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Case Scenario
 A 7 years old male boy was admitted with the chief complaints of
facial puffiness and passing smoky and frothy urine for 1 week. The
facial puffiness initially started off as periorbital edema. Urine output
was also decreased and had complaint of low grade fever for 1 week.
General examination revealed pallor, blood pressure of 139/96 mm
of Hg and an erythematous scaly circular skin lesion on right elbow.
Urine biochemistry revealed protein 3+, RBCs 4+, blood urea was
also raised. USG was suggestive of bilateral enlarged and pale
kidneys.
Nephrotic Syndrome
Presented by
Karan choudhary
CON AIIMS JODHPUR
Introduction
Nephrotic syndrome may be caused by primary (idiopathic) renal
disease or by a variety of secondary causes. Patients present with marked
oedema, proteinuria, hypoalbuminemia, and often hyperlipidaemia.
 It can happen when tiny filtering units (glomeruli) within the kidney are
damaged.
This damage within the kidney allows protein normally kept in body to
leak into the urine, which lowers the amount of protein in the blood.
Continued…
Definition
Nephrotic syndrome is a type of renal
failure characterized by increased
glomerular permeability and is manifested
by marked increase in protein (albumin) in
urine (proteinuria/albuminuria), a decrease
in albumin in blood (hypalbuminaemia),
diffuse oedema, high serum cholesterol, and
low-density lipoproteins (hyperlipidaemia).
Incidence
- Nephrotic syndrome is 15 times more common in children.
- Most cases in children are due to minimal-change disease.
- In adults, the most common form is membranous glomerulonephritis,
followed by FSGS.
- Diabetic nephropathy is emerging as a major cause of nephrotic
syndrome.
Focal Segmental Glomerulosclerosis
Classification
Nephrotic syndrome can be:
1. Primary, being a disease specific to the kidneys
2. Secondary, being a renal manifestation of a systemic general illness.
3. Congenital
Causes
Primary causes:
• Minimal-change nephropathy(70-90% children and 10-15% in adult)
• Focal glomerulosclerosis (15% in adult)
• Membranous nephropathy (30% in adult)
• Mesangial proliferative glomerulonephritis
• Rapidly progressive glomerulonephritis
Secondary causes:
• Diabetes mellitus
• Systemic Lupus Erythematosus
• Amyloidosis and paraproteinemia
• Viral infections (E.g. Hepatitis B, hepatitis C, HIV)
• Preeclampsia
Pathophysiology
It occurs with many intrinsic kidney
diseases and systemic diseases that
cause glomerular damage.
It is not a specific glomerular disease
but a constellation of clinical findings
that result from the glomerular damage.
Clinical Manifestations
Oedema (major manifestation): usually soft and pitting and most commonly
occurs around the eyes (periorbital), in dependent areas (sacrum, ankles, and
hands), and in abdomen (ascites).
Other symptoms:
• malaise
• headache
• irritability
• fatigue
• pleural effusion and pulmonary oedema
• hypertension
• anaemia
• anorexia
• abdominal pain
• diarrhoea
Assessment and diagnostic findings
1. History collection
2. Physical examination
3. Laboratory investigations
- Urine dipstick (confirm proteinuria)
- Random urine protein/creatinine ratio
- Serum creatinine (rule out acute renal failure, assess GFR)
- Serum albumin (assess degree of hypoalbuminemia)
- Lipid panel (assess degree of hyperlipidaemia)
Continued…
1. Protein electrophoresis may be performed on the urine to categorize the
type of proteinuria. The urine may also contain increased WBCs as well as
granular and epithelial casts.
2. A needle biopsy of the kidney may be performed for histologic
examination of renal tissue to confirm the diagnosis.
3. Serum markers: Anti – Clq antibodies are the most reliable markers for
assessing disease activity in lupus nephritis.
Complications
➢ Hypovolemia
➢ Infection (due to a deficient immune response)
➢ Thromboembolism (especially of the renal vein)
➢ Pulmonary emboli
➢ Acute renal failure (due to hypovolemia)
➢ Accelerated atherosclerosis (due to hyperlipidaemia)
➢ Progression to end-stage renal failure
Medical Management
The objective of management is to preserve renal function.
Treatment of most patients should include:
• fluid and sodium restriction,
• oral or intravenous diuretics, and
• angiotensin-converting enzyme inhibitors.
Some adults with nephrotic syndrome may benefit from
corticosteroid treatment.
Continued…
❖ Fluid and nutrition
- Creating a negative sodium balance will help reduce edema
- Restrict fluid intake to less than approx. 1.5L/day
❖ Diuretics
- Diuretics are the mainstay of medical management
- Loop diuretics – furosemide
❖ ACE inhibitors- reduce proteinuria and reduce progression of renal disease
❖ Albumin
- Intravenous albumin
❖ Corticosteroids or immunosuppressive agents
Nursing Management
Nursing assessment
1. Obtain history of onset symptoms including changes in characteristic
of urine and onset of edema
2. Perform physical examination looking for evidence of edema and
hypovolemia.
3. Assess vital signs, daily weights, intake and output, and laboratory
values.
Continued…
Nursing Diagnosis
1. Excess fluid volume related to fluid accumulation in tissues and third spaces.
2. Risk for imbalanced nutrition: less than body requirements related to anorexia.
3. Risk for impaired skin integrity related to edema.
4. Fatigue related to edema and disease process.
5. Risk for infection related to immunosuppression.
6. Deficient knowledge of the caregiver related to disease process, treatment, and
home care.
7. Compromised family coping related to care of a child with chronic illness
Patient education
- Teach client about sign and symptoms of nephrotic syndrome
- Review causes, purpose of prescribed treatments, and importance of long-
term therapy to prevent ESRD.
- Instruct client about the adverse effects of prescribed medications and
methods of preventing infection if taking immunosuppressive agents.
- Carefully review with client and family dietary and fluid restrictions.
- Discuss the importance of exercise, decreasing cholesterol intake and fat
intake.
SUMMARY:
In the above content, we have discussed about Nephrotic syndrome, its
definition, classification, causes, incidence, pathophysiology, clinical
manifestations, diagnostic finding, complications and management.
CONCLUSION:
Nephrotic syndrome is a type of renal failure characterized by increased
glomerular permeability and is manifested by massive proteinuria. Clinical
findings include a marked increase in protein (albumin) in urine
(proteinuria), a decrease in albumin in blood (hemoglobinemia), diffuse
oedema, high serum cholesterol, and low-density lipoproteins
(hyperlipidaemia). It can be primary or secondary. Management includes
medical and nursing management to preserve renal function.
REFERENCES
• Ross and Wilson, Anatomy & Physiology in Health and Illness,12th Edition, UN: Anne
Waugh and Allison Grant;2014, pg no. 224-238
• Brunner and Suddharths. Textbook of Medical Surgical Nursing.13th Edition. Volume II.
New Delhi: Wolter Kluwer Publication.
• Lewis. Medical Surgical Nursing Assessment and Management of Clinical Problems. 2nd
Edition. Volume II. New Delhi:Elsevier;2015.
• Joyce M. Black, Jane Hokanson Hawks. Medical Surgical Nursing Clinical Management
of positive outcomes. Volume II. New Delhi: Reed Elsevier India Private Limited;2015.
• Hockenberry J. and David Wilson. Wong’s essential of paediatric nursing,1st edition;
Elsevier;2015, pg no.340-448
Have a nice day !

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Nephrotic Syndrome .pdf

  • 1.
  • 2. Case Scenario  A 7 years old male boy was admitted with the chief complaints of facial puffiness and passing smoky and frothy urine for 1 week. The facial puffiness initially started off as periorbital edema. Urine output was also decreased and had complaint of low grade fever for 1 week. General examination revealed pallor, blood pressure of 139/96 mm of Hg and an erythematous scaly circular skin lesion on right elbow. Urine biochemistry revealed protein 3+, RBCs 4+, blood urea was also raised. USG was suggestive of bilateral enlarged and pale kidneys.
  • 3. Nephrotic Syndrome Presented by Karan choudhary CON AIIMS JODHPUR
  • 4. Introduction Nephrotic syndrome may be caused by primary (idiopathic) renal disease or by a variety of secondary causes. Patients present with marked oedema, proteinuria, hypoalbuminemia, and often hyperlipidaemia.  It can happen when tiny filtering units (glomeruli) within the kidney are damaged. This damage within the kidney allows protein normally kept in body to leak into the urine, which lowers the amount of protein in the blood.
  • 6. Definition Nephrotic syndrome is a type of renal failure characterized by increased glomerular permeability and is manifested by marked increase in protein (albumin) in urine (proteinuria/albuminuria), a decrease in albumin in blood (hypalbuminaemia), diffuse oedema, high serum cholesterol, and low-density lipoproteins (hyperlipidaemia).
  • 7. Incidence - Nephrotic syndrome is 15 times more common in children. - Most cases in children are due to minimal-change disease. - In adults, the most common form is membranous glomerulonephritis, followed by FSGS. - Diabetic nephropathy is emerging as a major cause of nephrotic syndrome.
  • 9. Classification Nephrotic syndrome can be: 1. Primary, being a disease specific to the kidneys 2. Secondary, being a renal manifestation of a systemic general illness. 3. Congenital
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  • 11. Causes Primary causes: • Minimal-change nephropathy(70-90% children and 10-15% in adult) • Focal glomerulosclerosis (15% in adult) • Membranous nephropathy (30% in adult) • Mesangial proliferative glomerulonephritis • Rapidly progressive glomerulonephritis Secondary causes: • Diabetes mellitus • Systemic Lupus Erythematosus • Amyloidosis and paraproteinemia • Viral infections (E.g. Hepatitis B, hepatitis C, HIV) • Preeclampsia
  • 12. Pathophysiology It occurs with many intrinsic kidney diseases and systemic diseases that cause glomerular damage. It is not a specific glomerular disease but a constellation of clinical findings that result from the glomerular damage.
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  • 14. Clinical Manifestations Oedema (major manifestation): usually soft and pitting and most commonly occurs around the eyes (periorbital), in dependent areas (sacrum, ankles, and hands), and in abdomen (ascites). Other symptoms: • malaise • headache • irritability • fatigue • pleural effusion and pulmonary oedema • hypertension • anaemia • anorexia • abdominal pain • diarrhoea
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  • 18. Assessment and diagnostic findings 1. History collection 2. Physical examination 3. Laboratory investigations - Urine dipstick (confirm proteinuria) - Random urine protein/creatinine ratio - Serum creatinine (rule out acute renal failure, assess GFR) - Serum albumin (assess degree of hypoalbuminemia) - Lipid panel (assess degree of hyperlipidaemia)
  • 19. Continued… 1. Protein electrophoresis may be performed on the urine to categorize the type of proteinuria. The urine may also contain increased WBCs as well as granular and epithelial casts. 2. A needle biopsy of the kidney may be performed for histologic examination of renal tissue to confirm the diagnosis. 3. Serum markers: Anti – Clq antibodies are the most reliable markers for assessing disease activity in lupus nephritis.
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  • 22. Complications ➢ Hypovolemia ➢ Infection (due to a deficient immune response) ➢ Thromboembolism (especially of the renal vein) ➢ Pulmonary emboli ➢ Acute renal failure (due to hypovolemia) ➢ Accelerated atherosclerosis (due to hyperlipidaemia) ➢ Progression to end-stage renal failure
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  • 24. Medical Management The objective of management is to preserve renal function. Treatment of most patients should include: • fluid and sodium restriction, • oral or intravenous diuretics, and • angiotensin-converting enzyme inhibitors. Some adults with nephrotic syndrome may benefit from corticosteroid treatment.
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  • 26. Continued… ❖ Fluid and nutrition - Creating a negative sodium balance will help reduce edema - Restrict fluid intake to less than approx. 1.5L/day ❖ Diuretics - Diuretics are the mainstay of medical management - Loop diuretics – furosemide ❖ ACE inhibitors- reduce proteinuria and reduce progression of renal disease ❖ Albumin - Intravenous albumin ❖ Corticosteroids or immunosuppressive agents
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  • 28. Nursing Management Nursing assessment 1. Obtain history of onset symptoms including changes in characteristic of urine and onset of edema 2. Perform physical examination looking for evidence of edema and hypovolemia. 3. Assess vital signs, daily weights, intake and output, and laboratory values.
  • 29. Continued… Nursing Diagnosis 1. Excess fluid volume related to fluid accumulation in tissues and third spaces. 2. Risk for imbalanced nutrition: less than body requirements related to anorexia. 3. Risk for impaired skin integrity related to edema. 4. Fatigue related to edema and disease process. 5. Risk for infection related to immunosuppression. 6. Deficient knowledge of the caregiver related to disease process, treatment, and home care. 7. Compromised family coping related to care of a child with chronic illness
  • 30. Patient education - Teach client about sign and symptoms of nephrotic syndrome - Review causes, purpose of prescribed treatments, and importance of long- term therapy to prevent ESRD. - Instruct client about the adverse effects of prescribed medications and methods of preventing infection if taking immunosuppressive agents. - Carefully review with client and family dietary and fluid restrictions. - Discuss the importance of exercise, decreasing cholesterol intake and fat intake.
  • 31. SUMMARY: In the above content, we have discussed about Nephrotic syndrome, its definition, classification, causes, incidence, pathophysiology, clinical manifestations, diagnostic finding, complications and management. CONCLUSION: Nephrotic syndrome is a type of renal failure characterized by increased glomerular permeability and is manifested by massive proteinuria. Clinical findings include a marked increase in protein (albumin) in urine (proteinuria), a decrease in albumin in blood (hemoglobinemia), diffuse oedema, high serum cholesterol, and low-density lipoproteins (hyperlipidaemia). It can be primary or secondary. Management includes medical and nursing management to preserve renal function.
  • 32. REFERENCES • Ross and Wilson, Anatomy & Physiology in Health and Illness,12th Edition, UN: Anne Waugh and Allison Grant;2014, pg no. 224-238 • Brunner and Suddharths. Textbook of Medical Surgical Nursing.13th Edition. Volume II. New Delhi: Wolter Kluwer Publication. • Lewis. Medical Surgical Nursing Assessment and Management of Clinical Problems. 2nd Edition. Volume II. New Delhi:Elsevier;2015. • Joyce M. Black, Jane Hokanson Hawks. Medical Surgical Nursing Clinical Management of positive outcomes. Volume II. New Delhi: Reed Elsevier India Private Limited;2015. • Hockenberry J. and David Wilson. Wong’s essential of paediatric nursing,1st edition; Elsevier;2015, pg no.340-448
  • 33. Have a nice day !