Urinary protein selectivity has no definite clinical value, is now less.

2. Hypoproteinemia: nephrotic syndrome is the second essential feature. Serum albumin less than 30g / L. Nephrotic syndrome when the liver synthesis of albumin increased, when the diet given enough protein and calories, the patient's liver synthesis of albumin per day about 22.6g, 15.6g than normal daily increase significantly. When the liver synthesis of albumin compensatory role is not enough to make up for the loss of urinary protein, will appear hypoproteinemia. Hypoalbuminemia and urinary protein excretion between the is not entirely consistent.

1), patients with nephrotic syndrome is usually negative nitrogen balance, high protein load, can be transferred to positive nitrogen balance, high protein load may be due to increased glomerular filtration protein excretion of urine protein, the plasma protein Not obvious, but at the same time taking blood angiotensin converting enzyme inhibitor, can prevent urinary protein excretion, serum albumin concentration can be significantly increased.

2), it is noteworthy that, hypoalbuminemia, the combination of drugs and albumin will be reduced, free drug concentration in the blood, may increase the toxicity of drugs.

3), nephrotic syndrome, a variety of plasma protein components can change, α2 and β globulin increased, α1 globulin and more normal. IgG, IgA, IgM, IgE levels were normal or increased, fibrinogen, coagulation factors Ⅴ, Ⅶ, Ⅷ, Ⅹ can be elevated, may be associated with increased liver synthesis, with increased platelet count, anticoagulation Blood enzyme Ⅲ (heparin-related factors) decreased, C protein and S protein concentration more than normal or increased, but the activity decreased. This will contribute to the occurrence of hypercoagulable state. Urinary fibrin degradation products (FDP) increased, reflecting the glomerular permeability changes. In short, blood coagulation and agglutination of a variety of pre-factors are increased, and anti-coagulation and fibrinolysis mechanism of damage. Due to the combined effects of hypercholesterolemia and hyperfibrinogenemia, plasma viscosity increases and spontaneous thrombosis occurs when the vascular endothelium is damaged.

4). In addition, the transport protein is also reduced, such as carrying important metal ions (copper, iron, zinc) protein decreased, and important hormones (thyroxine, cortisol, prostaglandin) and active 25- (OH) D3 Of the protein also decreased, which can lead to secondary hyperparathyroidism, calcium and phosphorus metabolism disorders, lead to renal bone disease. Continuous reduction of transferrin, the glucocorticoid in the treatment of patients with free and combined hormone ratio changes, leading to the drug metabolism and efficacy change.

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

4. edema of the most noticeable symptoms of patients is gradually aggravated systemic edema, the initial morning eyelid, facial, ankle edema; with the development of edema affected the body and the emergence of pleural effusion, ascites, pericardial effusion, mediastinal Fluid, scrotal or labia edema, pulmonary edema can also occur. Severe eyes can not open, head and neck thicker, the skin can be waxy pale, combined with the presence of chest and ascites, it appears obvious difficulty breathing, can not be supine only sitting position. If there is skin damage, the organization of fluid overflow and difficult to stop. Edema and postural relations, such as the emergence of postural edema, should not be suspected and venous thrombosis. The severity of edema is generally associated with the degree of hypoalbuminemia. Is generally believed that edema is caused by a large number of proteinuria plasma protein (especially albumin) decreased plasma colloid osmotic pressure decreased intravascular water to the tissue gap caused by the move. Another that the intrinsic edema and primary renal sodium and water retention, the possible factors are:

① glomerular filtration rate decreased;

② tubular reabsorption increased;

③ distal tubule on plasma atrial natriuretic peptide (ANP) decreased ability to respond.