Ускладнення нефротичного синдрому
Complication | Contributing Factors |
|---|---|
Edema (including ascites and pleural effusions) | Generalized capillary leak, due to hypoalbuminemia with decreased oncotic pressure Possibly renal sodium retention |
Infection (especially cellulitis and, in 2 to 6%, spontaneous bacterial peritonitis) | Unknown Possibly loss of opsonins and immunoglobulins |
Loss of erythropoietin and transferrin | |
Changes in thyroid function test results (among patients previously hypothyroid, increased dose requirement for thyroid replacement hormone) | Loss of thyroid-binding globulin |
Hypercoagulability and thromboembolism (especially renal vein thrombosis and pulmonary embolism, which occur in up to 5% of children and 40% of adults) | Loss of antithrombin III Increased hepatic synthesis of clotting factors Platelet abnormalities Hyperviscosity caused by hypovolemia |
Protein undernutrition in children (sometimes with brittle hair and nails, alopecia, and stunted growth) | Loss of proteins Decreased hepatic production Sometimes decreased oral intake secondary to mesenteric edema |
Increased hepatic lipoprotein synthesis | |
Coronary artery disease in adults | Dyslipidemia with atherosclerosis Hypercoagulability |
Hypertension in adults | Renal sodium retention |
Mineral bone disease | Corticosteroid use Vitamin D deficiency due to loss of vitamin D binding protein |
Unknown Possibly hypovolemia, interstitial edema, and use of nonsteroidal anti-inflammatory drugs (NSAIDs) | |
Proximal tubular dysfunction (acquired Fanconi syndrome), with glucosuria, aminoaciduria, potassium depletion, phosphaturia, renal tubular acidosis, bicarbonaturia, hypercitraturia, and uricosuria | Toxic effects on proximal tubular cells secondary to large amounts of protein that they reabsorb |