receptors which will result in a decrease in secretion of atrial
natriuretic peptide (ANP).
3- Renin secreted by juxta glomerular apparatus converts plasma
angiotensinogen into angiotensin I which is converted by
angiotensin converting enzyme (ACE) to angiotensin II. The latter
stimulates secretion of aldosterone from the suprarenal gland.
Aldosterone stimulates reabsorption of salt and water from the distal
convoluted tubules.
4- Antidiuretic hormone stimulates reabsorption of water from the
collecting ducts.
5- The decrease in the secretion of the atrial natriuretic peptide (ANP)
decreases water and salt excretion by the kidney; and
6- Salt and water retained through the stimulation of Renin, and
antidiuretic hormone secretion, and suppression of atrial natriuretic
peptide secretion-leak from the vascular space (due to low oncotic
pressure) to the interstitial space with more oedema formation.Hyperlipidemia:
Hyperlipidemia is secondary to hypoalbuminemia. This condition
is accompanied with increase in concentration of plasma cholesterol,
triglycerides, VLDL and a decrease in HDL. Urine examination may show
lipiduria and oval fat bodies.
Clinical Picture of Nephrotic Syndrome:
- Edema: is the main clinical feature of nephrotic syndrome. It starts
as morning puffiness of the face. Then, gradually progresses to
edema of lower limbs; especially on prolonged standing and at the
end of the day. In severe cases edema may progress to be
generalized anasarca with ascites- even pleural and pericardial
effusion.