Nephrotic syndrome is a kidney disorder characterized by heavy protein in the urine, low blood protein levels, fluid retention causing edema, and high cholesterol. It is caused by damage to the glomeruli in the kidneys, which allows protein to pass into the urine. Common causes include infections, cancers, autoimmune diseases, medications, and genetic factors. Symptoms include generalized edema, fatigue, loss of appetite, and shortness of breath. Diagnosis involves blood and urine tests to detect low protein and high protein in the urine. Treatment focuses on reducing edema with diuretics, lowering blood pressure and proteinuria with ACE inhibitors, and using steroids to reduce inflammation in some cases.

1. Nephrotic Syndrome
By Mwila B. C. (2009)

2. Definition
 Nephrotic syndrome is a renal disorder
due to damage to the renal glomeruli
resulting in heavy protein urea, low
plasma protein, hyper lipidemia and
generalized oedema(Anasarca).
 It is a renal disease characterized by
increased permeability of the glomeruli to
protein (Protein urea), low plasma
protein, hyperlipidemia and generalized
oedema

3. Causes
 Nephrotic syndrome has been associated
with allergic reactions such as;
 Insect bites
 Pollen
 Acute glomerulonephritis especially the minimal
change type
 Post-streptococcal glomerulonephritis
 Infections
 Herpes zoster, HIV, hepatitis B, hepatitis C,
syphilis, malaria, tuberculosis.

4. Causes cont
 Systemic diseases
 Diabetes mellitus
 Systemic Lupus erythematosus (a
chronic inflammatory disease)
 Amyloidosis (A disease in which a wax,
starch like , glycoprotein (or amyloid)
accumulates in the tissue and organs)
 Sickle cell disease
4. Circulatory problems
 Severe congestive heart failure
 Constrictive pericarditis

5. Causes cont
 Cancers
 Hodgkin’s
 Lung
 Colon
 Breast
 Renal transplantation
 Chronic kidney failure
 Pregnancy (Pre eclampsia)
 Chronic kidney failure
 The cause of nephrotic syndrome in children is
usually idiopathic

6. Causes cont
 Medicines, such as nonsteroidal
anti-inflammatory drugs,
penicillamine, gold therapy, or
captopril.

7. Incidence
 Males are more commonly affected
than females.

8. Pathophysiology
 The initial physiologic change is damage
to the cells in the glomerular basement
membrane from immune complex
deposition, nephrotoxic antibodies or any
other cause already mentioned.
 The damage results in increased
glomerular basement membrane porosity
and permeability to protein resulting in
proteinuria

9. Pathophysiology cont
 This results in reduced plasma protein
such as albumin.
 The reduced plasma protein leads to
reduced oncotic or osmotic pressure.
 This will lead to increase movement of
fluids from the intra vascular spaces into
the extra vascular as well as reduced
ability to pull back fluids into the
capillaries

10. Pathophysiology cont
 This will lead to edema
 Fluid loss from the vascular system to the
extra vascular will lead to reduced
circulatory volume (Hypovolaemia)
 This will lead to reduced cardiac out put
which will culminate in reduced renal
blood flow
 This will cause Reduced glomerular
filtration rate (GFR), causing renal
ischaemia.

11. Pathophysiology cont
 This will lead to the release of 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.
 Angiotensin will cause vasoconstriction in
order to increase renal blood flow.

12. Pathophysiology cont
 It will also lead to increased secretion of
aldosterone to retain more sodium and
water
 This will worsen the oedema causing it to
be generalized (Anasarca)
 Proteinuria: Occurs due to the structural
damage to the glomerular basement
membrane
 An increase in size and number of pores
allows passage of more and large protein
molecules

13. Pathophysiology cont
 Negatively charged fixed
components in the capillary walls of
the glomerular repel negatively
charged protein molecules
 Reduction of these fixed charged
components results in the genesis
of heavy proteinuria

14. Pathophysiology cont
 Hyperlipidaemia: Diminished
plasma oncotic pressure stimulate
hepatic lipoprotein synthesis
 Low-density lipoproteins and
cholesterol are elevated most
frequently causing the
Hyperlipidaemia.

15. Signs and symptoms
 Severe generalized oedema due to low
albumin level and retention of water and
sodium
 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.

16. 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, ascitis with impaired
absorption.

17. 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

18. 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
 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.

19. 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.
 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.

20. 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.

21. Nursing care
Refer to Glomerulonephritis

22. Nursing management
NURSING MANAGEMENT
 Monitor patient’s intake and output
 Weigh patient daily to monitor
oedema
 Assess skin condition for any skin
breakdown
 Observe for signs and symptoms of
infection and pulmonary oedema

23. Nursing management cont
 Promote adequate nutrition
 Offer oral hygiene regulary to help
reduce metallic taste
 Prevent infection because urinary
protein losses impair body defences
 When infection is suspected address
the problem immidiately

24. Nursing management cont
 Protect patient against sources of
infection
 Invasive procedures must be
avoided or performed under strict
aseptic technique
 Edematous tissue is susceptible to
skin breakdown and infection

25. Nursing management cont...
 Careful positioning and frequent
change of position increase comfort
and prevent infection
 Air or water matresses may
increase comfort and relieve skin
pressure

26. Nursing management cont
 Educate patient on medication
regimen
 Educate patient on dietary
adjustments and methods to meet
nutritional needs
 Educate patient to assess self for
fluid status

27. Nursing management cont
 Promote good habits to prevent
infection
 Emphasize need for follow- up care
to monitor renal function

28. Nursing management cont
 Kidney failure
 CCF due to fluid overload
 Pulmonary edema

29. End of the lecture
Thank your for your attention
And may our good lord bless and protect you all
(Mwila b. c. 2009)