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Language: en
Added: Jul 02, 2020
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NEPHROTIC SYNDROME MANITA UPADHYAY LECTURER
Introduction The syndrome is apparent in any condition that seriously damage the glomerular capillary membrane that results in increase glomerular capillary permeability to plasma proteins. Although liver is capable of increasing the production of protein. it can’t keep up with the daily loss of albumin through the kidney thus hypoalbuminemia results
DEFINITION It is a clinical disorder that is characterized by proteinuria , hypoalbuminemia , edema and hyperlipidemia . This occurs due to excessive leakage of plasma proteins in urine because of increase capillary permeability of the glomerulus.
INCIDENCE nephrotic syndrome is quite rare but has an important role to play in the development of kidney disease. in adults, the incidence of the condition is approximately 3 cases per 100,000 per year . the incidence of minimal change disease in caucasian children is reported to be 2 per 100,000
TYP E S category it is regarded as a sort of autoimmune phenomenon, especially since it responds well to immunosuppressive therapy. 1. Idiopathic NS: In childhood, the vast majority be l o n g s to
2. Secondary NS: I t occ u r s i n c h il d r e n (ab o ut 10 % ) o f all cases. Thi s co n dition m a y occur du e t o s o me form of chronic glomerulonephritis, or due to diabetes mellitus, SLE, malaria, h y p er t e n sion, endocarditic, he p a titis HIV/AIDS, malig n a n t B , i n f ecti v e drug t o xi c it y , lymphomas syphilis etc.
3. Congenital NS: It is rare but a serious and fetal problem usually associated with other congenital anomalies of kidney. It is inherited as autosomal recessive disease. Severe renal insufficiency & urinary infections along with this condition result is poor prognosis.
4. Infantile NS: The term is applied to NS occurring in infants between 4 – 12months of age. Its major causes are: NPHS2 Diffuse mesengial sclerosis (DMS)
ETIOLOGY 1. Primary renal cause : Minimal-change nephropathy(70-90% children and 10- 15%inadult) Glomerulosclerosis Acute post streptococcal glomerulonephritis Immune complex glomerulonephritis.
Pathop h ysiolo g y Decrease plasma oncotic pressure Compensatory synthesis of protein including lipoprotein by liver Due to E/F Increase renal catabolism albumin Hypoalbuminemia (less then 3.4 mg/DL)
Hyperlipidemia Fluid escape into the tissue Decrease plasma volume Edema Decrease GFR Generalized edema (Anasarca or dropsy) Decrease lipid catabolism due to low level of protein
CLINICAL MANIFESTATION Four main symptoms of nephritic symptoms:- Protein urea Hypoalbuminemia Hyperlipidemia Edema - Periorbital edema, pitting edema, ankle edema, Ascites, pleural effusion, Weight gain, hypertension
fatigue, headache, malaise and irritability foamy appearance of urine (decrease surface tension by severe proteinuria) hematuria thrombophilia (clot formation) lipiduria dyspnoea anemia fever, rash, joint pain Weakness Anorexia flank pain
DIAGNOSTIC EVALUATION palpation: due to edema and ascites kidney cannot be palpable. urine analysis hematuria 24 hour urinary total protein estimation – urine sample shows proteinuria (>3.5 g per liter per 24 hours) blood test BUN S.creatinine S.p r o t ei n lipid profile
Comprehensive metabolic panel(CMP) shows hypoalbuminemia, albumin level is <2.5g/dl Needle biopsy of kidney ECG KUB – X.ray Renal ultrasound Renal scan Intravenous urogram (IVU).
Management 1. Symptomatic treatment Edema – Rest – not for prolong time Nutrition – 1 gm protein/kg/day, not more that, sodium restriction, water not greater then the level of diuresis. Medication – Loop diuretics (furosemide) Hypoalbuminemia – moderate intake of protein, rich in animal protein. Hyperlipidemia – low saturated fat, high unsaturated fat, if unresponsive to nutrition therapy then take hypolipidemic drugs such as statin.
NURSING MANAGEMENT NURSING DIAGNOSIS: Risk for infection related to immunosuppressive drugs. Fluid and electrolyte imbalanced related to edema. Impaired skin integrity related to disease process. Altered nutrition related to Anorexia. Altered kidney function related to glomerural damage . Knowledge deficit related to disease process.