SILVER MAPLE COLLEGE
OF
HEALTH SCIENCES
STUDENT NAME: STUDENT ID:
FRED MWANSA 23010020
JENALA TEMBO 23010093
THELMA MWALE 23010025
1
INTRODUCTION
Nephrotic syndrome is a common kidney disorder in children,
characterized by significant proteinuria, hypoalbuminemia,
hyperlipidemia, and edema.
It results from the damage to the glomerular filtration barrier,
leading to protein leakage into the urine.
This condition poses a significant challenge in pediatric
healthcare due to its chronic nature, risk of complications, and
impact on the child’s growth and development.
2
This assignment explores the standard of causes, predisposing
factors, pathophysiology, signs and symptoms, medical
management, nursing care, complications and prevention of
nephrotic syndrome in children. The goal is to enhance
understanding and promote best practices in the care of children
with nephrotic syndrome.
3
GENERAL OBJECTIVES
At the end of this presentation students should have a general
understanding of what nephrotic syndrome and how it can be
managed.
SPECIFIC OBJECTIVES
At the end of the presentation students should be able to have a
deepened understanding on nephrotic syndrome in order to
improve patient care…
The pathophysiology of nephrotic syndrome and Identify the
key causes and risk factors associated with nephrotic syndrome.
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The recognition of the clinical manifestation and explore
diagnostic methods for nephrotic syndrome.
The medical management and treatment options and to also
outline the nursing care and interventions for patients with
nephrotic syndrome.
The identification of potential complications, exploration of
preventive measures and promotion of patient educationand
empowerment in managing nephrotic syndrome.
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DEFINITION
NEPHROTIC SYNDROME: Is a kidney disorder
characterized by a group of clinical signs and symptoms
resulting from damage to the glomeruli (the small filtering units
of the kidneys).
This damage increases the permeability (the ability to filter
substances) of the glomerular membrane, allowing proteins
(primarily albumin) to leak from the blood into the urine in
excessive amounts.
This condition leads to significant protein loss in the urine
(proteinuria), low protein levels in the blood
(hypoalbuminemia), high blood cholesterol levels
(hyperlipidemia) and swelling (edema), particularly in the legs, 6
feet and around the eyes.
CAUSES
The causes of nephrotic syndrome are categorized in two parts,
namely the primary and secondary causes.
Primary causes
The primary causes for nephrotic syndrome are; kidney diseases
that directly affect the glomeruli such minimal change disease,
focal segmental glomerulosclerosis (FSGS), and membranous
neuropathy.
Minimal Change Disease (MCD): this is a kidney disorder
that primarily affects the glomeruli and the glomeruli generally
lose their ability to retain large molecules like proteins,
resulting in significant protein leakage into the urine. 7
It’s a major cause of nephrotic syndrome characterized by high
levels of protein in urine, low levels of protein in blood, high
cholesterol levels and swelling (edema).
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It is the most common cause of nephrotic syndrome in children
but can also occur in adults. The diseases is named “minimal
change” because under a regular microscope, the glomeruli
appear almost normal, with only minor changes visible under an
electron microscope.
It is mainly idiopathic but can also be triggered by allergies or
recent infections (respiratory infections), toxins or vaccinations
(in rare cases) and autoimmune disorders (though less common)
Focal Segmental Glomerulosclerosis (FSGS): this is a type of
kidney disease characterized by scarring (sclerosis) of some
sections of the kidney’s filtering units called glomeruli.
This scarring is “focal” because it affects only some glomeruli
and “segmental” because it impacts only portions of each 9
affected glomerulus.
This is an idiopathic disease though it may be related to genetic
or immune factors that affect the glomeruli and can also be
caused by other factors such as obesity, sickle cell disease, viral
infections such as HIV, certain drugs like heroin and anabolic
steroids plus chronic kidney stress from reduced kidney mass or
injury
Membranous Nephropathy (MN): is a kidney disease
characterized by thickening of the glomerular basement
membrane, the part of the glomeruli responsible for filtering
waste and excess substances from the blood.
This thickening is due to the disposition of immune complexes
(antibodies and antigens) along the membrane, which triggers an
inflammatory response and leads to kidney damage. 10
It is also mostly an idiopathic disease but can also be caused by
auto-immune diseases such as systemic lupus erythematosus,
infections such as hepatitis B, hepatitis C and syphilis, certain
medications such as non-steroidal anti-inflammatory drugs
(NSAIDs), and cancer particularly solid tumors like lung or
colon cancer.
It is a common cause of nephrotic syndrome in adults but is rare
in children.
Secondary causes
The secondary conditions outside the kidneys that can lead to
glomerular damage including:
Diabetes mellitus
Systemic lupus erythematosus (SLE) 11
Infections such as hepatitis and HIV
PATHOPHYSIOLOGY
The pathophysiology of nephrotic syndrome involves
complex mechanisms that lead to increased permeability of
the glomerular filtration barrier in the kidneys.
This increased permeability causes significant protein loss in
the urine, resulting in a cascade of physiological changes that
characterize the syndrome.
STEP BY STEP BREAKDOWN
OF THE PROCESS
1. GLOMERULAR DAMAGE
Nephrotic syndrome begins with the damage of the glomeruli
and the damage can be as a result of primary glomerular diseases
and secondary causes such as systemic diseases, infections or 12
certain medications which can indirectly damage the glomeruli.
The glomeruli filtration barrier is made of three layers namely;
the endothelium (inner lining of blood vessels), the glomerular
basement membrane (GBM), and the specialized cells called
podocytes (specialized cells that line the outer layer of the
glomerular capillaries and are found in the bowman’s capsule).
Together these layers create a selective permeable barrier that
normally retains large molecules like proteins in the blood while
allowing waste products and small molecules to pass into urine
2. INCREASED GLOMERULAR PERMEABILIT
Due to glomerular damage, there is an alteration in the structure
or function of the glomerular filtration barrier.
Podocyte effacement: podocytes, the cells covering the
glomerular capillaries, have specialized foot processes that form
filtration slits. In nephrotic syndrome, these foot processes 13
become “effaced” or flattened, disrupting the filtration barrier
and allowing large molecules, especially proteins to leak
Basement membrane changes: In some types of nephrotic
syndrome, such as membranous nephropathy, immune
complexes deposit along the glomerular basement membrane,
thickening it and increasing permeability.
3. PROTEINURIA (EXCESSIVE PROTEIN LOSS IN
URINE)
The increased permeability allows proteins, primarily albumin,
to pass into urine a condition known as proteinuria.
Albumin is the main protein affected because of its relatively
small size and its role in maintaining blood oncotic pressure.
Proteinuria levels are typically very high in nephrotic syndrome,
with urine protein excretion exceeding 3.5 grams per day.
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4. HYPOALBUMINENMIA (LOW BLOOD ALBUMIN
LEVELS).
As albumin and other proteins re lost through urine, their levels
in the bloodstream decrease, leading to hypoalbuminemia.
Albumin is essential for maintaining oncotic pressure, which
helps keep fluid in the blood vessels. Without sufficient
albumin, the pressure drops, causing fluid to leak out of the
blood vessels and into surrounding tissues.
5. EDEMA (SWELLING)
Due to the in oncotic pressure, fluid moves from the blood
vessels into the interstitial spaces, causing edema (swelling).
Edema is typically seen in areas such as the legs, ankles, feet,
and around the eyes. It can also lead to generalized swelling or
anasarca, in severe cases. 15
Additionally, the kidneys often respond to low blood volume by
retaining more sodium water, which worsens edema.
6. HYPERLIPIDEMIA (ELEVATED BLOOD LIPIDS
The liver compensates for the loss of protein by increasing it’s
production of proteins, including albumin and lipoproteins
(which carry lipids or fats in the blood).
This overproduction of lipoproteins results in hyperlipidemia-
high levels of cholesterol and triglycerides in the blood.
Hyperlipidemia is common in nephrotic syndrome and
contributes to an increased risk of cardiovascular problems.
7. HYPERCOAGULABILITY (INCREASED RISK OF
BLOOD CLOTS)
Patients with nephrotic syndrome are at a higher risk for blood
clots (thrombosis) due to several factors:
Loss of anticoagulant proteins, such as antithrombin III, in the
urine, which would normally prevent clot formation. 16
Increased production of procoagulant factors by bthe liver as it
attempts to compensate for protein loss.
The hyperlipidemic and edematous state also contributes to a
higher risk of clotting.
8. INCREASED SUSCEPTIBILITY TO INFECTIONS
Protein loss also includes loss certain immunoglobulins
(antibodies), which weakens the immune response and makes
patients more vulnerable to infections, particularly respiratory
and peritoneal infections.
Edema may further compromise the immune system by
providing an environment conducive to bacterial growth,
especially in case of prolonged edema.
9. PROGRESSION TO CHRONIC KIDNEY DISEASE (CKD)
In some cases, especially if untreated, nephrotic syndrome can
lead to ongoing kidney damage.
17
Chronic proteinuria and inflammation can progressively scar the
kidneys (a process known as glomerulosclerosis), reducing their
filtering capacity and potentially leading to chronic kidney
disease (CKD) or end-stage renal disease (ESRD), requiring
dialysis or kidney transplantation.
SIGNS AND SYMPTOMS
Some of the signs and symptoms of nephrotic syndrome may
include:
Severe swelling (edema), especially around the eyes, legs,
ankles and feet as a result of protein loss in the urine and it
reduces the blood’s ability to retain fluids thereby leading to the
leakage of fluids out of the blood vessels to accumulate in the
surrounding tissues.
Foamy urine due to excess protein in the urine. 18
Weight gain from fluid retention.
Fatigue and loss of appetite.
Bloating and fluid in the abdomen
Generalized body swelling
Blood clots due to loss of proteins that prevent clotting
High blood pressure: excess fluid and changes in the kidney
function can lead to hypertension.
Urinary changes: one might notice changes in the color or
frequency of urination.
Muscle wasting: this can result from prolonged protein loss
Infections: individuals with nephrotic syndrome are more
susceptible to infections.
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MEDICAL MANAGEMENT
The medical management of nephrotic syndrome involves
addressing the underlying cause, controlling symptoms, preventing
complications and protecting kidney function.
1. MANAGEMENT GOALS
Alleviate symptoms (reduce edema)
Control proteinuria and prevent relapses.
Manage complications like infections, thromboembolism and
chronic kidney disease.
Treat underlying causes if secondary nephrotic syndrome is
diagnosed.
2. ASSESSMENT AND DIAGNOSIS
Clinical assessment:
20
Assess for hallmark symptoms: generalized edema, frothy urine
and weight gain.
Monitor blood pressure and assess for signs of complications
like infections or thromboembolic events.
Laboratory Investigations:
Urinalysis: check for proteinuria (>3.5g/24 hours).
Serum Albumin: Hypoalbuminemia (<2.5/dL).
Lipid profile: Hyperlipidemia
Renal function tests: Creatinine and urea levels.
Consider kidney biopsy if secondary causes or atypical features
are suspected.
21
3. Pharmacological management
Corticosteroids(first-line treatment):
Prednisolone: 1-2 mg/kg/day (maximum 60 mg/day) for 4-6
weeks then tapered gradually.
Monitor for side effects: hyperglycemia, hypertension and
infection.
Immunosupresssive Therapy (For Steroid-Resistant Cases):
Cyclophosphamide, cyclosporine or tacrolimus.
Monitor kidney function and drug levels as indicated
Diuretics:
Furosemide or spironolactone for edema control.
Use cautiously to avoid hypovolemia.
Albumin infusions:
For severe hypoalbuminemia with diuretic- resistant edema 22
Antihypertensives:
Angiotensin-converting enzyme inhibitors (ACEIs) or
angiotensin receptor blockers (ARBs) to reduce proteinuria.
Anticoagulants:
Low molecular weight heparin or warfarin for thromboembolic
complications.
Antibiotics:
Empirical treatment for suspected infections; prophylactic use in
high-risk cases.
4. NUTRITIONAL MANAGEMENT
Low sodium diet to manage edema.
Adequate protein intake to prevent malnutrition without
worsening proteinuria.
Monitor and manage dyslipidemia with diet or statins if 23
necessary.
5. MONITORING AND FOLLOW-UP
Regular monitoring of:
o Edema status, weight and blood pressure.
o Urine protein levels and renal function tests.
o Side effects of medications
Educate caregivers on recognizing relapse symptoms and the
importance of medication adherence.
6. COMPLICATION MANAGEMENT
Infections:
Prompt treatment of infections like peritonitis or pneumonia.
Routine vaccinations (avoid live vaccines during
immunosuppressive therapy).
Thromboembolic events
Early detection and management with anticoagulants if needed. 24
Chronic kidney disease:
Close monitoring and referral for progressive renal dysfunction.
7. REFERRAL AND MULTIDISCIPLINARY CARE
Refer to a pediatric nephrologist:
SRNS, atypical nephrotic syndrome or complications.
Multidisciplinary team involvement:
Collaborate with dietitians, psychologists and social workers for
holistic care.
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NURSING MANAGEMENT
1. Aims
Relieve symptoms of edema and proteinuria.
Prevent and manage complications such as infections,
malnutrition, and thromboembolism.
Educate the patient and family on disease management and
relapse prevention.
2. Assessment
History Taking:
Document onset and duration of symptoms (e.g., edema,
reduced urine output).
Inquire about recent infections, medications, and family history
26
of renal disease.
Physical Assessment:
Monitor for generalized edema (facial, periorbital, abdominal,
and lower extremities).
Check vital signs: blood pressure, heart rate, and temperature for
signs of infection or hypovolemia.
Assess for signs of complications, such as difficulty breathing
(pulmonary edema) or thrombosis (pain/swelling in extremities).
Urine Output and Appearance:
Measure and record urine output and note changes in color,
volume, or frothy appearance.
3. Nursing Interventions
a) Monitoring and Observation:
Measure and record weight daily to monitor fluid retention. 27
Monitor intake and output to assess fluid balance.
Regularly check vital signs, especially blood pressure, to detect
hypotension or hypertension.
Perform regular skin assessments for signs of breakdown due to
edema.
b) Symptom Management:
Edema:
Administer prescribed diuretics as ordered and monitor their
effectiveness.
Elevate edematous limbs and encourage the patient to change
positions frequently to reduce fluid pooling.
Proteinuria:
Encourage compliance with prescribed medications (e.g.,
corticosteroids, ACE inhibitors). 28
c) Infection Prevention:
Maintain strict hand hygiene and aseptic techniques during care.
Monitor for signs of infection (e.g., fever, increased white blood
cell count, redness, or warmth).
Educate caregivers about early signs of infections and the
importance of vaccination.
d) Nutritional Support:
Implement a low-sodium diet to reduce edema.
Encourage adequate protein intake within prescribed limits to
prevent malnutrition.
Collaborate with a dietitian for individualized dietary planning.
e) Skin Integrity:
Keep the skin clean and dry to prevent breakdown.
Apply barrier creams or dressings to protect edematous skin. 29
Reposition the patient frequently to avoid pressure ulcers.
f) Psychosocial Support:
Provide emotional support to alleviate anxiety about the
condition and its management.
Involve the family in care and provide education on home care
and relapse management.
Encourage interaction with peers or support groups for children
and families coping with chronic illnesses.
g) Medication Administration:
Administer medications as prescribed, such as:
Corticosteroids to reduce proteinuria.
Diuretics for fluid management.
Antihypertensives if required.
Monitor for side effects of medications and report any adverse 30
effects promptly.
4. Education and Discharge Planning
Teach the caregivers how to monitor for early signs of relapse
(e.g., edema, proteinuria using dipsticks).
Educate on the importance of adhering to medications and
follow-up appointments.
Encourage vaccination to prevent infections (avoid live vaccines
during immunosuppressive therapy).
Provide dietary advice on low-sodium and balanced nutrition.
5. Evaluation of Care
Evaluate the effectiveness of interventions by monitoring:
Reduction in edema and improvement in urine output.
Weight stabilization.
Adherence to medications and lifestyle changes. 31
Ensure the patient and family understand the disease process and
management plan.
COMPLICATIONS
1. Infections
Common Infections:
Peritonitis: Often caused by Streptococcus pneumoniae or
Escherichia coli.
Respiratory Infections: Increased susceptibility to pneumonia.
Urinary Tract Infections (UTIs): Frequent due to immune
suppression.
Sepsis: Systemic infection due to loss of immunoglobulins in
urine.
Skin Infections: Such as cellulitis.
Contributing Factors:
32
Hypoalbuminemia and protein loss, leading to immune
deficiency.
Use of corticosteroids or immunosuppressive drugs.
2. Thromboembolic Events
Complications:
Deep vein thrombosis (DVT).
Pulmonary embolism.
Renal vein thrombosis.
Cause:
Hypercoagulable state due to loss of antithrombin III, protein C,
and protein S in urine.
3. Hypovolemia
Manifestations:
Severe edema causing reduced effective circulating volume. 33
Symptoms include hypotension, tachycardia, and oliguria.
Cause:
Shift of fluid from intravascular to interstitial spaces.
4. Electrolyte Imbalance
Hyponatremia:
Caused by fluid retention and dilutional effect.
Hyperkalemia or Hypokalemia:
May occur due to diuretic therapy or kidney dysfunction.
Hypocalcemia:
Low serum calcium levels due to hypoalbuminemia.
5. Malnutrition
Manifestations: 34
Muscle wasting, fatigue, and delayed growth in children.
Cause:
Protein loss in urine combined with reduced appetite due to
edema.
6. Hyperlipidemia
Complication:
Increased cholesterol and triglyceride levels.
Cause:
Compensatory hepatic synthesis due to loss of protein in urine.
Risk:
Long-term cardiovascular complications if left untreated.
7. Acute Kidney Injury (AKI)
35
Manifestations:
Sudden decline in renal function.
Cause:
Hypovolemia, prolonged use of nephrotoxic drugs, or severe
infections.
8. Chronic Kidney Disease (CKD)
Risk:
Persistent proteinuria and repeated relapses may lead to
progressive kidney damage.
Cause:
Steroid-resistant nephrotic syndrome or secondary nephrotic
syndrome.
9. Psychosocial Issues
Manifestations: 36
Anxiety, depression, and poor self-esteem in children due to the
Family Burden:
Financial strain and caregiver stress due to frequent relapses and
prolonged treatments.
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PREVENTION
The preventive approach focuses on reducing triggers, managing
risk factors, and empowering families through education to
minimize the burden of nephrotic syndrome in children.
1. Preventing Primary Nephrotic Syndrome
Early Detection and Management:
Monitor children with a family history of nephrotic syndrome or
kidney disease for early signs such as edema and proteinuria.
Allergy and Infection Control:
Manage allergies and treat infections promptly to reduce
possible triggers.
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2. Preventing Secondary Nephrotic Syndrome
Infection Prevention:
Ensure timely vaccination, especially against Streptococcus
pneumoniae, Haemophilus influenzae, and varicella.
Practice good hygiene to prevent bacterial and viral infections.
Educate families about early treatment of respiratory and skin
infections.
Avoid Nephrotoxic Substances:
Minimize exposure to drugs such as NSAIDs and other
nephrotoxic agents.
Avoid herbal remedies or toxins that may harm the kidneys.
Manage Underlying Conditions:
39
Effectively control systemic diseases like diabetes or lupus that
may lead to nephrotic syndrome.
3. Lifestyle Modifications for Relapse Prevention
Balanced Diet:
Encourage a low-sodium diet to reduce edema risk.
Provide adequate protein intake to prevent malnutrition without
worsening proteinuria.
Hydration:
Encourage adequate fluid intake unless contraindicated by the
child’s condition.
Avoiding Stress:
Help families create a stress-free environment, as stress may
trigger relapses.
40
4. Preventing Complications
Regular Monitoring:
Advise caregivers to monitor urine protein levels using dipsticks
at home.
Schedule regular follow-ups to monitor renal function and
nutritional status.
Early Detection of Relapse:
Educate families on recognizing signs of relapse, such as
swelling or frothy urine, and seek early medical intervention.
Thrombosis Prevention:
Encourage mobility and prevent prolonged immobility in
children during illness. 41
5. Education and Awareness
Educate parents and caregivers on:
The importance of medication adherence, including
corticosteroids and immunosuppressants.
Recognizing early warning signs of infections or complications.
Provide age-appropriate education to children about their
condition to promote self-care as they grow older.
6. Access to Healthcare Services
Strengthen community healthcare services to provide
vaccinations, health education, and early interventions.
Advocate for timely referral to pediatric nephrologists for high-
risk children or those with persistent symptoms.
42
CONCLUSION
Nephrotic syndrome is a significant pediatric condition
characterized by proteinuria, hypoalbuminemia, edema, and
hyperlipidemia. It impacts the quality of life and overall health
of affected children, requiring timely diagnosis and effective
management to prevent complications.
While its exact cause often remains unknown, the condition can
result from primary kidney disease or secondary systemic
illnesses.
With appropriate medical interventions, including corticosteroid
therapy and supportive care, most children, particularly those
with steroid-sensitive nephrotic syndrome, achieve remission
and lead healthy lives. 43
Preventing complications such as infections, malnutrition, and
Education and awareness among healthcare providers and
caregivers are essential to ensure early recognition, proper
management, and adherence to treatment plans.
By adopting a holistic, patient-centered approach, nephrotic
syndrome can be effectively managed, enabling affected
children to achieve optimal growth and development.
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REFERENCES
1. Nelson Textbook of Pediatrics, 21st Edition
Kliegman, R. M., St. Geme, J. W., Blum, N. J., Shah, S. S., &
Tasker, R. C. (2020).
2. Kidney Disease: Improving Global Outcomes (KDIGO)
Guidelines (2012).
3. World Health Organization (WHO) Guidelines:
Management of conditions associated with malnutrition and
infections in pediatric populations.
4. Pediatric Nephrology, 7th Edition
Avner, E. D., Harmon, W. E., & Niaudet, P. (2016).
45
5. Nursing and Midwifery Council of Zambia (NMCZ) Standards
of Practice.
6. Nephrotic Syndrome in Children: A Toolkit for Primary Care
Providers.
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