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Complications of nephrotic syndrome

Dec 26, 2016
Infection and protein malnutrition, immune dysfunction and glucocorticoid treatment. The order of common infection site was respiratory tract, urinary tract and skin. Infection is a common complication of nephrotic syndrome, due to the application of glucocorticoid, clinical manifestations of the infection is not obvious, although there are many kinds of antibiotics are available, but if the treatment is not timely or not complete, infection remains the leading cause of nephrotic syndrome is one of the main causes of recurrence and poor curative effect, even causing death, should be highly pay attention to.

Two, thrombosis and embolism complications due to increased blood viscosity and blood concentration of hyperlipidemia; in addition, because some protein loss in the urine, and compensatory liver protein synthesis increase, caused by coagulation, anticoagulation and fibrinolysis imbalance; nephrotic syndrome and blood in hyperthyroidism, diuretics and glucocorticoid hormone have further aggravate hypercoagulability. Therefore, nephrotic syndrome prone to thrombosis and embolism complications, including renal vein thrombosis is the most common (incidence rate of about 10%-50%, of which 3/4 cases with chronic form, no clinical symptoms); thrombosis and embolism complications is important reason for nephrotic syndrome directly affect the treatment effect and prognosis of the syndrome.
Three, acute renal failure in patients with nephrotic syndrome can be reduced due to insufficient effective blood volume and renal blood flow, induced prerenal azotemia. After expansion, diuretic can be restored. A small number of cases of acute renal failure, especially in the majority of minimal change nephropathy, there is no obvious incentive, manifested as oliguria or even urine, expansion diuretic ineffective. Renal biopsy showed slight glomerular lesions, diffuse interstitial edema of renal interstitium, normal or partial cell degeneration and necrosis of renal tubules, and large number of protein tubules in renal lumen. The mechanism of acute renal failure is unknown, presumably with renal interstitial edema of renal tubular and a large number of high pressure tube blockage of renal tubules, namely the change of formation in the renal tubules caused by hypertension, glomerular filtration rate decreased abruptly, and can induce renal tubular epithelial cell damage, necrosis, leading to acute renal failure.
Four, protein and fat metabolism disorder of long-term hypoproteinemia can lead to malnutrition in children, growth retardation; immunoglobulin reduction caused by low immunity, prone to infection; metal binding protein loss can make the lack of trace elements; endocrine hormone can induce endocrine disorders with deficiency; drug binding protein may reduce effects of some drugs on behalf of the dynamics, the impact of drug efficacy. Promote glomerular sclerosis and tubulointerstitial lesions, promote chronic progression of renal lesions.

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