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单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,*,NEPHROTIC SYNDROME,NEPHROTIC SYNDROME,Nephrotic Syndrome,Proteinuria(“nephrotic range”3.5g/24h),Hypoalbumimenia(serum albumin 3.0 to 3.5 g/pe/24,hours),which leads to hypoproteinemia,decreased levels of serum albumin(albumin 3.5 g,Tubular proteinuria never exceeds 2 g per 24 h and,never causes NS,Urinary excretion of more than 3.5 g per 24 hours is,always glomerular disease,CAUSE OF PROTEINURIA AS RELATE,NON-PATHOLOGIC FORMS OF PROTEINURIA,Orthostatic proteinuria,typically in healthy teens and young adults,occurs upon assuming upright position,usually less than 2g/24 h,Functional proteinuria,patients with normal kidneys but experiencing:,-high fever,-congestive heart failure,-exposure to cold,-resolves with resolution of precipitating event,Persons younger than 30 years who excrete less than 2 g,of protein per day and who have a normal creatinine,clearance should be tested for orthostatic proteinuria,NON-PATHOLOGIC FORMS OF PROTE,HYPOALBUMINEMIA,most common clinical correlate of severe proteinuria,with almost always associated with hypoalbumemia,relationship between proteinuria and hypoalbuminia is,variable,variability partly depends on livers capacity to,synthesize albumin,6-10 percent of albumin pool normally catabolized,daily,HYPOALBUMINEMIA most common c,HYPOALBUMINEMIA IN NEPHROTIC SYNDROME MAY,RESULT FROM:,Increased loss(in urine)or catabolism(filtered,albumin increased tubular reabsorption enhanced,catabolism by tubular cells;increased renal catabolism,in part offset by decreased extrarenal catabolism.,Decreased synthesis of albumin(hepatic synthesis in,nephrotic syndrome is normal or increased,but below,maximal rate achieved in other hypoalbuminemic,states),Changes in albumin distribution(some evidence for,redistribution into other capillary beds),HYPOALBUMINEMIA IN NEPHROTIC S,HYPOALBUMINEMIA,High glomerular permeability leads to hyperalbuminuria,and,eventually,to hypoalbuminemia.,Hypoalbuminemia lowers the plasma colloid osmotic,pressure,causing greater transcapillary filtration of water,and the development of edema.,Capillary hydrostatic pressure and the gradient of plasma,to interstitial fluid oncotic pressure determine the,movement of fluid from the vascular compartment to the,interstitium.,Fluid that is not absorbed back into the vascular system,until it has reached the venous end of the capillary bed is,usually absorbed by the lymphatics and returned back to,the vascular space.,HYPOALBUMINEMIAHigh glomerul,HYPOALBUMINEMIA,Responses to decreased blood volume,Decreased renal perfusion,renin release,sequential,generation of angiotensin II,aldosterone,and,subsequent sodium reabsorption,ADH release and resultant water retention at,collecting duct,Decreased atrial naturetic peptide release and,resultant decreased sodium excretion,Edema is result of salt and water retention,HYPOALBUMINEMIAResponses to de,HYPERLIPIDEMIA,Clinical correlate of severe proteinuria,Total plasma cholesterol levels increase as proteinuria,becomes heavy,Levels of triglycerides only mildly increased,Pathogenesis,loss of albumin&associated hypoalbuminemia directly,or indirectly stimulates hepatic protein synthesis,reduced colloid osmotic pressure results in increased,albumin and lipoprotein synthesis and decreased,catabolism of lipoproteins in nephrotic syndrome,increase in total plasma and LDL cholesterol with a,normal or reduced HDL cholesterol increased risk of,premature atherosclerosis,HYPERLIPIDEMIA Clinical corre,HYPERCOAGULABILITY(I),Low zymogen factors,factor IX,factor XI.,Inreased prooagulatory cofators,factor V,factor VIII,Increased fibrinogen levels,Decreased oaulatory inhibitors:antithrombin III(but,protein C and S increased),Altered fibrinolytic system(,2-,antiplasmin increased,plasminogen decreased),Increased platelet reactivity:,thromoytosis,Increased release reaction,in vitro,(ADP,thrombin,collagen,arachidonic acid,epinephrine),Altered endothelial cell funtion,HYPERCOAGULABILITY(I)Low zym,HYPERCOAGULABILITY(II),Patients can develop spontaneous,peripheral arterial or,venous thrombosis,renal vein thrombosis,and,pulmonary,embolism,.,Clinical features of,acute renal vein thrombosis,include,sudden onset of flank or abdominal pain,gross hematuria,a left-sided varicocele(the left testicular vein drains into,the renal vein),increased proteinuria,and an acute decline in glomerular,filtration rate.,Chronic renal vein thrombosis,is asymptomatic.,HYPERCOAGULABILITY(II)Patient,METABOLIC COMPLICATIONS,Metabolic complications of NS,include protein,malnutrition and iron-resistant microcytic hypochromic,anemia due to transferrin loss.,High glomerular permeability causes the excretion of,vitamin Dbinding protein and complexes in the urine,leading to,(1)malabsorption of calcium,and development of bone,disease(eg,osteitis fibrosa cystica)because of,enhanced parathyroid hormone production and,(2)osteomalacia,because of impairment in,mineralization.,METABOLIC COMPLICATIONS Metab,SYMPTOMS
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