few glomerular diseases
description
Transcript of few glomerular diseases
![Page 1: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/1.jpg)
RENAL SYSTEMGLOMERULAR DISEASE
![Page 2: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/2.jpg)
GLOMERULAR DISEASES
• Nephrotic syndrome-Idiopathic-Secondary-Congenital
• Hemolytic uremic syndrome• Alport syndrome• IgA nephropathy• Glomerular Nephritis
![Page 3: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/3.jpg)
NEPHROTIC SYNDROMEIt is a manifestation of glomerular disease, characterized by:
- Nephrotic range proteinuria (Nephrotic range proteinuria - protein excretion of > 40 mg/ m2 /hr or a first morning protein: creatinine ratio of >2-3 : 1)
- the triad of clinical findings associated with massive proteinuriao hypoalbuminemiao edemao hyperlipidemia.
![Page 4: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/4.jpg)
INCIDENCE:
The annual incidence is 2-3 cases per 100,000 children per year in most Western countries and higher in underdeveloped countries resulting predominantly from malaria. Minimal change nephrotic syndrome constitutes 80% of nephrotic syndrome cases.
![Page 5: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/5.jpg)
ETIOLOGY• Idiopathic nephrotic syndrome
⁻ focal segmental glomerulosclerosis⁻ membranoproliferative glomerulonephritis⁻ membranous nephropathy ⁻ diffuse mesangial proliferation
• Associate with glomerular damage - Systemic lupus erythematosus- Lymphoma- Leukemia & infections
• Hereditary proteinuria syndromes - Alport syndrome- Sickle cell anemia.
![Page 6: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/6.jpg)
Company Logo
TYPES
Idiopathic
Secondary
Congenital
Nephrotic syndrome
![Page 7: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/7.jpg)
1.Idiopathic Nephrotic syndrome
• It is the primary disease which also known as childhood nephrosis, or minimal change nephrotic syndrome.
• Approximately 90% of children with nephrotic syndrome have idiopathic nephrotic syndrome.
• Idiopathic nephrotic syndrome is associated with primary glomerular disease without evidence of a specific systemic cause.
![Page 8: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/8.jpg)
2.Secondary Nephrotic Syndrome• It is a secondary disorder that occurs as a
clinical manifestation after or in association with glomerular damage. It occurs secondary to systemic diseases and infections.
• Nephrotic syndrome has also developed during therapy with numerous drugs and chemicals.
![Page 9: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/9.jpg)
3.Congenital Nephrotic Syndrome
It is inherited as autosomal recessive disorder. It is defined as nephrotic syndrome manifesting at birth or within the first 3 months of life. Congenital nephrotic syndrome may be classified as:
1. Primary2. Secondary
![Page 10: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/10.jpg)
• Primary congenital nephrotic syndrome is due to a variety of syndromes inherited as autosomal recessive disorders.- present at birth with edema due to massive proteinuria- delivered with an enlarged placenta (>25% of the
infant’s weight).- Severe hypoalbuminemia, hyperlipidemia, and
hypogammaglobulinemia result from loss of filtering selectivity at the glomerular filtration barrier.
• Secondary congenital nephrotic syndrome can be
occurred from underlying causes such as syphilis.
![Page 11: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/11.jpg)
PATHOPHYSIOLOGY
![Page 12: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/12.jpg)
![Page 13: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/13.jpg)
CLINICAL MANIFESTATIONS• Weight gain• Puffiness on face (facial
edema)o Especially around the eyeso Apparent on arising the
morningo Subsides during the day
• Abdominal swelling(ascitis)• Pleural effusion• Labial or scrotal swelling• Edema of intestinal mucosal
which result in:o Diarrhea
o Anorexiao Poor intestinal absorption
• Ankle / leg swelling• Irritability• Easily fatigued• Lethargic• BP normal or slightly
increased• Susceptible to infections• Urine alterations
o Decreased volumeo frothy
![Page 14: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/14.jpg)
DIAGNOSTIC EVALUATION• History collection
weight gain, anorexia, irritability, less active• Physical examination
Clinical manifestations• Urine dipstick test for protienuria• Blood tests
₋ Serum protein low concentration₋ Presence of casts, RBC₋ Reduced albumin₋ GFR normal or high₋ Hb normal or elevated₋ Elevated platelet count
• Renal biopsy if not respond to steroid treatment
![Page 15: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/15.jpg)
THERAPEUTIC MANAGEMENT
GOALS• Reduce excrtion of urinary protein• Reduce fluid retension• Preventing infection• Minimize complications related to treatment DIETARY MANAGEMENT• Low salt diet• Fluid restriction
![Page 16: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/16.jpg)
PHARMACOLOGICAL MANAGEMENT
• Diuretic therapy for temporary relief from edema• Infections are treated with
appropriate antibiotics• Corticosteroids for MCNS• Prednisolone – 2mg/kg body weight/day in one
or two divide doses• Relapse is treated with high dose steroid therapy• For children who do not respond to steroid
therapy, immune - suppressants are given.
![Page 17: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/17.jpg)
STEROID THERAPY
• Extended APN schedule• 60mg/m2/day as a single dose for 6 weeks• If remission is present , then 40 mg/m2/every
other day for next 6 weeks• If remission is maintained, taper steroids in
EOD in 2 weeks
![Page 18: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/18.jpg)
Definition of response• Remission
No albumin on three consecutive early morning urine samples
• Relapse2+ or more albumin on 3 consecutive early morning urine samples
• Frequent relapse3 or more relapses in 6 months or 4 or more relapses in 1 year
• Steroid resistanceNo remission after 8 weeks of adequate daily steroids
• Steroid dependenceRelapse within 15 days of stopping steroids after inducing remission or on tapering, on more than 2 occasions
![Page 19: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/19.jpg)
NURSING MANAGEMENTa. Focus Assessment
• Urinary System (oliguric, urine retention, proteinuria and urine discoloration).
• Fluid and electrolyte balance (excess fluid, edema, ascitis, weight gain, dehydration)
• Circulation (increased blood pressure)• Neurology (decreased level of consciousness due to
dehydration)• Breathing (shortness of breath, tachypnea)• Mobility (redness, malaise)
![Page 20: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/20.jpg)
b. Nursing Diagnosis
• Impaired Urinary Elimination related to Na and water retention.
• Excess Fluid Volume related to edema• Imbalanced Nutrition Less Than Body
Requirements related to damage protein metabolism
• Ineffective Breathing Pattern related to suppression of the diaphragm due to ascites
![Page 21: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/21.jpg)
c. Nursing interventions
• Administer medications• Stress the importance of adhering to the special
diet• meticulous skin care• Encourage activity and exercise• Frequently check of the patient’s urine• Monitor and document about edema.• Measure blood pressure• Monitor intake and output hourly.• Assess the patient’s response to prescribed
medications.
![Page 22: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/22.jpg)
COMPLICATIONS1.Due to drugs
Toxicity of drugs may occur– Furosemide,
siranolactone– Steroids– Cyclophosphamide– Levamisole– Anticoagulants
2.Due to the disease– Edema
– Biochemical hypothyroidism
– Hypocalcemic tetany– Anemia– Hypercoagulable states– Acute renal failure– Infection– Thromboembolic events– Cardiovascular disease– Steroid therapy
![Page 23: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/23.jpg)
IMMUNISATIONS• The children with NS should receive:• 23- serotype pneumococcal vaccine• 7-valent conjugate pneumococcal vaccine• routine childhood immunization schedule( for child is in
remission and off daily prednisone therapy)• Live virus vaccines should not be administered to children
who are receiving daily or alternate-day high-dose steroids• Vaccines can be administered after corticosteroid therapy has
been discontinued to nephrotic children in relapse• if exposed to varicella, should receive varicella-zoster
immunoglobulin• Influenza vaccine should be given on a yearly basis
![Page 24: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/24.jpg)
PROGNOSIS
Ultimate recovery in most cases is good. It is a self timing disease. In children who receives steroid therapy the tendency to relapse decreases with time. With early detection and treatment, the membrane damage could be minimized. About 80% of affected children have favorable prognosis.
![Page 25: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/25.jpg)
HEMOLYTIC-UREMIC SYNDROME (HUS)
It is one of the most common causes of community-acquired acute kidney failure in young children. It is characterized by the triad of:– micro angiopathic hemolytic anemia– thrombocytopenia– renal insufficiency
![Page 26: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/26.jpg)
CLINICAL DESCRIPTIONHUS is characterized by the acute onset of
microangiopathic hemolytic anemia, renal injury, and a low platelet count. Most cases of HUS occur after an acute gastrointestinal illness (usually diarrheal).
INCIDENCEOccurs in infants and small children between the ages of 6 months and 5 years.
![Page 27: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/27.jpg)
CASE CLASSIFICATION• Probable
An acute illness diagnosed as HUS that(a) has onset within 3 wk after onset of an acute or bloody diarrhea(b) meets the laboratory criteria except that microangiopathic changes are not confirmed.
• ConfirmedAn acute illness diagnosed as HUS that both meets the laboratory criteria and began within 3 wk after onset of an episode of acute or bloody diarrhea
![Page 28: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/28.jpg)
CLASSIFICATION OF HEMOLYTIC UREMIC SYNDROME
1.Infection Induced• Verotoxin-producing
Escherichia coli• Human immunodeficiency
virus2.Genetic• von Willebrand factor-
cleaving protease deficiency• Complement factor H
deficiency or mutation3.Other Diseases Associated
With Microvascular Injury
• Systemic lupus erythematosus
• Primary glomerulopathy• HELLP (hemolytic anemia,
elevated liver enzymes, low platelet count) syndrome
4.Medication-Induced• Calcineurin inhibitors• Cytotoxic, chemotherapy
agents• Quinine
![Page 29: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/29.jpg)
ETIOLOGY
• Rickettsia• Bacterial toxins (e-coli, salmonella, pneumococci)• Chemicals• Viruses (coxsackie virus, echovirus, adenovirus)• Usually transmitted by undercooked meat or
unpasteurized milk or apple cider• HUS outbreaks have also been associated with
municipal water supply; petting farms; swimming in contaminated ponds and consuming cheese, lettuce, or raw spinach contaminated with toxin
![Page 30: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/30.jpg)
PATHOPHYSIOLOGY
Primary injury in endothelial lining of small glomerular arterioles
Deposits of platelets and fibrin clots
Swelling in the glomerular arterioles
RBC damage resulted by the attempt to move through occluded blood vessels
Spleen removes the damage
Results in hemolytic anemia
Result in characteristic thrombocytopenia
![Page 31: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/31.jpg)
CLINICAL MANIFESTATIONS
• History of a prodromal disease (gastroenteritis or an upper respiratory infection)
• Acquired hemolytic anemia• Sudden onset of hemolysis• Thrombocytopenia• Renal injury• Central nervous system symptoms
![Page 32: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/32.jpg)
DIAGNOSTIC EVALUATION
• History collectuion• Clinical examination:– Triad of anemia, thrombocytopenia and renal failure
• Laboratory examination:o Urine - proteinuria, hematuria, urinary cast
presenceo Blood - Elevated blood urea, nitrogen, creatinine - Low hemobglobin, hematocrit - High reticulocyte count
![Page 33: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/33.jpg)
THERAPEUTIC MANAGEMENT• early recognition of the disease• monitoring for potential complications• meticulous supportive care.
– careful management of fluid and electrolytes– correction of volume deficit– control of hypertension– early institution of dialysis if the patient becomes anuric or
significantly oliguric– Red cell transfusions are usually required because hemolysis can be
brisk and recurrent until the active phase of the disease has resolved.
• Blood transfusion– Fresh, washed packed cells for anemic child with caution to prevent
circulatory overload– Fresh frozen plasma and plasma pherisis
![Page 34: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/34.jpg)
PROGNOSIS
Most recover renal function completely, but of surviving patients, 5% remain dependent on dialysis, and up to 20-30% are left with some level of chronic renal insufficiency. The recovery rate is about 95%, but residual renal impairment ranges from 10% to 50% in various cases.
![Page 35: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/35.jpg)
Immunoglobulin A Nephropathy (Berger Nephropathy)
IgA nephropathy is the most common chronic glomerular disease. The disease derives its name from deposits of Immunoglobulin A (IgA) in a granular pattern in the mesangium a region of the renal glomerulus.
![Page 36: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/36.jpg)
INCIDENCE
It is seen more often in male than in female patients.-is often benign in childhood in comparison to that of adults.-is an uncommon cause of end-stage renal failure during childhood.
![Page 37: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/37.jpg)
CLINICAL MANIFESTATIONS
• Gross hematuria associated with loin pain.• Proteinuria often <1000 mg/24 hr.• Mild to moderate hypertension.• Normal serum levels of C3
![Page 38: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/38.jpg)
DIAGNOSIS
• History collection• Physical examination (clinical features)• Laboratorical investiagations• Renal biopsy
![Page 39: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/39.jpg)
TREATMENT
• The primary treatment is appropriate blood pressure control
• Fish oil, which contains anti-inflammatory omega-3 polyunsaturated fatty acids
• Immunosuppressive therapy with corticosteroids• Angiotensin-converting enzyme inhibitors and
angiotensin II receptor antagonists are effective in reducing proteinuria and retarding the rate of disease progression.
• Kidney transplantation
![Page 40: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/40.jpg)
PROGNOSIS
Most children with IgA nephropathy do not display progressive renal dysfunction until adulthood, prompting the need for careful long-term follow-up. Poor prognostic indicators at presentation or followup include persistent hypertension, diminished renal function, and heavy or prolonged proteinuria.
![Page 41: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/41.jpg)
Alport Syndrome (hereditary nephritis)It is a genetically heterogeneous disease
caused by mutations in the genes coding for type IV collagen, a major component of basement membranes.
These genetic alterations are associated with marked variability in clinical presentation, natural history, and histologic abnormalities.
![Page 42: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/42.jpg)
GENETICS
Approximately 85% of patients have X-linked disease caused by a mutation. Autosomal recessive forms of AS are caused by mutations in the COL4A3 and COL4A4 genes on chromosome 2 encoding the α3 and α4 chains, respectively, of type IV collagen. An autosomal dominant form of AS linked to the COL4A3-COL4A4 gene locus occurs in 5% of cases.
![Page 43: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/43.jpg)
CLINICAL MANIFESTATIONS
• Asymptomatic microscopic Hematuria• Single or recurrent episodes of gross hematuria
commonly occurring 1-2 days after an upper respiratory infection.
• Proteinuria• Bilateral sensorineural hearing loss• Ocular abnormalities• Leiomyomatosis of the esophagus,
tracheobronchial tree, and female genitals in association with platelet abnormalities is rare.
![Page 44: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/44.jpg)
DIAGNOSIS
• Family history• Screening urinalysis of first-degree relatives• Audiogram,• Ophthalmologic examination• Diagnostic renal biopsy• Mutation screening or linkage analysis is not readily
available for routine clinical use.• Prenatal diagnosis is available for families with
members who have X-linked AS and who carry an identified mutation.
![Page 45: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/45.jpg)
TREATMENT
• No specific therapy is available to treat AS• Angiotensin converting enzyme inhibitors can
slow the rate of progression• Careful management of renal failure
complications such as hypertension, anemia, and electrolyte imbalance is critical.
• Patients with ESRD are treated with dialysis and kidney transplantation.
![Page 46: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/46.jpg)
PROGNOSIS
The risk of progressive renal dysfunction leading to end-stage renal disease (ESRD) is highest among hemizygotes and autosomal recessive homozygotes. Risk factors for progression are gross hematuria during childhood, nephrotic syndrome, and prominent GBM thickening.
![Page 47: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/47.jpg)
Acute Glomerulo Nephritis
AGN is an immune mediated inflammatory disease of the capillary loops in the renal glomeruli. AGN may be a primary event or a manifestation of a systemic disorder that can range from minimal to severe.
INCIDENCE-Acute post streptococcal glomerulo nephritis (APGN) is
the most common of post infectious renal disease in childhood.
-It is common in early school age children.-And male female ratio is 2:1.
![Page 48: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/48.jpg)
ETIOLOGY
It is an immune complex disease that occurs after an antecedent streptococcal infection with certain strains of group A β-hemolytic streptococcal infection. Acute post streptococcal glomerulonephritis is the most common. A latent period of 10 to 21 days occurs for the onset of clinical manifestations.
![Page 49: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/49.jpg)
PHASES
• Phase 1 – edema and oliguria present• Phase 2 – edema reduces and
urine output increases
![Page 50: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/50.jpg)
PATHOPHYSIOLOGYStreptococcal infection
Production of antigen antibody complex in glomerular loops
Inflammatory reaction
Proliferation and swelling of endothelial cells
Diminish the amount of glomerular filtrate and allow the
passage of blood cells and protein in the filtrate
Sodium and water retention
Damage of glomerular membrane
Progressive renal failure
![Page 51: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/51.jpg)
CLINICAL MANIFESTATIONS
• Sore throat/pyoderma/scabies/impetigo
• Oliguria• Edema• Periorbital puffiness• Pedal edema• Rapid weight gain• Hypertension• Circulatory congestion• Hematuria
• Proteinuria• Fever • Headache• Nausea and vomiting• Anorexia• Abdominal pain• Malaise• Hypertension
![Page 52: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/52.jpg)
DIAGNOSIS• History collection• Physical examination• Urine examination• Blood examination
-increased level of urea, creatinine, ESR, decreased Hb, hyponatremia, hyperkalemia, reduced C3(serum complement) in early stages.
• Throat swab culture-Streptococci from culture of the pharynx
• Chest X-ray-Cardiac enlargement, pulmonary congestion, pleural effusion.
![Page 53: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/53.jpg)
COMPLICATIONS
• CCF• Acyte renal failure• Hypertensive encephalopathy• Persistent hypertension• Anemia• Growth failure• Chronic glomerulonephritis
![Page 54: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/54.jpg)
MANAGEMENT-Bedrest for weeks till urine got free from RBC-Diet management-Daily weight recording to assess increase and decrease edema- Regular measurement of vital signs, body weight and input and output-administration of antibiotic-symptomatic management-Antihypertensive drugs-Tranquilisers for convulsions and encephalopathy-dialysis may be needed in renal failure and severe electrolyte imbalance-management of complications
![Page 55: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/55.jpg)
NURSING MANAGEMENT• Careful assessment of diseases status• Regular monitoring of vital signs• Maintain input and output• Children with restricted fluid intake and those
who does not have much edema should be observed for signs of dehydration if he lost weight.
• Administer antibiotics• Promote rest, sleep and comfortable position• Skin care for edematous part• Dietary management
![Page 56: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/56.jpg)
PROGNOSIS
Almost all children correctly diagnosed as having APSGN recover completely and specific immunity is conferred, so that subsequent recurrences are uncommon. A few of these children have been reported to develop chronic disease, but most of these cases are now believed to be different glomerular diseases misdiagnosed as post streptococcal disease.
![Page 57: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/57.jpg)
Chronic Glomerulo Nephritis
It is an advanced irreversible impairment of renal function with or without symptoms. It may develop as a primary disease or may occur in SLE or drug induced nephropathies.
![Page 58: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/58.jpg)
CLINICAL MANIFESTATIONS
• edema• Severe hypertension• Hematuria• Nocturia• Persistent anemia• Bone pain• Bony deformities• Failure to thrive
![Page 59: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/59.jpg)
DIAGNOSIS
• Urine examination• Blood examination- increase urea, creatinine• Urine analysis – protein, RBC, cast• USG
![Page 60: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/60.jpg)
MANAGEMENT
• It can be done with steroid therapy and other immune suppressive drugs.• Anti hypertensive drugs and
antibiotics are useful for symptomatic measurement.
![Page 61: few glomerular diseases](https://reader035.fdocuments.net/reader035/viewer/2022062312/554af568b4c90559058b4b87/html5/thumbnails/61.jpg)
THANK YOU..