ACUTE GLOMERULONEPHRITIS

Acute GN is defined as the sudden onset of hematuria, proteinuria, and red blood cell (RBC) casts. Common features: Oliguria Hematuria Proteinuria Edema Hypertension & circulatory changes

BP

Acute Poststreptococal
Glomerulonephritis (APSGN) is the most common of the noninfectious renal disease in childhood

APSGN primarily affects school-age

children with a peak age of 6 7 years.

It is an immune-complex disease. Occurs

as a by-product of an antecedent streptococcal infection with a certain strains of Group A Beta-Hemolytic Streptococci.

CLINICAL COURSE Acute Edematous Phase 4 10 days but may persists for 2 or 3 weeks Listless, anorexic, apathetic weight fluctuates urine remains smoky brown BP may suddenly reach dangerously high levels at any time during this phase First sign of improvement is small UO with a corresponding weight. BUN and creatinine levels during diuresis and usually return to normal. Proteinuria slight-moderate may persist for several weeks Gross hematuria diminishes but microscopic hematuria may persist for weeks or months

A latent period of 10 14 days occurs

between strep infection of the throat or skin and the onset of clinical manifestation. The kidney itself appears normal or moderately enlarged.

COMPLICATIONS: Hypertensive encephalopathy (Sx: HA, dizziness, abdL dsCft, vomitG) Acute cardiac decompensation (Cxd by hypervolemia) (Sx of circulatory congestion are evident) ARF

Glomerular capillary loops are almost

obliterated by swelling. Glomeruli appears dense & globulated.

Examination with the electron microscope

reveals discrete nodules or humps in the basement membrane, which are identified as deposits of immune complexes. This becomes evident after 6 weeks. CLINICAL MANIFESTATION: In some instances, there is no hxy of infxn, described only as mild cold. Initial signs of nephrotic reaction includes: Periorbital edema, more prominent in the AM Anorexia Dark-colored urine Urine is cloudy, smoky brown (tea/cola-colored), and decreased in volume Child is pale, irritable, lethargic, appears unwell but seldom expresses complaints. Older children: headaches, abdominal discomfort, and dysuria.

DIAGNOSTIC EVALUATION Urinalysis: (+) hematuria (+) proteinuria specific gravity (not more than 1.020) Dark-colored or tea-colored (reflecting RBC & Hgb content) Blood Exam Normal electrolytes BUN & Creatinine Increased (reflection of impaired glomerular filtration resulting to Azotemia) ASO Titer (Antistreptolysin O) - most familiar and readily available test for strep axbodies; useful, only if it follows a strep infxn but of less value if not. - appears approx. 10 days after initial infxn - Significant: > 250 Todd units; two samples taken 1 week apart Serum Complement Level (Serum C3 Level) - initially but returns to normal 8 10 weeks after onset of GN CXR
Reference: Wongs Nsg. Care of Infants and Children (8th edition)

generalized cardiac enlargement pulmonary congestion - pleural effusion during edematous phase THERAPEUTIC MANAGEMENT No specific treatment. Consists of general supportive measures and early recognition & treatment of complications. Short hospitalization is the rule in uncomplicated cases; prolonged hospitalization is required only for children with severely impaired renal fxn. Restrict activities during the most active phase. Monitor I/O Record daily weight at same time (the most useful means in assessing fluid balance) Sodium and water restriction (remember that the child is having edema)

Reference: Wongs Nsg. Care of Infants and Children (8th edition)

ACUTE GLOMERULONEPHRITIS (contd)

THERAPEUTIC MANAGEMENT Diuretics Furosemide (Lasix) Monitor VS esp. the BP (Significant but not severe HN is controlled with LOOP DIURETICS; In severe HN, axHN drugs may be needed such as Ca-channe blocker, Beta-blocker, or ACEI. Foods with substantial amounts of K is restricted during the period of oliguria. Prolonged oliguria azotemia CHON restriction Antibiotics indicated for children with evidence of strep infection; given to prevent transmission of nephritogenic strep to other family members and not to alter the course of dSE NURSING CARE MANAGEMENT Monitor VS Monitor I & O. Note the character of the urine Weight the child daily Assess for sx of cerebral complication Seizure precautions DAT but no added salt; eliminate foods high in Na and salted treats. Advised not to give potato chips and pretzels Provide special attention to meal preparation and serving because the child has a poor appetite. Facilitate meal planning; collaborate with the parents and dietitian. Activities should be planned, allow frequent rest periods and avoid fatigue. Strenuous activity is usually restricted until there is no evidence of proteinuria or macroscopic hematuria Parent education and support Follow-up, weekly then monthly, for evaluation and UA.

Reference: Wongs Nsg. Care of Infants and Children (8th edition)

NEPHROTIC SYNDROME
Defined as a massive proteinuria, hypoalbuminemia, hyperlipidemia and edema.

Major presenting symptom of renal dSE in

pedia CLASSIFICATIONS: (A) Primary syndrome is restricted to glomerular injury (B) Secondary when it develops as a part of systemic illness TYPES OF NEPHROTIC SYNDROME (1) Minimal Change NS 80% of cases aka idiopathic / minimal lesion / lipoid / childhood / uncomplicated nephrosis, or nil dSE Predominant in preschool Rare in younger than 6mos Precipitating fxr: viral URTI (2) Secondary NS - occurs during the course of collagen vascular dSE or as a result of toxicity to drugs. (3) Congenital NS CLINICAL MANIFESTATION Weight gain Periorbital edema (puffiness of the face) esp. in the morning but subsides during the day Swelling of the abdomen and lower extremities, more prominent in the afternoon Anasarca generalized edema Ascites fluid accumulation in the abdomen Diarrhea Loss of appetite Poor intestinal absorption Decreased UO; appears darkly opalescent and frothy Extreme skin pallor Irritable Easily fatigued or lethargic Changes in the nails appear as white (Muercke) lines parallel to lunula w/c are cx by prolonged hypoalbuminemia BP usually normal or slightly decreased Child is more susceptible to infection esp. cellulites, pneumonia, peritonitis, or sepsis. DIAGNOSTIC EVALUATION

Urinalysis - massive proteinuria > 2g/m2 of body surface/day - with few RBC - with sluggish and oval fat bodies - specific gravity: high Plasma lipids elevated Serum cholesterol m/be as high as 450 to 1500 mg/dL Protein concentration reduced: <2 g/dL Platelet count (d/t hemoconcentration) serum Needs attended (130-135 mEq/L) THERAPEUTIC MANAGEMENT Primary Objective: reduce the excretionof urinary protein and maintain protein-free urine Generalized Measures: Bed rest during edema phase Activity not restricted during remission Antibiotics for acute infections Diet Remission: Regular diet During massive edema: salt (+) azotemia & RF: CHON Corticosteroid Therapy Primary therapeutic agent in mgmt of NS PO 60 mg/ m2 /day in evenly divided doses Prednisone is the safest and least expensive, steroid of choice Continued daily for 6 weeks then changed to 40mg/ m2 on alternate days for 6 more weeks Complications: growth retardation cataracts obesity HN GI bleeding Bone demineralization Infections Hyperglycemia Immunosuppressant Therapy Given to chidren who does not respond to steroid therapy Cyclophosphamide (Cytoxan) or chlorambucil Leucopenia are anticipated Cyclophosphamide may cause azoospermia with potential sterility in males treated for more than 2 to 3 months and variable effects on gonadal fxn in females. Diuretics
Reference: Wongs Nsg. Care of Infants and Children (8th edition)

 NS is usually unresponsive with diuretics though; Loop diuretics (usually furosemide) in combination with metolazone are sometimes useful Plasma expanders may be administered to severely edematous NURSING CARE MANAGEMENT Monitor I & O; weighing diapers in younger children Weigh daily Measure abdominal girth Assess edema; esp in periorbital area Assess color and texture of the skin Monitor VS; to detect early signs of complications (ie., shock) Salt and water restriction during edematous phase Vulnerable to URTI, protect from infected person Skin surfaces of areas with edema should be cleaned and separated with clothing, cotton, or antiseptic powder.

Reference: Wongs Nsg. Care of Infants and Children (8th edition)

ACUTE RENAL FAILURE

Renal failure is the inability of the kidneys to excrete waste material, concentrate urine, and converse electrolytes

Acute renal failure exist when the kidneys

suddenly are unable to appropriately regulate volume and composition of urine in response to food an fluid intake

Principal feature: oliguria with azotemia,

acidosis, diverse electrolyte disturbance

Oligoanuria 1.8 to 4 dl/m2/24hr

CLINICAL MANIFESTATION Oliguria UO <1ml/kg/hr Edema Drowsiness Circulatory congestion Cardiac arrhythmia from hyperkalemia Metabolic acidosis tachypnea Hyponatremia or hypocalcemia seizure

When nourishment is provided by the IV route, careful monitoring is essential to prevent fluid overload. Maintain optimum thermal environment; reduce elevation of body temp. Reduce anxiety and restlessness to decrease rate of tissue catabolism. Monitor ECG and serum potassium ion levelregularly to prevent cardiac arrhythmia and cardiac arrest Any signs of hyperkalemia should be reported immediately (serum K >7mEq/L, ECG: loss of Pwave, prolonged RS complex, depressed ST segment, tall and tented Twave, bradycardia, or heart block. Monitor VS esp BP q4-6H May administer Labetalol (B-blocker) IV bolus or continuous drip to prevent hypertensive encephalopathy

DIAGNOSTIC EVALUATION BUN plasma Creatinine

Azotemia Hyponatremia Hypocalcemia Hyperkalemia Metabolic acidosis

NURSING MANAGEMENT Most effective is prevention. Monitor central venous pressure. Initially, Foley Cath inserted; may or may not be removed Mannitol, furosemide or both may be administered in the presence of oliguria. - If urine flow is generated to the extent of 6 to 10 ml/kg of BW in 1 to 3 hours, initial dosage is reduced and continued - If unresponsive within 2 hours after single dose, drugs are NOT repeated CHO & fat; CHON, K, Needs attended IV rout of nourishment is generally preferred consisting of amino acids administered by the central venous pressure Regular measurement of plasma electrolytes, pH, BUN, and creatinine level Major goal of nursing mgmt is reestablishment of renal fxn Monitor intake and output

Reference: Wongs Nsg. Care of Infants and Children (8th edition)

CHRONIC RENAL FAILURE

Begins when the diseased kidney can no longer maintain the normal chemical structure of body fluids under normal condition ESRD (end-stage renal diseae) is the final stage of CRF, irreversible CLINICAL MANIFESTATIONS fatigue on exertion Pallor; skin develops a sallow, muddy appearance as a result of anemia BP sometimes elevated Falling behind on the growth chart is often the first measurable sign Weight loss Headache mLe cramps Nausea Facial puffiness Malaise Growth retardation Bone demineralization Dryness or itching of the skin Bruised skin Amenorrhea is common in adolescent girls (+) uremia Anemia Bloody diarrheal stools Metabolic acidosis Hypertension CHF Pulmonary edema Dulling of the sensorium Tremors, muscular twitching Seizure

Reference: Wongs Nsg. Care of Infants and Children (8th edition)