Nephrotic syndrome in patients with decreased resistance to infection is mainly due to:
Urine loss of a large number of immunoglobulin; b lack of factors leading to bacterial immunomodulation defects; malnutrition, the body's non-specific immune response weakened, resulting in impaired immune function; a large number of transferrin and zinc loss from the urine, Transferrin is required to maintain normal lymphocyte function and zinc ion concentration is associated with thymosin synthesis.
Local factors, pleural effusion, ascites, skin edema caused by skin rupture and severe edema local humoral factor dilution, decreased defensive function, are susceptible factors in patients with nephrotic syndrome, before the advent of antibiotics, bacterial infections were kidney disease One of the major causes of death in patients with syndrome, severe infections occur mainly in children and the elderly, adults are rare, clinically common infections are: primary peritonitis, cellulitis, respiratory tract infections and urinary tract infections, once infected Diagnosis is established, should be treated immediately.
Hypercoagulable state and venous thrombosis. Nephrotic syndrome, when the plasma albumin is less than 2.0g / d1, the risk of renal vein thrombosis increased, the majority of thrombosis in the formation of a small vein, and then extended to eventually involving the renal vein, renal vein thrombosis, in the membrane In nephrotic patients up to 50%, in other pathological types, the incidence of 5% to 16%, acute renal vein thrombosis patients can be manifested as sudden onset of back pain, hematuria, leukocyturia, increased urinary protein and Renal dysfunction, chronic patients without any symptoms, but often after renal thrombosis proteinuria aggravated, or poor response to treatment.
Tubular dysfunction. Nephrotic syndrome renal tubular dysfunction, more common in children, the mechanism that the tubular reabsorption of a large number of filtration proteins, tubule epithelial cells are damaged, often manifested as diabetes, amino aciduria, hyperphosphatemia, kidney Tubular loss of potassium and high chloride acidosis, where a variety of renal tubular defects often prompted poor prognosis.
Abnormal bone and calcium metabolism. Nephrotic syndrome, the blood circulation in the vitd binding protein and vitd complex loss from the urine, so that the blood 1,25 (oh) 2vitd3 levels, resulting in intestinal calcium malabsorption and bone tolerance to pth, and thus nephrotic syndrome Often manifested hypocalcemia, and sometimes occur due to osteomalacia and hyperparathyroidism caused by fibrocystic osteitis, renal failure in the progression of nephrotic syndrome complicated by osteodystrophy, in general than non-renal disease caused by uremia More serious.