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Complication of nephrotic syndrome


The main reason for the decline of resistance to infection in patients with nephrotic syndrome is that the majority of IgG is lost in the urine. The deficiency of B factor (the component of alternative pathway) leads to the defect of the immune modulation of bacteria. When malnutrition occurs, the nonspecific immune response of the organism is weakened and the immune function of the organism is impaired...View more

Hypercoagulable state and Venous thrombosis

Nephrotic syndrome have hypercoagulable state, mainly due to the change of coagulation factor in blood. Including IX, Xi and VIII factor decreased, V factor, X fibrinogen, beta thromboglobulin and platelet levels increased. Adhesion and aggregation of platelets are enhanced. Antithrombin III and plasmin activity decreased. Therefore, the increase of procoagulant and procoagulant factors, the decrease of anti coagulation factors and the damage of fibrinolysis mechanism are the causes of hypercoagulability in nephrotic syndrome...View more

Acute renal failure

Acute renal failure are the most serious complications of nephrotic syndrome, and dialysis treatment is often needed. Common causes include: the change of hemodynamics: nephrotic syndrome often hypoalbuminemia and vascular lesions, especially in elderly patients with renal arteriosclerosis, is very sensitive to blood volume and blood pressure, so when the acute hemorrhagic, vomiting and diarrhea caused by fluid loss, surgical injury, ascites, a diuretic and antihypertensive drug use after all...View more

Renal tubular hypofunction

In nephrotic syndrome is more common in children with tubular hypofunction. The mechanism is that the large reabsorption of the filtration protein by the renal tubule results in damage to the tubular epithelial cells. Often manifested as diabetes, amino acid urine, high phosphate urine, renal tubular potassium loss and high chloride acidosis, where a variety of renal tubular dysfunction, often suggesting poor prognosis.

Renal anomalies of bone and calcium metabolism

In comprehensive blood circulation in VitD binding protein (Mw65000) and VitD syndrome complex in the urine in the blood loss, 1, 25 (OH) 2VitD3 level decreased, resulting in intestinal calcium malabsorption and bone of PTH tolerance, thus nephrotic syndrome often occurs in hypocalcemia, fiber cystic osteitis and sometimes caused by hyperparathyroidism osteomalacia. In patients with nephrotic syndrome, progression of renal failure is generally more severe than uremia, which is not associated with kidney disease.

Endocrine and Metabolic syndrome

Nephrotic syndrome, loss of thyroid binding protein (TBG) and corticosteroid binding protein (CBG) in urine. Clinically, thyroid function is normal, but serum TBG and T3 are usually decreased. The levels of free T3 and T4 and TSH are normal. Since both CBG and 17 cortisol decrease in blood, the ratio of free and bound cortisol can be altered and the tissue response to cortisol in pharmacological doses is also different from normal. The ceruloplasmin (Mw151000), transferrin (Mw80000) and urinary albumin loss from nephrotic syndrome, often with serum copper, zinc and iron concentrations decreased. Zinc deficiency can cause impotence, taste disorders, wound healing and cell mediated immune damage. Continue to reduce transferrin can cause clinical treatment of anemia of iron resistant small cell with low pigment. In addition, severe hypoproteinemia can lead to persistent metabolic alkalosis, which results in a decrease in plasma bicarbonate levels by 3mmol/L, due to a decrease in plasma protein 10g/L.

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Nephrotic Syndrome| Kidney Failure| Uremia| Polycystic Kidney| Nephritis| Hypertensive Nephropathy| Diabetic Nephropathy

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