Hypoproteinemia is seen in most nephrotic syndrome patients, that is to say serum albumin levels below 30g/l. The main reason is the loss of albumin in urine, but the two are not completely parallel, because the plasma albumin value is the result of the balance between the synthesis and catabolism of albumin. Mainly affected by the following factors.
Albumin increased in liver synthesis. The absolute value of albumin dissociation rate is normal or even decreased when hypoproteinemia and albumin pool volume decrease. Synthesis by the liver albumin increased, if the diet can give enough protein and calories, liver daily albumin synthesis of more than 20g. Patients with strong constitution and high protein diet do not show hypoproteinemia. It has been suggested that plasma colloid osmotic pressure may play an important role in regulating the synthesis of albumin by the liver.
The ability of renal tubules to break down albumin increased. Albumin 10% in the liver of normal people is metabolized in the renal tubules. In nephrotic syndrome, the metabolism of the kidney increases to 16% - 30% because of the increase of the uptake and dissociation of the protein in the proximal tubule.
Severe edema and decreased gastrointestinal absorptive capacity often lead to negative nitrogen balance in patients with nephrotic syndrome. Age, duration of disease, chronic liver disease and malnutrition all affect the level of plasma albumin. Patients with nephrotic syndrome, the intake of high protein diet can lead to increased urinary protein and plasma albumin did not increase or have increased but little, and in severe malnutrition, if taking angiotensin converting enzyme inhibitor, high protein diet can increase plasma albumin concentration. If limiting protein intake, urine protein will decrease, and plasma albumin levels do not change, or although there is little.
Because of hypoalbuminemia, the combination of the drug and albumin decreases and the free drug levels in the blood rise, even if the normal dose can cause toxicity. In the presence of hypoproteinemia, the binding of four acids to plasma proteins decreases, resulting in increased platelet aggregation and thromboxane, which can aggravate proteinuria and kidney damage.
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