Overview of Heavy Proteinuria and The: Nephrotic Syndrome
Overview of Heavy Proteinuria and The: Nephrotic Syndrome
Overview of Heavy Proteinuria and The: Nephrotic Syndrome
nephrotic syndrome
INTRODUCTION AND TERMINOLOGY
Proteinuria
• There are three basic types of proteinuria;
1) Glomerular ;
2) Tubular ; and
3) overflow .
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• In the nephrotic syndrome, protein loss is due
to glomerular proteinuria, characterized by
increased filtration of macromolecules across
the glomerular capillary wall.
Conditions
• The podocyte appears to be the major target
of injury in diseases that cause idiopathic
nephrotic syndrome in adults and children
(membranous nephropathy , minimal change
disease, and focal segmental
glomerulosclerosis [FSGS]),
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• In patients with nephrotic syndrome, albumin
is the principal urinary protein, but other
plasma proteins including clotting inhibitors,
transferrin, immunoglobulins, and hormone
carrying proteins such as vitamin D-binding
protein may be lost as well.
Hypoalbuminemia
• — The mechanism of hypoalbuminemia in
nephrotic patients is not completely
understood.
• Most of albumin loss is due to urinary
excretion.
Edema
• — Two mechanisms have been proposed to
explain the occurrence of edema in the
nephrotic syndrome.
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• In some patients, marked hypoalbuminemia
leads to egress of fluid into the interstitial
space by producing a decrease in plasma
oncotic pressure.
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• In most patients however , there is a parallel
fall in the interstitial protein concentration and
little change in the transcapillary oncotic
pressure gradient.
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• In the latter patients,edema appears to be the
consequence of primary renal sodium
retention in the collecting tubules mediated
through the epithelial sodium channel and the
basolateral Na-KA TPase .
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• The lack of major arterial underfilling has
important implications for diuretic therapy
since the excess fluid can usually be removed
without inducing volume depletion.
Hyperlipidemia and lipiduria
• — The two most common lipid abnormalities
in the nephrotic syndrome are
1) hypercholesterolemia and
2) hypertriglyceridemia.
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• Decreased plasma oncotic pressure appears to
stimulate hepatic lipoprotein synthesis
resulting in hypercholesterolemia.
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• Diminished clearance may also play a role in
the development of hypercholesterolemia.
• Impaired metabolism is primarily responsible
for nephrotic hypertriglyceridemia.
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• Lipiduria is usually present in the nephrotic
syndrome.
• Urinary lipid may be present in the sediment,
a) entrapped in casts (fatty casts),
b) enclosed by the plasma membrane of
degenerative epithelial cells (oval fat bodies),
or
c) free in the urine.