Hematuria
Presence of at least 5RBC/Microliter of urine, micro(less than 
100), macro(more than 100)
Prevalence 0.5-2%among school children, screening urine 
analysis should be obtained of well child once at 5years old
then once during 2nd decade of life.
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 Haematuria
1- UTI, 2- meatal stenosis, 3- perinatal irritation, 4- trauma, 5- 
stone, 6- caogulopathy, 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 parietooccipital areas on T2-weighted 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 of1- 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 infection-induced,
genetic, medication- induced, and HUS associated with systemic diseases
characterized by microvascular injury
The most common form of HUS is caused by toxin-producing Escherichia
coli that cause prodromal acute enteritis and is commonly termed diarrheaassociated HUS. In the subcontinent of Asia and southern Africa, the shiga
toxin of Shigella dysenteriae type 1 is causative, whereas in Western
countries verotoxin-producing 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 restaurants
Pathogenasis
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 is most common in preschool and school-aged children, but it can
occur in adolescents. In HUS caused by exotoxin-producing E. coli, onset
of HUS occurs a few days (as few as 3) after onset of gastroenteritis with
fever, vomiting, abdominal pain, and diarrhea.
The prodromal intestinal symptoms may be severe and require
hospitalization, but they can be relatively mild and considered trivial. The
diarrhea is often bloody, but not necessarily so, especially early in the
illness. Following the prodromal illness, the sudden onset of pallor,
irritability, weakness, and lethargy herald the onset of HUS
. Oliguria can be present in early stages but may be masked by ongoing
diarrhea because the prodromal enteritis often overlaps the onset of HUS.
Thus, patients can present with HUS either with significant dehydration or
volume overload, depending on whether the enteritis or renal insufficiency
from HUS predominates and the amount of fluid that was administered.
Patients with pneumococcus-associated HUS usually are ill with
pneumonia and empyema when they develop HUS. Onset can be insidious
in patients with the genetic forms of HUS, with HUS triggered by a variety
of illnesses, including mild, nonspecific gastroenteritis or respiratory tract
infections
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.
DIAGNOSIS
1- CBP HB=5-9 G/L, wbc up to 30000, platelet 20000-100000, retic increased,
coombs test -ve, The blood peripheral smear reveals helmet cells, burr
cells, and fragmented RBCs
2- GUA low grade protienurea, micro.hematuria
3- PT, PTT normal
4- RFT mild to moderate RF require dialysis
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,
for diarrhea-associated HU has <5% mortality in most major medical centers.
Half of the patients require dialysis support during the acute phase of the disease.
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 prognosis for HUS not associated with diarrhea is more severe.
Pneumococci-associated HUS causes increased patient morbidity, with mortality
reported as 20%. 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
in patient passing acute phase , should flow because HT, decrease in renal 
function may be seen 20 years after.
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 patients suffering severe
manifestations of HUS, primarily serious CNS involvement. other genetic forms of HUS, such as
undefined familial (recessive or dominant) or sporadic but recurrent HUS.