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Seminar on nephrotic syndrome

Submitted by, Mrs Bibi Baby 2 nd year MSc Nursing PION.

Submitted to, Mrs. Prasanna Balaji HOD of Medical Surgical Nursing PION.

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Content

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Introduction . Objectives . a. General objectives:At the end of the class student will have adequate knowledge about nephrotic syndrome. b. Specific objectives:At the end of the seminar students will able to:
1. describe nephrotic syndrome. 2. explain the incidence and risk factors of nephrotic syndrome. 3. enumerate the causes of nephrotic syndrome.

4. describe the pathophysiology of nephrotic syndrome.


5. enumerate the clinical manifestation of nephrotic syndrome. 6. explain the diagnosis of nephrotic syndrome.

7. describe the medical and nursing management of nephrotic syndrome. 8. enlist the nursing diagnosis and intervension of nephrotic syndrome.
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Journal /abstract. Bibliography .

NEPHROTIC SYNDROME INTRODUCTION

Nephrotic syndrome is usually caused by damage to the clusters of small blood vessels in kidneys that filter waste and excess water from blood. When healthy, these vessels keep blood protein from seeping into urine and out of body. When damaged, they don't perform this function effectively, and protein can leak out of blood and lead to swelling all over body (edema). DEFINITION Nephrotic syndrome is a primary glomerular disease characterized by the following: Marked increase in protein in the urine (proteinuria) Decrease in albumin in the blood (hypoalbuminemia) Edema High serum cholesterol and low-density lipoproteins (hyperlipidemia) The syndrome is apparent in any condition that seriously damages the glomerular capillary membrane and results in increased glomerular permeability. INCIDENCE Estimates on the annual incidence of nephritic syndrome range from 2-7 per 100,000 children, and prevalence from 12-16 per 100,000 in India . About 2 out of 100,000 children in the US develop nephrotic syndrome each year. About 3 out of 100,000 adults in the US develop nephrotic syndrome each year.

RISK FACTORS Factors that can increase risk of nephrotic syndrome include:

Medical conditions that can damage kidneys. Certain diseases and conditions increase risk of developing nephrotic syndrome, such as diabetes, lupus, amyloidosis, minimal change disease and other kidney diseases. Certain medications. Examples of medications that can cause nephrotic syndrome include nonsteroidal anti-inflammatory drugs and drugs used to fight infections. Certain infections. Examples of infections that increase the risk of nephrotic syndrome include HIV, hepatitis B, hepatitis C and malaria.

ETIOLOGY Nephrotic syndrome is usually caused by damage to the clusters of tiny blood vessels (glomeruli) of kidneys. The glomeruli filter blood as it passes through kidneys, separating things which body needs from those it doesn't. Healthy glomeruli keep blood protein (mainly albumin) which is needed to maintain the right amount of fluid in body from seeping into urine. When damaged, glomeruli allow too much blood protein to leave body, leading to nephrotic syndrome. Many possible causes Many diseases and conditions can cause glomerular damage and lead to nephrotic syndrome, including:
1.

Minimal change disease. The most common cause of nephrotic syndrome in children, this disorder results in abnormal kidney function, but when the kidney tissue is examined under a microscope, it appears normal or nearly normal. The cause of the abnormal function typically can't be determined.

2.

Focal segmental glomerulosclerosis. Characterized by scattered scarring of some of the glomeruli, this condition may result from another disease or a genetic defect or occur for no known reason.

3.

Membranous nephropathy. This kidney disorder is the result of thickening membranes within the glomeruli. The exact cause of the thickening isn't known, but it's sometimes associated with other medical conditions, such as hepatitis B, malaria, lupus and cancer.

4.

Diabetic kidney disease. Diabetes can lead to kidney damage (diabetic nephropathy) that affects the glomeruli.

5.

Systemic lupus erythematosus. This chronic inflammatory disease can lead to serious kidney damage.

6.

Amyloidosis. This disorder occurs when substances called amyloid proteins accumulate in organs. Amyloid buildup often affects the kidneys, damaging their filtering system.

7.

Blood clot in a kidney vein. Renal vein thrombosis, which occurs when a blood clot blocks a vein connected to the kidney, can cause nephrotic syndrome.

8.

Heart failure. Some forms of heart failure, such as constrictive pericarditis and severe right heart failure, can cause nephrotic syndrome.

PATHOPHYSIOLOGY Nephrotic syndrome can occur with almost any intrinsic renal disease or systemic disease that affects the glomerulus. Although generally considered a disorder of childhood, nephrotic syndrome does occur in adults, including the elderly. Nephrotic syndrome is characterized by the loss of plasma protein, particularly albumin, in the urine. Although the liver is capable of increasing the production of albumin, it cannot keep up with the daily loss of albumin through the kidneys. Thus, hypoalbuminemia results
Damage to the glomerular capillary membrane
Loss of plasma protein(albumin)

Stimulates synthesis of Hyperlipidemi a

Hypoalbuminemia Decreased oncotic pressure Generalized edema (fluid moves from vascular space to extracellular fluid)

Activation of reninangiotensin system Sodium retention Edema

CLINICAL MANIFESTATIONS The major manifestation of nephrotic syndrome is


1. Edema:-It is usually soft and pitting and most commonly occurs around the eyes

(periorbital), in dependent areas (sacrum, ankles, and hands), and in the abdomen (ascites).
2. Foam in the toilet water, which may be caused by excess protein in urine

3. Weight gain due to excess fluid retention Other symptoms: 4. Malaise. 5. Headache. 6. Irritability . 7. Fatigue .

DIAGNOSIS
1. Blood tests.

A blood test may show low levels of the protein albumin (hypoalbuminemia) specifically and decreased levels of blood protein overall. Loss of blood protein may cause an increase in blood cholesterol and blood triglycerides. Serum creatinine and blood urea also may be measured to assess your overall kidney function. Proteinuria (predominately albumin) exceeding 3 to 3.5 g/day is sufficient for the diagnosis of nephrotic syndrome. 2. Urine analysis. Protein electrophoresis and immunoelectrophoresis 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.
3. Needle biopsy of the kidney may be performed for histologic examination of

renal tissue to confirm the diagnosis.


4. Recent studies have confirmed the usefulness of serum markers as a means of

assessing the disease process.


5. Anti-C1q antibodies are the most reliable markers for assessing disease activity in

lupus nephritis

COMPLICATIONS
1. Blood clots. The inability of the glomeruli to filter blood properly can lead to loss

of blood proteins that help prevent clotting. This increases risk of developing a blood clot (thrombus) in veins.
2. High blood cholesterol and elevated blood triglycerides. When the level of the

protein albumin in blood falls, liver makes more albumin. At the same time, liver releases more cholesterol and triglycerides.( Accelerated atherosclerosis)
3. Poor nutrition. Loss of too much blood protein can result in malnutrition. This

can lead to weight loss, but it may be masked by swelling.

4. High blood pressure. Damage to glomeruli and the resulting buildup of wastes in

bloodstream (uremia) can raise blood pressure.


5. Acute kidney failure. If kidneys lose their ability to filter blood due to damage to

the glomeruli, waste products may build up quickly in blood. (due to hypovolemia ).If this happens, emergency dialysis an artificial means of removing extra fluids and waste from blood typically with an artificial kidney machine (dialyzer).
6. Chronic kidney failure. Nephrotic syndrome may cause kidneys to gradually lose

their function over time. If kidney function falls low enough, may require dialysis or a kidney transplant.
7. Infections. People with nephrotic syndrome have an increased risk of infections.

(due to a deficient immune response). MEDICAL MANAGEMENT The objective of management is to preserve renal function.
1. Diuretic agents may be prescribed for the patient with severe edema;

however,caution must be used because of the risk of reducing the plasma volume to the point of impaired circulation with subsequent prerenal acute renal failure.
2. The use of angiotensin-converting enzyme (ACE) inhibitors in combination with

diuretics often reduces the degree of proteinuria but may take 4 to 6 weeks to be effective.
3. Other medications used in treating nephrotic syndrome include: antineoplastic agents (cyclophosphamide [Cytoxan]) or

immunosuppressant medications (azathioprine [Imuran], chlorambucil [Leukeran], or cyclosporine). It may be necessary to repeat treatment with corticosteroids if relapse occurs.
4. Treatment of the associated hyperlipidemia is controversial. The usual

medications used to treat hyperlipidemia are often ineffective or have serious consequences, including muscle injury.

5. The patient may be placed on a low-sodium, liberal-potassium diet to enhance the

sodium/potassium pump mechanism, thereby assisting in elimination of sodium to reduce edema.


6. Protein intake should be about 0.8 g/kg/day, with emphasis on high biologic

proteins (dairy products, eggs, meats), and the diet should be low in saturated fats. NURSING MANAGEMENT 1. Monitor intake and output; note sings of low plasma volume and impaired circulation with prerenal acute renal failure. 2. Instruct patient receiving steroids or cyclosporine regarding medication and signs and symptoms that must be reported to physician.
3. Measure blood pressure while the patient is in a supine position and also while

hes standing, be alert for a drop in blood pressure that exceeds 20 mm Hg. 4. Instruct patient in selecting a high-protein diet while restricting cholesterol and fat intake.
5. The patient who is receiving corticosteroids or cyclosporine requires instructions

about the medications and signs and symptoms that should be reported to the physician.
6. Dietary instructions may also be necessary. :-

Patients with nephrotic syndrome need adequate instruction about the importance of following all medication and dietary regimens so that their condition can remain stable as long as possible. 7. Provide good skin care because the patient with Nephrotic syndrome usually has edema, if needed provide antiembolism stockings To avoid thrombophlebitis, encourage activity and exercise
8. Offer the patient and family reassurance and support, especially during the acute

phase, when edema is severe and the patients body image changes.

NURSING DIAGNOSIS
1. Imbalanced nutrition less than body requirements related to poor appetite &

restricted diet. Interventions:


Assess the nutritional status . Encourage small frequent meals. Increase food intake especially protein intake daily. Encourage well balanced diet to maintain normal growth pattern. Provide supplementary vitamins and iron as per doctors orders. 2. Fluid volume excess (total body)related to fluid accumulation in tissues.

Interventions:
Monitor sodium and fluid intake orally and intravenously. Check the weight daily. Maintain intake and output chart. Assess the venous stasis of ascites. 3. Impaired skin integrity related to edema, lowered body defenses.

Interventions:
Change the position frequently to prevent tissue breakdown. Opposing skin surface should be kept clean separated with soft cotton &

apply powder.
Edematous eyelids are cleansed with warm saline compresses. Avoid exposure to heat or cold. Provide loose clothing to avoid irritation. Keep the childs nails trimmed to avoid scratching and excoriation. 4. Ineffective family coping process related to serious disease.

Interventions:
Teach the caregivers about the home care. The nurse can assist the family members for problem solving. Explain the caregivers about various therapies used.

Nurse should provide positive feed back. 5. Knowledge deficit related to chronic illness.

Interventions:
Asses the knowledge status of the caregivers. Teach the caregivers about the home care after the acute phase of disease. Provide instructions to the caregivers about the medication before

discharge.
Tell the family members about the follow-up visits.

JOURNAL/ABSTRACT The Nephrotic Syndrome: Current Concepts The nephrotic syndrome, an entity of multiple causes, is characterized by edema, proteinuria, hypercholesterolemia, and hypoalbuminemia. It occurs in the child or adult

with primary renal disease or a systemic disease involving the kidney. The percutaneous renal biopsy has enabled clinicians to study the natural history of the underlying renal disease and to prognosticate more carefully the outcome of therapies. Other clinical featuresage of onset, urinary protein selectivity, urinary enzyme concentrationshave been helpful as prognostic indexes. Immunofluorescent studies of renal tissue are valuable in diagnosis, prognosis, and patient management. Immunologic and inflammatory mechanisms are involved with the glomerular basement membrane, and further study of them may provide more specific and effective therapies. Corticosteroids are effective in the management of the nephrotic syndrome in children and, to a lesser degree, in adults. Azathioprine, cyclophosphamide, and methotrexate appear to be valuable in steroid-resistant and relapsing cases, although long-term experience with toxicity and survival time is limited at present. BIBLIOGRAPHY
1) Suzanne C, Brend G. Medical surgical nursing. 10th edition. Philadelphia:

Lippincott William & Wilkins; 2004


2) Lewis, Heitkemper, Dirksen, OBrien, Bucher. Medical surgical nursing. 7th

edition. Missouri: Elsevier; 2008


3) Ignatavicius D, Workman L, Mishler A. Medical surgical nursing. 2nd edition.

Philadelphia: W.B Saunders company; 2000


4) Doenges E, Moorhouse F, Murr C. Nursing care plans. 7th edition. New delhi:

Jaypee Brothers; 2007


5) Harvey gonick. Annals of internal medicine journal.

http://www.annals.org/content/76/3/463.abstract

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