Inroduction Nephrotic syndrome is one of the bcommon cause of hospitalization among children. Incidence of the condition is 2 to7 per1000. It is more common in male child. Mean age of occurrence is 2 to 5 years. It is a symptom complex manifested by massive oedema, hypoalbuminemia, marked albuminuria and hyperlipidemia  Classification Congenital nephrotic syndrome Idiopathic or primary nephrotic syndrome Secondary nephrotic syndrome  Congenital nephrotic syndrome It is rare but serious and fatal problem usually associated with other congenital abnormalities of kidney. It is inherited as autosomal recessive disease. Severe renal insufficiency and urinary infections along with this condition result is poor prognosis.  Idiopathic or primary nephrotic syndrome It is the most common type(about 90%) and regarded as autoimmune phenomenon as it responds to immunosuppressive therapy. Subgroup of this type◦ Minimal change nephrotic syndrome(85%)◦ Proliferative nephrotic syndrome(5%)◦ Focal sclerosis nephrotic syndrome(10%) 

1. Nephrotic syndrome
BY:
PH.MOEEN EMGHARI
CLINICAL PHARMACY

2. Outlines:
1. Inroduction
2. Classification
3. pathophysiology
4. Clinical features
5. Complications
6. Demographic Details
7. History of patient illness
8. plan of therapy
9. Laboratory tests

3. Inroduction
 Nephrotic syndrome is one of the bcommon cause of hospitalization
among children.
 Incidence of the condition is 2 to7 per1000.
 It is more common in male child.
 Mean age of occurrence is 2 to 5 years.
 It is a symptom complex manifested by massive oedema,
hypoalbuminemia, marked albuminuria and hyperlipidemia

4. Classification
 Congenital nephrotic syndrome
 Idiopathic or primary nephrotic syndrome
 Secondary nephrotic syndrome

5. 1. Congenital nephrotic syndrome
 It is rare but serious and fatal problem usually associated with
other congenital abnormalities of kidney.
 It is inherited as autosomal recessive disease.
 Severe renal insufficiency and urinary infections along with
this condition result is poor prognosis.
2. Idiopathic or primary nephrotic syndrome
 It is the most common type(about 90%) and regarded as autoimmune
phenomenon as it responds to immunosuppressive therapy.
 Subgroup of this type
◦ Minimal change nephrotic syndrome(85%)
◦ Proliferative nephrotic syndrome(5%)
◦ Focal sclerosis nephrotic syndrome(10%)

6. 3. Secondary nephrotic syndrome
 It occur in children about 10% of all cases.
 This condition may occur due to some form of chronic
glomerularnephritis or due to diabetes mellites,systimic lupus
erythematosis(SLE), malaria,malignant hypertension, hepatitis
‘B’,infective endocarditis, drug toxicity, lymphomas and
syphilis

7. pathophysiology
 The pathological changes of nephrotic syndrome may be
due to loss of charge selectivity and thickening of the foot
plate of the glomerular basement membrane.
 These result in increased glomerular permiability which
permits the negatively charged protein, mainly albumin to
pass through the capillary walls into the urine.
 Excess loss of albumin result in decrease in serum albumin
 As a result of hypoalbuminemia,there is reduction in plasma
oncotic pressure.

9.  Thus fluid flows from the capillaries into the interstitial space and
produce oedma. The sift fo fluid from the plasma to the
interstitial spaces the intravascular fluid volume resulting
hypovolemia,which stimulate ranin angiotension axis and
volume receptor to secret aldosterone and antidiuretic hormone these
lead to reabsorption of Na & H2O in distal tubules
resulting oedema.
 Loss of protein & immunoglobulin predisposes to infection in the child.
Diminished oncotic pressure leades to
hepatic lipoprotein synthesis which result
in hyperlipidemia.

10. Damaged glomerular capillary membrane
Loss of plasma protein (albumin)
HypoalbuminemiaStimulates synthesis of lipoproteins
Sodium retention
Generalized edema
(fluid moves from vascular space to
extracellular fluid)
Decreased oncotic pressure
Activation of renin–angiotensin system
Hyperlipidemia
Edema

11. 1. Child may present with periorbital
puffiness.
2. Oedema may be minimal or massive.
3. Profound weight gain with in a short
period.
4. Dependent oedema develops in the
ankle, feet, genitalia(scrotum) & hand.
5. Oedmatus part soft & pits easily on
pressure.
6. Striae may be appear on the skin due to
Fluid accumulate in the body space
resulting ascites,pleural effusion with
respiratory distress and generalized
oedema
7. Urine out put is reduce GI disturbances
usually found as vomiting, loss of appetite
& diarrhea
8. Other features include fatigue, lethergy,
pallor & irritability, hypertension,
hematuria, hepatomegaly & wasting of
muscle may found in some cases.
Clinical features

12. Complications
1. Ascitis
2. Pleural effusion
3. Generalized oedema(anasarca)
4. Coagulation disorder
5. Thrombosis
6. Recurrent infection
7. Growth retardation
8. Calcium & Vitamin D deficiency
9. Protein energy malnutrition

13. Demographic Details
 NAME : ‫حسن‬ ‫سعد‬ ‫حسن‬‫زعرب‬
 ID:44052054
 NUMBER :
 D.O.B : 20/2/2018
 GENDER : boy
 AGE : 10 MONTH OLD
 Ht:50cm
 Wt:5kg
 DATE AND TIME OF ADMISSION : 10/4/2018
 DATE OF DISCHARGE: -
 ADDRESS : ‫الغربية‬ ‫.رفح‬

14. History of patient illness
 Two month old male neonate product of NSVD , birth weight 2.8 kg ,
diagnosed anenataly with bilateral enlarged kidneys with history of
oligohydromnios , admitted after one week of birth to NIC Due to
generalized EDEMA ,The investigation show massive protein urea &low
total body protien,he had received multiple Albumin transfusion,
 The parent are first cousin
 The patint have 2 sobling healthy girls
 No similar condition in the family

15. plan of therapy
1. H.albumin
2. Furosamid
3. Hydrocortison
4. Hypertonic normal
5. Salbutamol
6. L.Thyroxin
7. Alpha D3 0.25
8. Enalpril
9. CaCo3 600

16. Laboratory tests
1. Total proten
2. TSH
3. CRP
4. Blood culture
5. CBC
6. Urine Test

17. thanks