Nephrotic Syndromes

Clinical manifestations: Renal protein losses combined with partially maladaptive responses by the kidney and liver cause many of the observed clinical phenomena, including ↑ CV risk factors.
1. Nephrotic-range proteinuria (>3.5g per 1.73m2 body weight): Normal urinary albumin excretion is <100mg/day (an additional 500mg-2g/day is filtered, reabsorbed and catabolized for a total of 600-2.1mg/day total filtered)
2. Hypoalbuminemia: Due to urinary losses and inadequate compensation in liver albumin synthesis.
3. Edema: albumin is an important component of intravascular oncotic pressure; edema is caused:
a) Directly by decreased intravascular oncotic pressure, which in turn causes intravascular hypovolemia
b) Indirectly: relative intravascular hypovolemia is sensed by the kidney, which responds by increasing sodium and water reabsorption via renin-angiotensin-aldosterone and ADH
4. Hyperlipidemia and Lipiduria: multifactorial. LDL most commonly elevated, VLDL and IDL often elevated, HDL variable, but sometimes reduced. Can cause advanced atherosclerosis.
5. Thromboembolism: multifactorial, but severe enough to CAUSE renal vein thrombosis. Renal loss of antithrombin III (ATIII) makes these patients refractory to heparin therapy.
6. Immune dysfunction/infection: partly caused by urinary loss of immunoglobulins and complement, complicated by immunosuppressive agents used for treatment.
7. Abnormal calcium and bone metabolism: caused by urinary loss of VitD-binding protein

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