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NEPHROTIC
SYNDROME
MANITA UPADHYAY
LECTURER
INTRODUCTION
The syndrome is apparent in any condition that
seriously damage the glomerular capillary
membrane that results in increase glomerular
capillary permeability to plasma proteins.
Although liver is capable of increasing the
production of protein. it can’t keep up with the daily
loss of albumin through the kidney thus
hypoalbuminemia results
DEFINITION
It is a clinical disorder that is characterized by
proteinuria, hypoalbuminemia, edema and
hyperlipidemia.
This occurs due to excessive leakage of
plasma proteins in urine because of increase
capillary permeability of the glomerulus.
INCIDENCE
• nephrotic syndrome is quite rare but has an
important role to play in the development of
kidney disease.
• in adults, the incidence of the condition is
approximately 3 cases per 100,000 per year.
the incidence of minimal change disease in
caucasian children is reported to be 2 per
100,000
TYPES
category it is regarded as a sort of
autoimmune phenomenon, especially since
it responds well to immunosuppressive
therapy.
1. Idiopathic NS:
In childhood, the vast majority belongs to
2. Secondary NS:
•It occurs in children (about 10%) of all
cases.
•This condition may occur due to some form
of chronic glomerulonephritis, or due to
diabetes mellitus, SLE, malaria,
hypertension,
endocarditic,
hepatitis
HIV/AIDS,
malignant
B, infective
drug toxicity,
lymphomas syphilis etc.
3. CongenitalNS:
•It is rare but a serious and fetal problem
usually associated with other congenital
anomalies of kidney.
•It is inherited as autosomal recessive disease.
•Severe renal insufficiency & urinary infections
along with this condition result is poor
prognosis.
4. InfantileNS:
•The term is applied to NS occurring in infants
between 4 – 12months of age. Its major
causes are:
A. NPHS2
B. Diffuse mesengial sclerosis (DMS)
ETIOLOGY
1. Primary renal cause:
 Minimal-change nephropathy(70-
90% children and 10- 15%inadult)
 Glomerulosclerosis
 Acute post streptococcal
glomerulonephritis
 Immune complex glomerulonephritis.
2. Systemic cause
• Infections
• Toxins – mercury, bismuth, gold
• Allergic – bee sting, inhaled pollen, food
allergy
• Cardiovascular – sickle cell disease, renal
vein thrombosis, congestive heart failure
• Malignancies – leukemia
• Others – systemic lupus erythematous,
anaphylactic purpura
PATHOPHYSIOLOGY
Decrease plasma oncotic
pressure
Compensatory synthesis of protein
including lipoprotein by liver
Due to E/F
Increase renal catabolism albumin
Hypoalbuminemia (less then 3.4 mg/DL)
Hyperlipidemia
Fluid escape into
the tissue
Decrease plasma
volume
Edema Decrease GFR
Generalized edema
(Anasarca or dropsy)
DECREASE LIPID
CATABOLISM DUE TO
LOW LEVEL OF
PROTEIN
CLINICAL MANIFESTATION
Four main symptoms of nephritic symptoms:-
• Protein urea
• Hypoalbuminemia
• Hyperlipidemia
• Edema- Periorbital edema, pitting edema, ankle
edema, Ascites, pleural effusion, Weight gain,
hypertension
• fatigue, headache, malaise and irritability
• foamy appearance of urine (decrease surface tension by
severe proteinuria)
• hematuria
• thrombophilia (clot formation)
• lipiduria
• dyspnoea
• anemia
• fever, rash, joint pain
• Weakness
• Anorexia
• flank pain
DIAGNOSTIC EVALUATION
palpation: due to edema and ascites kidney cannot be palpable.
urine analysis
hematuria
24 hour urinary total protein estimation – urine
sample shows proteinuria (>3.5 g per liter per 24
hours)
blood test
BUN
S.creatinine
S.protein
lipid profile
• Comprehensive metabolic panel(CMP)
shows hypoalbuminemia, albumin level is
<2.5g/dl
 Needle biopsy of kidney
 ECG
 KUB – X.ray
 Renal ultrasound
 Renal scan
 Intravenous urogram (IVU).
MANAGEMENT
1. Symptomatic treatment
• Edema –
 Rest – not for prolong time
 Nutrition – 1 gm protein/kg/day, not more that, sodium
restriction, water not greater then the level of diuresis.
 Medication – Loop diuretics (furosemide)
• Hypoalbuminemia – moderate intake of protein, rich
in animal protein.
• Hyperlipidemia – low saturated fat, high unsaturated
fat, if unresponsive to nutrition therapy then take
hypolipidemic drugs such as statin.
• Thrombophilia – Heparin
• Infection – Antibiotics
• ACE inhibitors – to control hypertension
• Achieve better blood glucose level
2. Kidney damage
• Corticosteroid – prednisone
• Immunosuppressant – Cyclophosphamide
COMPLICATION
• infection
• thromboembolic complication
• pulmonary edema
• hypovolemia
• growth retardation
• altered drug metabolism
• ESRD
NURSING MANAGEMENT
NURSING DIAGNOSIS:
•Risk for infection related to immunosuppressive drugs.
•Fluid and electrolyte imbalanced related to edema.
•Impaired skin integrity related to disease process.
•Altered nutrition related to Anorexia.
•Altered kidney function related to glomerural
damage.
•Knowledge deficit related to disease process.
Nephrotic syndrome(nursing managment)

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Nephrotic syndrome(nursing managment)

  • 2.
  • 3. INTRODUCTION The syndrome is apparent in any condition that seriously damage the glomerular capillary membrane that results in increase glomerular capillary permeability to plasma proteins. Although liver is capable of increasing the production of protein. it can’t keep up with the daily loss of albumin through the kidney thus hypoalbuminemia results
  • 4. DEFINITION It is a clinical disorder that is characterized by proteinuria, hypoalbuminemia, edema and hyperlipidemia. This occurs due to excessive leakage of plasma proteins in urine because of increase capillary permeability of the glomerulus.
  • 5. INCIDENCE • nephrotic syndrome is quite rare but has an important role to play in the development of kidney disease. • in adults, the incidence of the condition is approximately 3 cases per 100,000 per year. the incidence of minimal change disease in caucasian children is reported to be 2 per 100,000
  • 6. TYPES category it is regarded as a sort of autoimmune phenomenon, especially since it responds well to immunosuppressive therapy. 1. Idiopathic NS: In childhood, the vast majority belongs to
  • 7. 2. Secondary NS: •It occurs in children (about 10%) of all cases. •This condition may occur due to some form of chronic glomerulonephritis, or due to diabetes mellitus, SLE, malaria, hypertension, endocarditic, hepatitis HIV/AIDS, malignant B, infective drug toxicity, lymphomas syphilis etc.
  • 8. 3. CongenitalNS: •It is rare but a serious and fetal problem usually associated with other congenital anomalies of kidney. •It is inherited as autosomal recessive disease. •Severe renal insufficiency & urinary infections along with this condition result is poor prognosis.
  • 9. 4. InfantileNS: •The term is applied to NS occurring in infants between 4 – 12months of age. Its major causes are: A. NPHS2 B. Diffuse mesengial sclerosis (DMS)
  • 10. ETIOLOGY 1. Primary renal cause:  Minimal-change nephropathy(70- 90% children and 10- 15%inadult)  Glomerulosclerosis  Acute post streptococcal glomerulonephritis  Immune complex glomerulonephritis.
  • 11. 2. Systemic cause • Infections • Toxins – mercury, bismuth, gold • Allergic – bee sting, inhaled pollen, food allergy • Cardiovascular – sickle cell disease, renal vein thrombosis, congestive heart failure • Malignancies – leukemia • Others – systemic lupus erythematous, anaphylactic purpura
  • 12. PATHOPHYSIOLOGY Decrease plasma oncotic pressure Compensatory synthesis of protein including lipoprotein by liver Due to E/F Increase renal catabolism albumin Hypoalbuminemia (less then 3.4 mg/DL)
  • 13. Hyperlipidemia Fluid escape into the tissue Decrease plasma volume Edema Decrease GFR Generalized edema (Anasarca or dropsy) DECREASE LIPID CATABOLISM DUE TO LOW LEVEL OF PROTEIN
  • 14. CLINICAL MANIFESTATION Four main symptoms of nephritic symptoms:- • Protein urea • Hypoalbuminemia • Hyperlipidemia • Edema- Periorbital edema, pitting edema, ankle edema, Ascites, pleural effusion, Weight gain, hypertension
  • 15. • fatigue, headache, malaise and irritability • foamy appearance of urine (decrease surface tension by severe proteinuria) • hematuria • thrombophilia (clot formation) • lipiduria • dyspnoea • anemia • fever, rash, joint pain • Weakness • Anorexia • flank pain
  • 16. DIAGNOSTIC EVALUATION palpation: due to edema and ascites kidney cannot be palpable. urine analysis hematuria 24 hour urinary total protein estimation – urine sample shows proteinuria (>3.5 g per liter per 24 hours) blood test BUN S.creatinine S.protein lipid profile
  • 17. • Comprehensive metabolic panel(CMP) shows hypoalbuminemia, albumin level is <2.5g/dl  Needle biopsy of kidney  ECG  KUB – X.ray  Renal ultrasound  Renal scan  Intravenous urogram (IVU).
  • 18. MANAGEMENT 1. Symptomatic treatment • Edema –  Rest – not for prolong time  Nutrition – 1 gm protein/kg/day, not more that, sodium restriction, water not greater then the level of diuresis.  Medication – Loop diuretics (furosemide) • Hypoalbuminemia – moderate intake of protein, rich in animal protein. • Hyperlipidemia – low saturated fat, high unsaturated fat, if unresponsive to nutrition therapy then take hypolipidemic drugs such as statin.
  • 19. • Thrombophilia – Heparin • Infection – Antibiotics • ACE inhibitors – to control hypertension • Achieve better blood glucose level 2. Kidney damage • Corticosteroid – prednisone • Immunosuppressant – Cyclophosphamide
  • 20. COMPLICATION • infection • thromboembolic complication • pulmonary edema • hypovolemia • growth retardation • altered drug metabolism • ESRD
  • 21. NURSING MANAGEMENT NURSING DIAGNOSIS: •Risk for infection related to immunosuppressive drugs. •Fluid and electrolyte imbalanced related to edema. •Impaired skin integrity related to disease process. •Altered nutrition related to Anorexia. •Altered kidney function related to glomerural damage. •Knowledge deficit related to disease process.

Editor's Notes

  1. minimal change ns – this predominant type, seen 86% of the cases. significant change ns – this is infrequent. mesangial proliferation is seen in 5% cases and focal sclerosis in 10% of cases.
  2. Renal insufficiency is poor function of the kidneys that may be due to a reduction in blood-flow to the kidneys caused by renal artery disease. Normally, the kidneys regulate body fluid and blood pressure, as well as regulate blood chemistry and remove organic waste.
  3. Diffuse mesangial sclerosis (DMS) is a histopathologic finding in some children with congenital (CNS) or infantile nephrotic syndrome (INS). In DMS, there is an increase in mesangial matrix without mesangial cellular proliferation, leading to obliteration of glomerular capillaries and eventual glomerulosclerosis
  4. Anaphylactoid purpura: A form of blood vessel inflammation that affects small capillaries in the skin and the kidneys. It results in skin rash associated with joint inflammation (arthritis) and cramping pain in the abdomen