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The glomerular membrane, which is normally impermeable to albumin and other large proteins,
becomes permeable to proteins, especially albumin, which leak through the membrane and are
lost in urine (hyperalbuminemia). This reduces the serum albumin level(hypoalbuminemia),
which decreases the COP in the capillaries. As a result, the hydrostatic pressure exceeds the pull
of the COP, and fluid accumulates in the interstitial spaces and body cavities, particularly the
abdominal cavity (ascites). The shift of the fluid from the plasma to the interstitial spaces reduces
the vascular fluid ( hypovolemia ) which inturn stimulates the renin angiotensin systemand the
secretion of antidiuretic hormone and aldosterone. Tubular reabsorption of sodium and water
increased in an attempt to increase intravascular volume. The elevation of serum cholesterol,
phospholipids , and triglycerides is unexplained
Predisposing factors: Precipitating factors:
Age
Gender Medical condition
Genetic Medication
Unknown Infection
Direct glomerular
damage
Inflammation
Fatigue, difficulty of
Sodium and water breathing, anemia,
Increased urinary retention nausea and vomiting
frequency, proteinuria,
albuminuria, hematuria
Diuretics
Decreased urinary output,
Edema, Hypertension
LEGEND:
Causes
Diet modifications: low
salt, low fat, low protein Disease process
diet. Fluid restrictions as
Reaction/compensation
advised
Signs and symptoms
Complications