Hematuria
Presence of at least 5RBC/Microliter of 
urine, micro(less than 100), macro(more
than 100)
Prevalence 0.5-2%among school 
children
Haematuria either heme +ve (RBC, 
myoglobin) ,
heme-ve(just red discoloration) caused 
by
1-drugs(deferoxamine, ibubrufin, 
metranidazole, iron sorbitol, nitrfurantion,
refampcin, salicylic acid
2- dyes (beets, food coloring,
3- hemogenstic acid, urate, porphyrin
Common Causes OF Grosse Hematuria
1- UTI,
2- meatal stenosis
3- perinatal irritation
4- trauma
5- stone
6- coagulopathy
7- tumor
8- glom ruler diseases(IgA
nephropathy, post infectious GN, HSP,
SLE)
Evaluation
1- careful history,physical examination, GUA
-level of Haematuria upper=brown in color, 
more than2++ protienurea, RBCcast, deformed
RBC(glomerl, tubuler, interstitial),
Lower=pc system, ureter, blader, 
urethra)(gross, clot, less protienurea, normal
shape RBC)
-Tea color, edema, HT, hiegh blood urea 
suggest acute GN(PSGN)
-Reccurent URI, GI system suggest acute GN, 
HUS
-Frequency , dysurea, fever suggest UTI
-Renal colick,
renal stone
-Flank mass
hydronephrosis, cystic 
disease, RVT
-Headache, visual disturbances, epistaxis, 
significant HT,
suggest PSGN
-Family history of deafness
Alport 
syndrome
-The child of persistent asymptomatic isolated 
microscopical Haematuria more than 2weeks
need further evaluation.
IgA nephropathy(Beurger disease)
common chronic glo.disease
-predominate IgA within messengeal deposits
of glo with abscense of systemic disease like
SLE, HSP
Clinical feature
Micro Haematuria, protienurea , nephritis,
nephrotic, male more than female, Crosse
Hematuria associated with URI, GIT disorder,
mild to moderate HT, normal C3 level
incontrast to PSGN, serum IgA IS NOT
DIAGNOSTIC, ONLY 50% (increased)
Prognosis and treatment
NOT lead to significant renal damage,
progressive disease in 20-30%
Poor prognostic factors
1- persistent HT 2- decrease in renal function
3- heavy and persistent protienurea
The proper management of HT is the aim,
immune suppressive , steroid some benefit
Acute post sterptoccocal GN(PSGN)
Sudden onset of Grosse hematuria(30-50%), 
edema(85%) , HT, degree of renal
insufficiency(usaualy mild). Is the most common
G-disease supper passed by IgA nephropathy.
Etiology and Epidemiology
Flow throat (serotype 12)in winter, and 
skin(serotype 49) in summer, infection by certain
nephrogenic strain of GABH strept.
Pathology
Both kidneys enlarged symmetrically, on light 
microscope all glomeruli appears enlarged ,
diffuse messengeal cell proliferation with
increase in matrix.
Pathogenesis
Precise mechanism is still undetermined, 
although low C3 level strongly suggestive of
immune e mediated by activation of alternative
pathway of complement rather than classical.
C/F
most common age (5-15)years,and 
uncommon less than 3 years
-1-2week after 
throat(strept.pharangitis) and 3-6weeks
after skin infection (pyioderma)
-The severity of renal range from 
asymptomatic hematuria with normal
renal function to acute renal failure with
hematuria
-Various degree of edema, HT, oligurea, 
encephalopathy or and heart failure
owing to HT, or hypervolemia.
- Encephalopathy result from HT or 
toxic material of strept.
-Edema result from salt and water 
retention or nephrotic(less than 5%).
Fever, malaise, lethargy , flank pain are 
common.
- The acute phase resolved at 6-8 weeks, 
although protienurea and HT usually
resolved by 4-6 weeks after onset,
persistent microscopical hematuria may
persist up to 1-2years
Diagnosis
1- GUA RBC, RBC cast, protienurea, WBC,
2- CBP
mild anemia(hemodilution, low grade hemolysis)
3- RFT
b.urea and s.cr either normal; or increased
4- C3 level decreased markedly (return to normal at 6-8 weeks)
5- clear evidence of invasive st.pharangitis, by +ve throat culture or
Antistreptolysin test( ASO) commonly increased markedly after URI
but not skin infection (normally 200 TOD)
6- the best one after skin infection is Dexoyribonuclase B(DANase
B)
7- the streptozyme test include all (ASO, DANase B, streptokinase,
hyalinrridase)
Magnetic resonance imaging of the brain is indicated in patients
with severe neurologic symptoms and can demonstrate reversible
posterior leukoencephalopathy in the parieto-occipital areas on T2weighted images.
Chest x-ray is indicated in those with signs of heart failure or
respiratory distress, or physical exam findings of a heart gallop,
decreased breath sounds, rales, or hypoxemia.
The clinical diagnosis child 
with acute nephritis, low C3
level , evidence of recent strpt.
Infection.
DDX
IgA , focal segemental GN, 
membroprolefrative, SLE, HSP, acute
exacerbation of chronic GN
Indication of renal biopsy
1- in the presence of renal failure
2- in the presence of nephrotic syndrome
3- absence of evidence of recent strpt.
Infection.
4- normal C3,C4 level
5- hematuria, decrease renal function, low C3
level persist more than 8 weeks after the onset.
NOTE
Acute GN, may flow other infection(coagalase
–ve staph, st.pneumonia, G-ve, fungal,
viral(influenza), ricketetial.
Complication
1- mainly due to HT 60%, 10% encelopathy.
2- acute renal failure acidosis, hyperkalemia,
hypocalcaemia, hyperphosphetemia, seizure.
Prevention
1- Early institution of AB for st.pharangitis, skin infection, does 
not eliminate the risk of GN
2- family member of patient with PSGN should be cultured for 
GABH st. if +ve , give treatment
Treatment
1-Proper management of HT, RF, 
2-10 days course of treatment with penicilline to prevent the 
spread of infection and dose not affect the natural history of the
disease.
3- salt restriction , diuretics, CA cannel blocker , ACE, are 
standard treatment of HT.
Prognosis
95%complete recovery , mortality rate decreased by appropriate 
management of HT, HF, RF.
Acute phase may pass to chronic renal disease
Recurrence are extremely rare.
Hemolytic-Uremic Syndrome
Hemolytic-uremic syndrome (HUS) is one of the most
common causes of community-acquired acute kidney failure
in young children. It is characterized by the triad of
1- microangiopathic hemolytic anemia
2- thrombocytopenia
3- renal insufficiency
CLINICAL DESCRIPTION
Hemolytic uremic syndrome (HUS) is characterized by the
acute onset of microangiopathic hemolytic anemia, renal
injury, and a low platelet count. Thrombotic
thrombocytopenic purpura (TTP) also is characterized by
these features but can include central nervous system (CNS)
involvement and fever and can have a more gradual onset.
Most cases of HUS (but few cases of TTP) occur after an
acute gastrointestinal illness (usually diarrheal).
DEFINITION OF POSTDIARRHEAL
HEMOLYTIC UREMIC SYNDROME DISEASE
LABORATORY CRITERIA FOR DIAGNOSIS
The following are both present at some time during the illness:
• Anemia (acute onset) with microangiopathic changes (i.e.,
schistocytes, burr cells, or helmet cells) on peripheral blood smear and
• Renal injury (acute onset) evidenced by hematuria, proteinuria, or
elevated creatinine level: ≥1.0 mg/dL in a child <13 yr or ≥1.5 mg/dL in
a patient 13 yr or older or ≥50% increase over baseline.
Note: A low platelet count can usually, but not always, be detected early
in the illness, but it can then become normal or even high. If a platelet
count obtained within 7 days after onset of the acute gastrointestinal
illness is not <150,000/mm3, other diagnoses should be considered.
CASE CLASSIFICATION
Probable • An acute illness diagnosed as HUS or TTP
that meets the laboratory criteria in a patient who does
not have a clear history of acute or bloody diarrhea in
the preceding 3 wk, or
• An acute illness diagnosed as HUS or TTP that (a)
has onset within 3 wk after onset of an acute or bloody
diarrhea and (b) meets the laboratory criteria except
that microangiopathic changes are not confirmed.
Confirmed • An acute illness diagnosed as HUS or
TTP that both meets the laboratory criteria and began
within 3 wk after onset of an episode of acute or bloody
diarrhea
Etiology
The various etiologies of HUS allow classification into
1-infection-induced
2- genetic
3-medication- induced, and
4-HUS associated with systemic diseases characterized by
microvascular injury
The most common form of HUS is caused by toxin-producing
s Escherichia coli that cause prodromal acute enteritis and is
commonly termed diarrhea-associated HUS. In the subcontinent of
Asia and southern Africa, the shiga toxin of Shigella dysenteriae
type 1 is causative, whereas in Western countries verotoxinproducing E. coli (VTEC) are the usual causes.
Several serotypes of E. coli can produce verotoxin, and the
O157:H7 type is most common in Europe and the Americas. The
reservoir of VTEC is the intestinal tract of domestic animals, usually
cows. Disease is usually transmitted by undercooked meat or
unpasteurized milk or apple cider. Epidemics have followed
ingestion of undercooked, contaminated hamburger at fast food
restaurant
Pathogenesis
1-Endothelial cell damage localized thrombus,
2- anemia mechanical damage of RBC, due to passing 
via altered vasculature
3- thrombocytopenia intrarenal platelets adhetion
4- HSM engulfed damaged RBC, platelets by liver and 
spleen
-.
Clinical Manifestations
HUS often begins with vomiting and diarrhea, which may be bloody. Within a week, the
person may become weak and irritable. Persons with this condition may urinate less than
normal. Urine output may almost stop.
Red blood cell destruction leads to symptoms of anemia.
Early symptoms:
Blood in the stools
Irritability
Fever
Lethargy
Vomiting and diarrhea
Weakness
Later symptoms:
Bruising
Decreased consciousness
Low urine output
No urine output
Pallor
Seizures -- rare
Skin rash that looks like fine red spots (petechiae)
Yellow skin (jaundice)
Liver or spleen swelling
Nervous system changes
The majority of patients with HUS have some central
nervous system (CNS) involvement. Most have mild
manifestations, with significant irritability, lethargy, and
nonspecific encephalopathic features. Severe CNS
involvement occurs in ≤20% of cases. Seizures and
significant encephalopathy are the most common
manifestations in those with severe CNS involvement and
result from focal ischemia secondary to microvascular CNS
thrombosis.
DDX
TTP
SLE, malignant HT, RVT,(marked renal
enlargement, absent of renal vien flow via Doppler
US.
Complication
1- renal acidosis, hyperkalemia, hypocalcaemia,
hyperphosphetemia, seizure
2- extrarenal GIT, intessuception, perforation
CNS, infarction, cortical blindness
HEART pericarditis, arrythemia.
Prognosis and Treatment
The acute prognosis, with careful supportive care,
1-For diarrhea-associated HU has <5% mortality in most major medical
centers.
2-Half of the patients require dialysis support during the acute phase of
the disease.
3-Most recover renal function completely, but of surviving patients, 5%
remain dependent on dialysis,
4-And up to 20-30% are left with some level of chronic renal
insufficiency.
5-The prognosis for HUS not associated with diarrhea is more severe.
Pneumococci-associated HUS causes increased patient morbidity, with
mortality reported as 20%.
6-The familial, genetic forms of HUS can be insidiously progressive
or relapsing diseases and have a poor prognosis
The primary approach that has substantially improved acute outcome in
HUS is early recognition of the disease, monitoring for potential
complications, and meticulous supportive care
Supportive care includes
careful management of fluid and electrolytes including correction of volume deficit
, control of hypertension
, and 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
. In pneumococci-associated HUS, it is recommended that any administered red cells be
washed before transfusion to remove residual plasma
Anticoagulation, antiplatelet, and fibrinolytic therapy is specifically contraindicated because
they increase the risk of serious hemorrhage.
Antibiotic therapy to clear the toxigenic organisms can result in increased toxin release,
potentially exacerbating the disease, and therefore is not recommended.
Prompt treatment of any underlying pneumococcal infection is importan
Plasma infusion or plasmapheresis has been proposed for
1-patients suffering severe manifestations of HUS,
2- primarily serious CNS involvement.
3-other genetic forms of HUS, such as undefined familial (recessive or dominant)
4-or sporadic but recurrent HUS.