Y


Y
BY,
PUTRI NOOR ZULAIKHA
 YY

! Triad of proteinuria
! pot urine protein:creatinine ratio
! Hypoalbuminaemia
! Oedema
! evere hyperlipidaemia
 
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ALL GROMERULONEPHRITIE AND MINIMAL CHANGE OF

GLOMERULU LE ION

Y TEMIC VA CULITIDE , MAINLY Y TEMIC LUPU ERYTHEMATO U

DIABETIC GLOMERULO CLERO I

AMYLOIDO I

DRUG

ALLERGIE
  Y
Primary causes of nephrotic syndrome include, in
approximate order of frequency:

! Minimal-change nephropathy
! Focal glomerulosclerosis
! Membranous nephropathy
! Hereditary nephropathies
 econdary causes include, again in order of
approximate frequency:

! Diabetes mellitus
! ystemic Lupus erythematosus
! Amyloidosis
! Viral infections (eg, hepatitis B, hepatitis C,
human immunodeficiency virus [HIV] )
! Preeclampsia
Y
! 
! The first sign of nephrotic syndrome in children is
usually swelling of the face; this is followed by swelling
of the entire body.
! Adults can present with dependent edema.
! Foamy urine may be a presenting feature.
! A thrombotic complication, such as deep vein
thrombosis of the calf veins or even a pulmonary
embolus, may be the first clue indicating nephrotic
syndrome.
! Additional historical features that appear can be
related to the cause of nephrotic syndrome. Thus, the
recent start of a nonsteroidal anti-inflammatory drug
(N AID) or a 10-year history of diabetes may be very
relevant.
! 
! Edema is the predominant feature of nephrotic
syndrome and initially develops around the eyes and
legs. With time, the edema becomes generalized and
may be associated with an increase in weight, the
development of ascites, or pleural effusions.
! Hematuria and hypertension manifest in a minority
of patients.
! Additional features on exam will vary according to
cause and as a result of whether or not renal function
impairment exists. Thus, in the case of longstanding
diabetes, there may be diabetic retinopathy, which
correlates closely with diabetic nephropathy. If the
kidney function is reduced, there may be
hypertension and/or anemia.
  
! Urinalysis
! Time collection of urinary protein
! erum tests for kidney function
! urine protein electrophoresis.
! The serum albumin
! Ultrasonographic
! Granular cast
G
 
     
 
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! has generalized edema severe enough to cause
respiratory distress
! tense scrotal or labial edema, if he or she has
complications (eg, bacterial sepsis, peritonitis,
pneumonia, thromboembolism)
! Diuretics will be needed; furosemide (1
mg/kg/d) and spironolactone (2 mg/kg/d) will
help when fluid retention is severe, provided no
signs of renal failure or volume contraction are
evident. Achieving a satisfactory diuresis is
difficult when the patient's serum albumin level
is less than 1.5 g/dL. Albumin at 1 g/kg may be
given, followed by intravenous furosemide.
Complications may occur, including pulmonary
edema. ome evidence suggests that albumin
may delay the response to steroids and may even
induce more frequent relapses, probably by
causing severe glomerular epithelial damage.
Fluid removal and weight loss remain transient
unless proteinuria remits
! With regard to infection, oral penicillin can be
prescribed as prophylaxis for children with gross
edema. Abdominal paracentesis should be
performed if the patient develops signs of
peritonitis, and any bacterial infection should be
treated promptly. A nonimmune patient with
varicella should receive zoster immunoglobulin
therapy if exposed to chickenpox, and
acyclovir should be given if the patient develops
chickenpox
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! Diuretics will be needed; furosemide,
spironolactone, and even metolazone may be
used. Volume depletion may occur with diuretic
use, which should be monitored by assessment
of symptoms, weight, pulse, and blood pressure
! Anticoagulation has been advocated by some for
use in preventing thromboembolic
complications, but its use in primary
prevention is of unproven value.
! Hypolipidemic agents may be used, but if the
nephrotic syndrome cannot be controlled, there
will be persistent hyperlipidemia
! In secondary nephrotic syndrome, such as that
associated with diabetic nephropathy,
angiotensin-converting enzyme (ACE) inhibitors
and/or angiotensin II receptor blockers are widely
used. These may reduce proteinuria by reducing
the systemic blood pressure, by reducing
intraglomerular pressure, and also by direct
action on podocytes.
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