🔹
Types of hematuria:
Gross hematuria:
seen with the naked eye as red, brown or smoky urine depending on the
🔹> 5Microscopic
amount of red cells.
hematuria:
red cells/high power field (HPF) in centrifuged freshly voided
sample of urine (10ml).
it may be:
🔸
Defnition
The neprotic syndrome (NS) is a glomerular disorder characterized by freq uent remission andrelapses
and consisting of a tetrad of:
– Asymptomatic (silent)
– Symptomatic (accompanied by other manifestations as edema, fever,
etc.)Hyperttension
– Proteinuria (mainly albuminuria) > 1gram/ m2/24 hours.Selective proteinria of low molecular weight
protein
– Hypoproteinemia (mainly albumin): total s.protein<5.5 g/dl & s. albumin <2.5 g/dl.
– Hypercholesterolemia: >220 mg/dl Due loss of lipase enzyme, and loss protein the liver makes proteins 🔹
Causes of heamturia:
Glomerular diseases:
– Acute poststreptococcal glomerulonphritis.
including lipoprotiens
– Edema. – Recurrent gross hematuria syndrome:
1• IgA nephropathy.
2• Benign familial (idiopathic) hematuria.
Classification
1. Idiopathic nephrotic syndrome ( classical NS occurring in 90% of cases) 🔹
3• Alport syndrome With deafness .
🔹 Membranous glomerulopathy
A. Minimal change nephrotic syndrome (MCN S): 77% of cases. أشهرهم
B . NS with mesangial proliferation: 4% of cases.
🔹
🔹
Membranoproliferative glomerulonephritis.
Hemolytic-uremic syndrome.
C. Nephrotic syndrome with focal segmental glomerulosclerosis: 9 % of cases. 🔹
🔹
Nenoch-shonlein (anaphylacttoid) purpura.
Systemic lupus erythematosus .
2.Secondary nephrotic syndrome: (10% )
(nephritis then progress to nephrotic)
🔹
🔹
N ephritis of chronic infection.
Rapidly progressive glomerulonphritis.
i.Glomerulonephritis (most commonly).
– Membranous glomerulopathy.
🔹 Goodpasture disease.
Infection (bacterial, tuberculosis, viral, schistosomoasis).
• Exercise-induced hematuria.
– Membrano proliferative glomerulonphritis. • Traumatic
i. Other causes:
a.Chronic infections: schistosoma, hepatitis, malaria, syphilis.
b.Systemic disease: SLE , Henoch-schönlein purpura, sickle cell dis., diabetes.
🔹
• Stones and hypercalcuria.
Hematologic:
It can make red urine but not hematuria*
c. Malignancies: Wilms tumor. – Thrombocytopenia
d. Drugs: mercurials, penicillamine, trimethadione, gold salts. – Coagulopathies.
e. Allergies: bee sting, serum sickness. – Sickle cell nephropathy.
3- Congenital NS
very rare, autosomal recessive, presenting at birth or during 1st 6 months
Hematuria
🔹
– Renal vein thrombosis.
congenital abnormalities:
• Polycystic kidneys.
• Hydronephrosis due to pelvi-ureteric obstruction.
Pathology
3 main morphologic patterns:
1)Minimal change NS: (85% oftotal cases)
🔹
• Vascular abnormalities.
🔹 Tumors: e.g. Wilms tumor(most common)
Drugs: e.g. (cyclophosphamide: cause Hemorrhagic cystitis ) ,
2)Mesangial proliferation: (5% oftotal cases) chloroquine, metronidazole, rifampicin, phenolphthalein
3) Focal segmental sclerosis (10 %of total cases)
Pathophysiology
• Proteinuria: Work-up of a child with hematuria
• Edema:
• Hyperlipidemia:
• History: present, past, family.
• Physical examination stressing on:
– Height, weight, blood pressure, optic fundi.
– Skin: edema, rash, purpura, ecchymosis (to exclud SLE ,PSAGA)
– Abdominal masses, ascites.
• Laboratory:
– U rine analysis, urine culture.
– Protein and calcium in 24 hours urine.
– Complete blood picture.
– B lood urea, creatinine, complement (C3)
– Rapid slide test for streptococcal antigens.
• Nephrosonogram and /or IV pyelogram
Diagnosis of hematuria:
1.Edema (severe) • Is the color of urine due to blood?
• is the usual presenting manifestation. • Is this true hematuria (red blood cells) orhemoglobinuria /
• Start as periorbital puffiness + pitting edema of lower limbs. myoglobinuria?Truma or convulsions
• Progresses to generalized edema →weight gain ±↓ urinevolume. • Is the hematuria of renal or non-renal origin?
• May be associated with ascitis ± pleural effusion ± edema of genitalia. • What caused the hematuria?
• More in dependent parts: back (if recumbent), abdominal wall, perineum, scrotum Clinical manifestations
, legs (if sitting) • Commonest type of N S: MCNS
• Age: peak incidence between 2-6 years, can occure in 1st year
-The important part we must see the edema is the scrotum الgenitalia قالت حتى مهم or in adult (uncommon)
باالمتحان العملي • Sex: more in Boys, male: female ratio = 2: 1
🔹 Weight gain: due to accumulation of edema.
2.Diminished urine output: may occur with development of edema.
•Response to prednisolone
•The initial attack and subsequent relapsesmay follow a viral
3.Pain and respiratory difficulty: due toascitis and plural effusion and upper respiratory infection.
pulmonaryedema.
4. Diarrhea: due to edema of intestine wall.
5. Blood pressure: hypertension is uncommon, if we found Hypertension it must
looking for other cause than MCN S
Definition: (Type 3 immune reaction )
🔹urine analysis
Laboratory finding
AGN is an acute diffuse inflammatory disease of glomeruli mediated
– amount: normal or ↓
– appearance : clear ,if boiled → turbidity
Renal Diseases 1 by immune complex deposition and presenting as acute nephritic
syndrome
– specific gravity : ↑ It is a clinical complex of acute onset characterized by:
– proteins :>1 g/m2/24 hours ,or 3+ to 4+ bydipstick • Hematuria with RB C casts in urine
– proteinuria is of selective type (mainly albumin + low molecular weight proteins ) Nephrotic Syndrome • Oliguria• Azotemia• Hypertension
🔹
– microscopically: hyaline casts ± transient microscopic hematuria.
Serum and blood :
– Total plasma proteins: < 5.5 g/dl.
• Mild proteinuria (<1 gram/day ) It's severe in nephrotic syndrome
• Edema ( usually mild )
– Serum albumin: <2.5 g/dl.
– Serum cholesterol: >220 mg/dl. Etiology
– Serum triglycerides ↑. Deposition of immune complex these complexes may be:
• Post-infectious (exogenous antigen) Post
– Total serum Calcium ↓ due to reduction in albumin-bound fraction.
streptococcal glomerulonephritis and
– Normal complement C3. • non Post streptococcal glomerulonephritis: like
– Hematocrite and hemoglobin may be ↑. bacterial,viral , fungal, parasitic ,
🔹
– Erythrocyte sedimentation rate may be ↑.
renal functions:
• Non-infectious (endogenous antigen)Antigen
🔸
_antibody reaction
Post streptococcal acute glomerulonphritis
– Creatinine clearance may be ↓due to ↓ renal perfusion (hypovolemia).
(PSAGN)the commen one
🔹
– Blood urea may be slightly ↑ due to ↓ renal perfusion (hypovolemia).
Renal biopsy is not required for diagnosisin most children.Children with: hematuria, hypertension, renal
insufficiency, hypocomplementemia, age < 1 year or > 8 years should be considered for renal biopsy
before treatment .
Definition:
PSAGN represent the classical "acute nephritic syndrome".
It is due to non-bacterial inflammation of the glomeruli secondary to a
Complications previous group A β-hemolytic streptococcal (GABHS) infection of
1. Increased susceptibility to infection. pharynx or skin.
2. Arterial or venous thrombosis **BurThe most common nephropathys is IGA ** إمتحان سؤال
🔶 Why are nephrotic patients more susceptible to infection?
• Edema fluid in tissues is a good culture medium. Epidemiology:
• Hypoproteinemia. – Age: >3 years, usually 5-10 years.
• ↓ Immunoglobulin levels. – Sex: male: female ratio 2:1
• Impaired T-cell function.
• ↓ Bactericidal activity of leukocytes. Etiology:
PSAGN occurs1-3 weeks after infection of pharynx or
• ↓ complement activity.But its normal value skin(impetigo\pyoderna)"with certain "nephritogenic" strains of GABHS
• Loss of complement factor in urine (Properdin factor B that opsonize certain bacteria). (serotypes12,49.et)
• ↓Splenic function.
• Immunosuppressive therapy.
🔶
• Thrombo-embolic complications
The risk of thrombosis is related to:
a-Increase prothrombotic factors:
pathogenesis:
it is mediated via immune complex.
-Fibrinogen -Thrombocytosis -Hemo-concentration -Relative immobilization -Sterpotococcal antigen and its antibody make an antigen-antibody
b-Decrease fibrinolytic factors: complex-->activation of Complement and Deposition of both
-Urinary losses of anti-thrombin III, Proteins C and S. complexs and complement in the basement membrane of glomeruli
and in mesangium -->infammatory reaction.
5- Specific therapy:
Acute glomerulonephritis • Clinical picture:
• Induction:
oral prednisone 60 mg /m2/day dividedin 3 doses until urine free for 3 cosecutive days
Post streptococcal acute 1. Asymptomatic PSAGN :
• Maintenance: glomerulonphritis (PSAGN) presenting only with asymptomatic microscopic hematuria
2. Classical presentation with the nephritic triad of :
Oral prednisone 60 mg / m2 every other day (singledose) for 6 weeks.45 mg / m2 every other day (single
• Edema: in 75 % of cases
dose) for 2weeks.30 mg / m2 every other day (single dose) for 2weeks.15mg / m2 every other day (single
• Gross hematuria: in 65 % of cases
dose) for 2weeks.G radual withdrawal over 2 weeks.
• Hypertension: in 60 % of cases
🔶
🔸 Patient may be classified according to their response to prednisone into 4 types:
» steroid responsive:
• This may be accompanied by systemic manifestation as: mild fever,
headache, anorexia, nausea, vomiting, and abdominal pain.
3-Presentation by complication (s):
respond to prednisone in 1-4 weeks (usually 2 weeks),remission is maintained during alternate day
• hypertensive encephalopathy (Convulsion )يدخل
🔸
therapy.
» steroid dependent:
respond to daily dose and relapse on altemate day therapy or within 4 weeks of discontinued of
• Heart failure and pulmonary edema
• Acute renal failure
prednisone.
🔸
Renal biopsy is indicated.
» steroid resistant:
proteinuria 2+ or greater after 8 weeks of daily prednisone therapy.
• Laboratory findings
1.Urinary changes:
– Volume : oligouria ( urine volume <400 ml/m2/24 hours)
🔸
renal biopsy is indicated and cytotoxic drugs are given.
» frequent relapsers :(Protienuria +edema)
patient who respond well to prednisone therapy but relapse 4 or more times in a 12 month period
by fatema okoff – Color :normal, microscopic or gross hematuria→ smoky , red, tea-or
cola-colored
– Specific gravity ↑ Oliguria
6- Cytotoxic drugs:
🔸 Indications:
o Frequent relapsers and steroid dependence
– Mild to moderate proteinuria ( < 1 gm / m2/24 hours )
– Microscopically( in freshly voided sample ): red blood cells,
↑polymorphonuclear leukocytes,casts (red cell casts, granular casts )
o Corticosteroid toxicity 2-Blood:
Treatment of NS
🔸
o Steroid resistant NS
What to use:
Cyclophosphamide 3 mg/kg/day in a single daily dose for 8-12 weeks + ample fluids.
The principles lines of treatment are:
– Effort to reduce edema.
• Mild normochromic anemia ( due to hemodilution )
• ↑ Erythrocyte sedimentation rate( ESR)النهinfection
maintenance dose: يوم ايوه و يوم ال – Specific therapy with prednisone. • ↓Serum complement ( C3) level
🔸 Alternate-dayprednisone therapy is ofen continued during the
1- Hospitalization, investigations and exclusion of contraindications to steroids.
2-Physical activity: not restricted, as tolerance by child.
• Serum protein : normal or slight ↓ ( due to hemodilution
• Blood urea usually dl ↑( normal < 40 mg /dl)
🔸
course of cyciophosphamide therapy.
Toxicity and side effects;
alopecia, sterility, disseminated varicela, hemorhagic cystitis, leucopenia (do weekly WBC count
3-Diet and fluids: if edema is severe
– Salt: do not add salt to diet or restrict it to 2g/day until edema resolves. • Serum creatinine : usually ↑( normal < 0.7 mg/ dl)
• ↓Creatinine clearance
– Water: moderate restriction.
&stopdrugs if WBCs <5000/mm”). 3-Evidence of recent GABHS infection:
7-all children with NS should receive polyvalent pneumococcal vaccine.
It may be given once the chid is in remission and off of daily prednisone
🔹
4- Diuretics: are used cautiously
For mild edema: • Positive throat cultures
• Streptozyme rapid slide test for detection of antibodies to GABHS
therapy. 🔹
Hydrochlorothiazide 2-4 mg/kg/day in 2 divided doses + spironolactone 3-5mg/kg/day in divided doses
For marked edema:
oral furosemid (lasix) 1- 2mg/kg/dose every 4 hours + Metolazone (zaroxolyn) 0.1-0.2 mg/kg/12 hours. N ot I.V
• ↑ASO titer (in throat infection only), ↑anti-DNase B antibodies.
🔸
Prognosis ofsteroid-responsive MCNS:
Repeated relapses with complete spontaneous resolution by
🔸
Treatment
No specific treatment. Prognosis
🔸
the end of 2nd decade.
🔸 No residual renal dysfunction • Hospitalization and monitoring
• Restriction of activity In complection
• Complete recovery in > 95% of cases G ood
prognosis
🔸 Notheloss of fertility(unless cyclophosphamide was used)
diseases is not hereditary • Diet No restrictions except in oliguric phase
• Treatment of streptococcal infection
• Infrequent : glomerular hyalinization →chronic
renal failure
• 5-Treatment of hypertension 10 days must with • Death from complications can occur in acute
penicillin الزم stage if not properly treated.
• Recurrences are extremely rare .If recurrent
• Treatment of heart failure andpulmonary edema we must Think other cause than streptococcal
• Treatment of acute renal failure
Types of hematuria:
Gross hematuria:
seen with the naked eye as red, brown or smoky urine depending on the
🔹> 5Microscopic
amount of red cells.
hematuria:
red cells/high power field (HPF) in centrifuged freshly voided
sample of urine (10ml).
it may be:
🔸
Defnition
The neprotic syndrome (NS) is a glomerular disorder characterized by freq uent remission andrelapses
and consisting of a tetrad of:
– Asymptomatic (silent)
– Symptomatic (accompanied by other manifestations as edema, fever,
etc.)Hyperttension
– Proteinuria (mainly albuminuria) > 1gram/ m2/24 hours.Selective proteinria of low molecular weight
protein
– Hypoproteinemia (mainly albumin): total s.protein<5.5 g/dl & s. albumin <2.5 g/dl.
– Hypercholesterolemia: >220 mg/dl Due loss of lipase enzyme, and loss protein the liver makes proteins 🔹
Causes of heamturia:
Glomerular diseases:
– Acute poststreptococcal glomerulonphritis.
including lipoprotiens
– Edema. – Recurrent gross hematuria syndrome:
1• IgA nephropathy.
2• Benign familial (idiopathic) hematuria.
Classification
1. Idiopathic nephrotic syndrome ( classical NS occurring in 90% of cases) 🔹
3• Alport syndrome With deafness .
🔹 Membranous glomerulopathy
A. Minimal change nephrotic syndrome (MCN S): 77% of cases. أشهرهم
B . NS with mesangial proliferation: 4% of cases.
🔹
🔹
Membranoproliferative glomerulonephritis.
Hemolytic-uremic syndrome.
C. Nephrotic syndrome with focal segmental glomerulosclerosis: 9 % of cases. 🔹
🔹
Nenoch-shonlein (anaphylacttoid) purpura.
Systemic lupus erythematosus .
2.Secondary nephrotic syndrome: (10% )
(nephritis then progress to nephrotic)
🔹
🔹
N ephritis of chronic infection.
Rapidly progressive glomerulonphritis.
i.Glomerulonephritis (most commonly).
– Membranous glomerulopathy.
🔹 Goodpasture disease.
Infection (bacterial, tuberculosis, viral, schistosomoasis).
• Exercise-induced hematuria.
– Membrano proliferative glomerulonphritis. • Traumatic
i. Other causes:
a.Chronic infections: schistosoma, hepatitis, malaria, syphilis.
b.Systemic disease: SLE , Henoch-schönlein purpura, sickle cell dis., diabetes.
🔹
• Stones and hypercalcuria.
Hematologic:
It can make red urine but not hematuria*
c. Malignancies: Wilms tumor. – Thrombocytopenia
d. Drugs: mercurials, penicillamine, trimethadione, gold salts. – Coagulopathies.
e. Allergies: bee sting, serum sickness. – Sickle cell nephropathy.
3- Congenital NS
very rare, autosomal recessive, presenting at birth or during 1st 6 months
Hematuria
🔹
– Renal vein thrombosis.
congenital abnormalities:
• Polycystic kidneys.
• Hydronephrosis due to pelvi-ureteric obstruction.
Pathology
3 main morphologic patterns:
1)Minimal change NS: (85% oftotal cases)
🔹
• Vascular abnormalities.
🔹 Tumors: e.g. Wilms tumor(most common)
Drugs: e.g. (cyclophosphamide: cause Hemorrhagic cystitis ) ,
2)Mesangial proliferation: (5% oftotal cases) chloroquine, metronidazole, rifampicin, phenolphthalein
3) Focal segmental sclerosis (10 %of total cases)
Pathophysiology
• Proteinuria: Work-up of a child with hematuria
• Edema:
• Hyperlipidemia:
• History: present, past, family.
• Physical examination stressing on:
– Height, weight, blood pressure, optic fundi.
– Skin: edema, rash, purpura, ecchymosis (to exclud SLE ,PSAGA)
– Abdominal masses, ascites.
• Laboratory:
– U rine analysis, urine culture.
– Protein and calcium in 24 hours urine.
– Complete blood picture.
– B lood urea, creatinine, complement (C3)
– Rapid slide test for streptococcal antigens.
• Nephrosonogram and /or IV pyelogram
Diagnosis of hematuria:
1.Edema (severe) • Is the color of urine due to blood?
• is the usual presenting manifestation. • Is this true hematuria (red blood cells) orhemoglobinuria /
• Start as periorbital puffiness + pitting edema of lower limbs. myoglobinuria?Truma or convulsions
• Progresses to generalized edema →weight gain ±↓ urinevolume. • Is the hematuria of renal or non-renal origin?
• May be associated with ascitis ± pleural effusion ± edema of genitalia. • What caused the hematuria?
• More in dependent parts: back (if recumbent), abdominal wall, perineum, scrotum Clinical manifestations
, legs (if sitting) • Commonest type of N S: MCNS
• Age: peak incidence between 2-6 years, can occure in 1st year
-The important part we must see the edema is the scrotum الgenitalia قالت حتى مهم or in adult (uncommon)
باالمتحان العملي • Sex: more in Boys, male: female ratio = 2: 1
🔹 Weight gain: due to accumulation of edema.
2.Diminished urine output: may occur with development of edema.
•Response to prednisolone
•The initial attack and subsequent relapsesmay follow a viral
3.Pain and respiratory difficulty: due toascitis and plural effusion and upper respiratory infection.
pulmonaryedema.
4. Diarrhea: due to edema of intestine wall.
5. Blood pressure: hypertension is uncommon, if we found Hypertension it must
looking for other cause than MCN S
Definition: (Type 3 immune reaction )
🔹urine analysis
Laboratory finding
AGN is an acute diffuse inflammatory disease of glomeruli mediated
– amount: normal or ↓
– appearance : clear ,if boiled → turbidity
Renal Diseases 1 by immune complex deposition and presenting as acute nephritic
syndrome
– specific gravity : ↑ It is a clinical complex of acute onset characterized by:
– proteins :>1 g/m2/24 hours ,or 3+ to 4+ bydipstick • Hematuria with RB C casts in urine
– proteinuria is of selective type (mainly albumin + low molecular weight proteins ) Nephrotic Syndrome • Oliguria• Azotemia• Hypertension
🔹
– microscopically: hyaline casts ± transient microscopic hematuria.
Serum and blood :
– Total plasma proteins: < 5.5 g/dl.
• Mild proteinuria (<1 gram/day ) It's severe in nephrotic syndrome
• Edema ( usually mild )
– Serum albumin: <2.5 g/dl.
– Serum cholesterol: >220 mg/dl. Etiology
– Serum triglycerides ↑. Deposition of immune complex these complexes may be:
• Post-infectious (exogenous antigen) Post
– Total serum Calcium ↓ due to reduction in albumin-bound fraction.
streptococcal glomerulonephritis and
– Normal complement C3. • non Post streptococcal glomerulonephritis: like
– Hematocrite and hemoglobin may be ↑. bacterial,viral , fungal, parasitic ,
🔹
– Erythrocyte sedimentation rate may be ↑.
renal functions:
• Non-infectious (endogenous antigen)Antigen
🔸
_antibody reaction
Post streptococcal acute glomerulonphritis
– Creatinine clearance may be ↓due to ↓ renal perfusion (hypovolemia).
(PSAGN)the commen one
🔹
– Blood urea may be slightly ↑ due to ↓ renal perfusion (hypovolemia).
Renal biopsy is not required for diagnosisin most children.Children with: hematuria, hypertension, renal
insufficiency, hypocomplementemia, age < 1 year or > 8 years should be considered for renal biopsy
before treatment .
Definition:
PSAGN represent the classical "acute nephritic syndrome".
It is due to non-bacterial inflammation of the glomeruli secondary to a
Complications previous group A β-hemolytic streptococcal (GABHS) infection of
1. Increased susceptibility to infection. pharynx or skin.
2. Arterial or venous thrombosis **BurThe most common nephropathys is IGA ** إمتحان سؤال
🔶 Why are nephrotic patients more susceptible to infection?
• Edema fluid in tissues is a good culture medium. Epidemiology:
• Hypoproteinemia. – Age: >3 years, usually 5-10 years.
• ↓ Immunoglobulin levels. – Sex: male: female ratio 2:1
• Impaired T-cell function.
• ↓ Bactericidal activity of leukocytes. Etiology:
PSAGN occurs1-3 weeks after infection of pharynx or
• ↓ complement activity.But its normal value skin(impetigo\pyoderna)"with certain "nephritogenic" strains of GABHS
• Loss of complement factor in urine (Properdin factor B that opsonize certain bacteria). (serotypes12,49.et)
• ↓Splenic function.
• Immunosuppressive therapy.
🔶
• Thrombo-embolic complications
The risk of thrombosis is related to:
a-Increase prothrombotic factors:
pathogenesis:
it is mediated via immune complex.
-Fibrinogen -Thrombocytosis -Hemo-concentration -Relative immobilization -Sterpotococcal antigen and its antibody make an antigen-antibody
b-Decrease fibrinolytic factors: complex-->activation of Complement and Deposition of both
-Urinary losses of anti-thrombin III, Proteins C and S. complexs and complement in the basement membrane of glomeruli
and in mesangium -->infammatory reaction.
5- Specific therapy:
Acute glomerulonephritis • Clinical picture:
• Induction:
oral prednisone 60 mg /m2/day dividedin 3 doses until urine free for 3 cosecutive days
Post streptococcal acute 1. Asymptomatic PSAGN :
• Maintenance: glomerulonphritis (PSAGN) presenting only with asymptomatic microscopic hematuria
2. Classical presentation with the nephritic triad of :
Oral prednisone 60 mg / m2 every other day (singledose) for 6 weeks.45 mg / m2 every other day (single
• Edema: in 75 % of cases
dose) for 2weeks.30 mg / m2 every other day (single dose) for 2weeks.15mg / m2 every other day (single
• Gross hematuria: in 65 % of cases
dose) for 2weeks.G radual withdrawal over 2 weeks.
• Hypertension: in 60 % of cases
🔶
🔸 Patient may be classified according to their response to prednisone into 4 types:
» steroid responsive:
• This may be accompanied by systemic manifestation as: mild fever,
headache, anorexia, nausea, vomiting, and abdominal pain.
3-Presentation by complication (s):
respond to prednisone in 1-4 weeks (usually 2 weeks),remission is maintained during alternate day
• hypertensive encephalopathy (Convulsion )يدخل
🔸
therapy.
» steroid dependent:
respond to daily dose and relapse on altemate day therapy or within 4 weeks of discontinued of
• Heart failure and pulmonary edema
• Acute renal failure
prednisone.
🔸
Renal biopsy is indicated.
» steroid resistant:
proteinuria 2+ or greater after 8 weeks of daily prednisone therapy.
• Laboratory findings
1.Urinary changes:
– Volume : oligouria ( urine volume <400 ml/m2/24 hours)
🔸
renal biopsy is indicated and cytotoxic drugs are given.
» frequent relapsers :(Protienuria +edema)
patient who respond well to prednisone therapy but relapse 4 or more times in a 12 month period
by fatema okoff – Color :normal, microscopic or gross hematuria→ smoky , red, tea-or
cola-colored
– Specific gravity ↑ Oliguria
6- Cytotoxic drugs:
🔸 Indications:
o Frequent relapsers and steroid dependence
– Mild to moderate proteinuria ( < 1 gm / m2/24 hours )
– Microscopically( in freshly voided sample ): red blood cells,
↑polymorphonuclear leukocytes,casts (red cell casts, granular casts )
o Corticosteroid toxicity 2-Blood:
Treatment of NS
🔸
o Steroid resistant NS
What to use:
Cyclophosphamide 3 mg/kg/day in a single daily dose for 8-12 weeks + ample fluids.
The principles lines of treatment are:
– Effort to reduce edema.
• Mild normochromic anemia ( due to hemodilution )
• ↑ Erythrocyte sedimentation rate( ESR)النهinfection
maintenance dose: يوم ايوه و يوم ال – Specific therapy with prednisone. • ↓Serum complement ( C3) level
🔸 Alternate-dayprednisone therapy is ofen continued during the
1- Hospitalization, investigations and exclusion of contraindications to steroids.
2-Physical activity: not restricted, as tolerance by child.
• Serum protein : normal or slight ↓ ( due to hemodilution
• Blood urea usually dl ↑( normal < 40 mg /dl)
🔸
course of cyciophosphamide therapy.
Toxicity and side effects;
alopecia, sterility, disseminated varicela, hemorhagic cystitis, leucopenia (do weekly WBC count
3-Diet and fluids: if edema is severe
– Salt: do not add salt to diet or restrict it to 2g/day until edema resolves. • Serum creatinine : usually ↑( normal < 0.7 mg/ dl)
• ↓Creatinine clearance
– Water: moderate restriction.
&stopdrugs if WBCs <5000/mm”). 3-Evidence of recent GABHS infection:
7-all children with NS should receive polyvalent pneumococcal vaccine.
It may be given once the chid is in remission and off of daily prednisone
🔹
4- Diuretics: are used cautiously
For mild edema: • Positive throat cultures
• Streptozyme rapid slide test for detection of antibodies to GABHS
therapy. 🔹
Hydrochlorothiazide 2-4 mg/kg/day in 2 divided doses + spironolactone 3-5mg/kg/day in divided doses
For marked edema:
oral furosemid (lasix) 1- 2mg/kg/dose every 4 hours + Metolazone (zaroxolyn) 0.1-0.2 mg/kg/12 hours. N ot I.V
• ↑ASO titer (in throat infection only), ↑anti-DNase B antibodies.
🔸
Prognosis ofsteroid-responsive MCNS:
Repeated relapses with complete spontaneous resolution by
🔸
Treatment
No specific treatment. Prognosis
🔸
the end of 2nd decade.
🔸 No residual renal dysfunction • Hospitalization and monitoring
• Restriction of activity In complection
• Complete recovery in > 95% of cases G ood
prognosis
🔸 Notheloss of fertility(unless cyclophosphamide was used)
diseases is not hereditary • Diet No restrictions except in oliguric phase
• Treatment of streptococcal infection
• Infrequent : glomerular hyalinization →chronic
renal failure
• 5-Treatment of hypertension 10 days must with • Death from complications can occur in acute
penicillin الزم stage if not properly treated.
• Recurrences are extremely rare .If recurrent
• Treatment of heart failure andpulmonary edema we must Think other cause than streptococcal
• Treatment of acute renal failure
