Notes

1. NEPHROTIC SYNDROME
G.T.P only…

2. General Objective
 At the end of this lecture/discussion:
 Students should be able to
demonstrate their basic knowledge of
nephrotic syndrome and be able to
provide nursing care to patients with
nephrotic syndrome.

3. Specific Objectives
 Define nephrotic syndrome.
 State the causes of nephrotic syndrome.
 State the signs and symptoms of nephrotic
syndrome.
 Outline the pathophysiology of nephrotic
syndrome.
 Discuss the diagnosis for nephrotic
syndrome.
 Describe the management of nephrotic
syndrome.
 Outline the complications of nephrotic
syndrome.

4. INTRODUCTION
 Although not a disease, nephrotic
syndrome is characterized by
proteinuria, hyperlipidemia,
hypoalbuminemia, and oedema.
 The treatment and prognosis is variable
depending on the underlying cause
 Age plays no part in the prognosis
 Some forms of nephrotic syndrome may
result in renal failure.
 So knowledge of the condition is
important to be able to provide the care
needed.

5. Introduction cont’
Paediatric nephrotic syndrome
proteinuria exceeding 40mg/m2/hour
while in an adult is 3.5g/ 24 hours
 Is not a disease itself but a
manifestation of many different
glomerular diseases.

6. Definition
This is a condition characterized by
heavy proteinuria, hypoalbinaemia,
oedema with hyperlipidemia.
OR

7. Definition
 Nephrotic Syndrome, group of
symptoms caused by the excretion of
large amounts of protein in the urine
due to kidney impairment or
 where the 'filters' in the kidney
become 'leaky' and large amounts of
protein leak from the blood into the
urine
(Lewis, 2007).

8. Definition cont’
 It is a renal disease characterized by
variety of symptoms that accompany
any condition that seriously impairs,
the glomerular capillary membrane
resulting in increased permeability to
protein (proteinuria), low plasma
protein (hypoalbuminemia),
hyperlipidemia(high fat levels) and
generalized oedema (anasarca)
especially around the eyes, feet, and
hands.

9. Nephrotic syndrome oedema

10. Nephrotic syndrome oedema

11. causes
 Are divided into primary and secondary
 Primary – also called idiopathic is associated
with diseases intrinsic to the kidney such
 Diseases affecting the glomerular.
 Minimal change disease
 'minimal change- there is virtually no change
detectable in the glomeruli if a sample of
kidney is looked at under the microscope.
 The glomeruli look normal under the
microscope, but may have some minor
change that allows leakage of protein.

12. Causes cont’
 The cause of minimal change disease is
not clear.
 Something to do with a slight change in
the immune system, or a reaction of
parts of the immune system to some
unidentified factor.
 causes about 9 in 10 cases of nephrotic
syndrome in children under the age of
five years.
 about 1 in 5 cases of nephrotic
syndrome in adults.

13. Causes cont’
 Membranous nephropathy
 There is some thickening of the
membrane in the glomeruli (the 'filter'
of the glomeruli) which makes the
glomeruli 'leaky' to protein.
 The thickening may be caused by
abnormal reaction of the immune
system to some infections or drugs
can cause this disease.
 It’s very common in adults unlike
children

14. Causes cont’
 Lipoid nephrosis commonly in children,
glomeruli show degenerative changes with
no thickening of the basement membranes.
 Focal segmental glomerulosclerosis
(FSGS)
 condition where small scars (sclerosis)
develop on some glomeruli as a reaction of
the immune system to kidney
transplantation, or heroin injection.
 accounts for up to 1 in 10 cases of
nephrotic syndrome in children but a higher
percentage of cases in adults

15. Causes cont’
 Allergic reaction Insect bites, Pollen,
Snake venom.
Secondary– refers to the causes outside
the kidney such as
 Systemic diseases
 Systemic lupus erythematosus(a
chronic inflammatory disease).
 Amyloidosis -accumulation of a protein-
based substance amyloid (waxy protein
resembling starch) in the glomeruli
tissues.

16. Causes cont’
 Diabetic nephropathy (diseased
kidney/nephrone because of diabetes)
there is thickening of glomerular
basement membrane and mesangial
expansion affecting the glomerular
filtration rate.
 Sickle cell disease

17. Causes cont’
 Neoplasm:
 Hodgkin’s disease, carcinoma ( renal
cell, lung, neuroblastoma, breast, and
etc)
 Infection:
 HBV/Hepatitis C, HIV, syphilis,
Schistosomiasis,, malaria,
tuberculosis Herpes zoster, these
conditions cause thickening of
membranes within the glomeruli.

18. Causes cont’
 Drug/Toxins:
 Mercury, vaccine, pellicillamine,
Heroin, gold therapy, or captopril,
Non-steroid anti-inflammatory drugs.
 Circulatory problems
 Such as constrictive pericarditis and
severe congestive heart failure.
 Chronic kidney failure and kidney
transplantation.

19. Causes cont’
 Genetic abnormalities- infantile NS
presenting before the age of 3
months and congenital NS presenting
at the age of 4- 12 months
 This is due to abnormal formation of
gene called nephrin.

20. Pathophysiology
 Normally, urine contains virtually no protein.
 In nephrotic syndrome the urine contains large
amounts of protein.
 What happens is that filters in the kidneys (the
glomeruli) become 'leaky' and protein, instead of
remaining in the blood, leaks out into the
urine( proteinuria).
 The initial physiologic change is
damage/disturbance to the arrangement of cells
in the glomerular basement membrane from
immune complex deposition, nephrotoxic
antibodies or any other causes.
 Results in increased glomerular basement
membrane porosity and permeability to protein
resulting in proteinuria

21. Pathophysiology cont
 Protein loss leads to reduced plasma
protein such as albumin
 Decreased plasma protein leads to
reduced oncotic or osmotic pressure.
 Proteins in the blood exert an osmotic
pressure which tends to pull fluid into the
capillary vessels. If the concentration of
protein reduces, the osmotic pressure
reduces, and fluid leaks out of the blood
vessels (intravascular spaces of
capillaries) into the body tissues (extra
vascular).

22. Pathophysiology cont
 This causes swelling and puffiness of the
affected tissues (oedema).
 The swelling is usually painless, but the
swollen tissues may feel tight.
 Fluid loss from the vascular system to the
extra vascular will lead to reduced
circulatory volume (Hypovolaemia)
 Leading to reduced cardiac out put
which will culminate in reduced renal
blood flow
 This will cause Reduced glomerular
filtration rate (GFR), causing renal

23. Pathophysiology cont
 Macula dense cells of the juxtaglomerular
apparatus are stimulated to secrete
rennin.
 Rennin will cause the activation of
angiotensinogen to angiotensin I
 Angiotensin I will later be converted to
angiotensin II with the help of angiotensin
converting enzyme from the
pneumocytes.
 Angiotensin will cause vasoconstriction in
order to increase renal blood flow.

24. Pathophysiology cont
 It also acts directly on the adrenal
cortex to cause secretion of
aldosterone which increases sodium
reabsoprtion in the proximal tubules
and as sodium is being retained, water
is passively retained too.
 This will worsen the oedema causing it
to be generalized (Anasarca).
 An increase in size and number of
pores allows passage of more and
large protein molecules

25. Pathophysiology cont
 Then body responds to
Hypoalbuminemia by stimulating the liver
to synthesis of generalized protein (
including lipoprotein ) and lipid in the
liver ,the lipoprotein high molecular
weight is not lost in urine instead
accumulates leading to hyperlipidemia.
 Some patients develop progressive renal
insufficiency and ultimately may lead to
end-stage renal disease requiring
dialysis or transplantation.

26. Summary of pathophysiology
The underlying problem in nephrotic
syndrome is caused by the loss of
charge selectivity of the glomerular
basement membrane which permits
negatively charged proteins primarily
albumin to pass through the capillary
walls into urine.
Excessive urine loss of protein leads to
a decrease in serum protein (hypo
albinaemia).

27. The choroidal osmotic pressure that holds
water in the vascular compartment is reduced
because of the decrease in the amount of
serum albumin.
This allows fluids to flow from the capillaries
into the interstitial space thus producing
oedema.
The shift of fluid from plasma to the interstitial
spaces reduces the intravascular volume
(hypovolemia) which in turn stimulates the
renin-angiotensin system and the secretion of
antidiuretic hormone thus producing
hypertension.
The loss of proteins particularly immunoglobins

28. Signs and symptoms
 Severe generalized oedema due to
low albumin level and retention of
water and sodium.
- Oedema maybe minimal or massive
- It is faced apparent around the eyes
- Dependant oedema occurs in areas of
the body such as ankles, hands, feet
and genitalia
- Fluids that accumulate in the body
spaces may give rise to ascites
- Striae may appear on the skin from
over stretching

29.  Pronounced proteinuria due to damage
to the glomerular basement membrane
 Hypoalbuminemia due to albiminuria
 Hyperlipidemia due to increased hepatic
synthesis of lipids
 Urine volume and renal function may be
either normal or greatly reduced to
damage to the kidney.
 Profound weight gain due to oedema
and child may actually double normal
weight
 Decreased urine output during
oedematous stage and urine appears
concentrated/frothy

30. Signs and symptoms cont
 Dyspnea due to pulmonary oedema or
congestion.
 Peri orbital edema due to low plasma
protein
 Fatigue is common as renal function
reduces dramatically.
 Anorexia is common due to GIT
involvement, ascites with impaired
absorption.
 Pallor,irritability,lethargy,fatigue due to
anaemia
 GIT disturbances including vomiting,
diarrhoea and anorexia

31. Diagnosis
 Blood for serum albumin will be low
 Blood for serum cholesterol will be
increased
 Blood for Urea and electrolytes will
show electrolyte imbalance such as
low potassium levels.
 Renal biopsy will help to confirm the
diagnosis or reveal the extent of renal
damage
 Urinalysis will show proteinuria 2+or
greater, haematuria

32. Diagnosis cont’
 Creatinine and creatinine clearance.
Results of these tests give information
on how well your kidneys are working.
 History may reveal predisposing
factors like gold poisoning, diabetes,
etc
 Clinical feature will show generalized
oedema
 24 hour urine protein and frequently it
will show 2g/m²/day

33. Diagnosis cont’
 Kidney ultrasound to look at the
kidneys. This exam can rule out other
cause.
 A 24-hour urine collection, which
measures the total amount of protein
in the urine collected over 24 hours> it
will show that protein loss is high.
 Blood examination total protein will be
reduced, albumin will be less than
2g/dl, cholesterol increased 200mg/dl

34. Treatment
 Treatment of nephrotic syndrome
depends on the cause of the disease
and may include:
 Diuretics, such as or furosemide
(Lasix), to reduce oedema dose 0.5-
1.5mg/kg body weight.

35. Treatment
 Medications, such as angiotensin-
converting enzyme (ACE) inhibitors
and angiotensin II receptor blockers
(ARBs), to reduce the amount of
protein lost in the urine, lower blood
pressure, and slow the progress of the
disease.
 In rare cases, salt-free albumin given
through a vein (IV). Albumin helps
remove extra fluid from the tissues.

36. Treatment cont
 Corticosteroids may be useful in
controlling the illness, e.g.
hydrocortisone 25-100mg. Or
predinisolone5-25mg daily.
 Bed rest in patients with severe
oedema or those with infections
 Antibiotics if infection suspected or for
prophylaxis e.g. Amoxyl 62.5-250mg
tds for 5/7
 Dietary protein is prescribed at 1g/kg
body weight.

37. Steroid therapy
Prednisolone is usually the drug of choice
because it is less likely to induce salt
retention and potassium loss.
Dose : 60mg/m²/day or 2mg/kg/day.
Maximum dose is 80mg/kg for 4 weeks.
After daily steroid therapy the prednisolone
should be discontinued slowly to avoid
complications of steroid withdrawal
particularly intracranial hypertension.
Use alternate day prednisolone over a
period of 8 weeks

38. Other drugs
These should be considered when the child lapses
frequently (4-6/year) or becomes steroid resistant
or steroid dependant or demonstrates
unacceptable S/E of steroid therapy.
1. Levamisole
2. Cyclosporine
3. Cyclophosphamide
4. Intravenous albumin 25% to shift fluid from
interstitial spaces into the vascular system.
This is a temporal treatment to relieve oedema in
severe cases that causes respiratory distress and
severe discomfort.

39. Nursing management(specific)
 Problems identified
 Altered nutrition
 Fluid volume deficit
 Body image disturbance
 Risk of injury and infection
 Altered tissue perfusion

40. Specific Nursing Management
 Aims :
 To reduce oedema
 To protect the child from infection
 To correct the fluid deficit
 To maintain the serum albumin levels
 Enhance the nutritional status

41. Specific Nursing care cont’
 Environment
 Patient should be nursed in the general
ward separate from infectious conditions
to reduce risk of contracting infections
because of reduced immunity due to
protein loss.
 The room should be well ventilated, dust
free with necessary accessories such as
bed extra pillows for upright position in
respiratory distress episodes.
 All objects that can cause injury should
be removed from the room to prevent
injuries and the floor should not be
slippery

42. Position
 Position the child so that areas with oedema
are not in contact
 Place a pillow in between the child’s legs
when lying on sides to prevent edematous
areas to be in contact with each other
 Patient can assume a position of comfort
coupled with frequent change of position to
prevent pressure sore formation.
 careful positioning is important to prevent
infection and promote comfort.
 Preferably air mattresses or reduced
pressure mattresses should be used as they
promote comfort and prevent pressure sore
formation.

43. Nursing care cont’
 Rest and activity
 Complete bed rest is encouraged in
severe oedema and patient can hardly
tolerate any activity in the acute
phase.
 Passive exercises to be done to
prevent deep vein thrombosis or
thrombophlebitis

44. observations
 Monitor patient’s intake and output
chart
 Weigh patient daily to monitor oedema
 Assess skin condition for any skin
breakdown
 Observe for signs and symptoms of
infection like raised temperature and
pulmonary oedema such as dyspnoea
 If dyspnoea present patient should be
propped up to allow for good lung
expansion.

45.  Observe for S/E and complications of
therapy such as Cushing Syndrome
manifested by increased body hair,
rounding face (moon face), abdominal
distension, increased appetite and
acne.
 Vital signs 4 hourly
 Daily urinalysis

46. Nursing care cont’
 Psychological care
 Explain the condition to the patient and
the family to make them know what is
wrong.
 Encourage frequent visiting and allow as
much parental participation in child’s
care to allay anxiety.
 Allow the child and relatives verbalize
fears, concerns and worries, for example
patient and parents may worried about
the body disfigurement because of
oedema and give appropriate
reassurance to allay anxiety

47. Nursing management cont
 Nutrition and Fluids
 Promote adequate nutrition
 Low sodium intake should be
encouraged to prevent more fluid
retention which can worsen oedema.
 Recommended protein intake should
be 1g/kg body weight to replace lost
proteins as well as prevent buildup of
wastes in the blood.

48. Nutrition cont’
 Dietetic guidelines should be drafted in to
know the quantities of the calories and
vitamins to boost energy and the immunity.
 Fluid intake should restricted to 1 litre in 24
hours and a fluid balance chart should be
maintained to monitor the intake and output.
 Low fat, low sugar intake should be provided.
 Provide food choices that appeal to the child
that are easy to eat.
 Offer foods high in potassium like bananas,
grapes, milk.

49. Hygiene
 Bath the child frequently and apply
powder on oedematous areas.
 Areas of concern are moist parts of
the body and oedematous male
genitalia
 Support the scrotum with cotton pads
for the child’s comfort
 Offer oral hygiene regularly to help
reduce metallic taste.

50.  Prevent infection because urinary
protein losses impair body defenses.
 Invasive procedures must be avoided
or performed under strict aseptic
technique
 Edematous tissue is susceptible to
skin breakdown and infection hence
ensure skin care is important.

51. Infection Prevention
 Provide meticulous skin care to the
edematous child to prevent infection.
 If possible avoid invasive procedures
such as femoral vein punctures and
IM injections to reduce chances of
infection

52. Nursing management cont
Heath education
 Teach the parents about the child’s
medication
 Encourage continued medical follow up
visits
 Teach the parents how to recognize S/S of
infection
 Teach S/S of relapse that is increased
oedema, reduced urine out put
 Emphasize the importance of taking
medication according to the prescribed

53.  Disease information and how to prevent
infection should be discussed with the
patient.
 Explain to the patient the need to take
prescribed drugs and follow the
frequency
 If patient on steroids, explain to him that
adverse effects will subside as therapy
stops and patient should be warned not
to stop drugs abruptly or without the
doctor’s advice as this might worse the
condition.

54. Health education
 Encourage the patient to observe the
review dates to monitor the progress his
condition.
 Educate patient to assess self for fluid
status
 Explain to the patient importance of
adhering to dietary restrictions to meet
nutritional needs
 The patient should be taught how to do
urinalysis and if possible provide albustix
to use at home

55. Nursing management cont’
 Patient and the family should be
taught on how to identify signs of
infection and respiratory distress.
 He should be encouraged to report to
hospital immediately once identifies
raised temperature, ascites or
dyspnea.
 Promote good habits to prevent
infection
 Emphasize need for follow- up care to

56. Complication
 A high cholesterol level. If this persists
long-term it is a risk factor for developing
heart disease.
 Pulmonary edema due to fluid leak,
sometimes it leaks into lungs
causing hypoxia and dyspnoea
 CCF due to fluid overload
 Kidney failure due to hypovolaemia
 Infection: An increased risk of developing
infections due to loss/ leakage of
immunoglobulin (antibodies) in the urine
 Vitamin D deficiency can occur. Vitamin D
binding protein is lost.

57.  Susceptibility to infections
 Peritonitis
 Septicemia
 Cellulitis
 Thrombosis
 Acute renal failure

58. Summary
 Nephrotic syndrome is a condition that is
characterized by very high levels of protein in
the urine (proteinuria), low levels of protein in
the blood, swelling (oedema), and high
cholesterol.
 The cause of nephrotic syndrome is unknown
but there are predisposing factors such as
infections, systemic diseases, amyloidosis or
allergic reactions
 Therefore prevention of nephrotic syndrome
relies on controlling these factors/diseases.
 Treatment of nephrotic syndrome is based on
the underlying cause.

59. END OF LECTURE
 REFERENCES
 Haesh Mohan (2002), Textbook of
Pathology, 4th edition, Jaypee Brothers
medical publishers, New Delhi, India
 Nicholas A. B, Nicki R. C, Brian R. W and
John A. A. H (2007),Davidson’s principles &
practice of medicine, 20th edition, Churchill
Livingstone Elsevier. London. UK.
 Suzanne C. S, Janice.L. H, Brenda G. B and
Kerry H. C (2010), Brunner & Suddarth’s
Textbook of Medical-Surgical Nursing, 12th
edition, Wolters Kluwer Health, Hong Kong,
China