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  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