hematuria pptx - فرح

Dr.Farah sameer yahya

M.B.CH.B.C.A.B.P
Lecturer in department of pediatrics / Mosul college of medicine
CHILD WITH
HEMATURIA
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DEFINITION OF HEMATURIA

Presence of red blood cells (RBC) in urine >10 RBC per mm3 of freshly voided, unspun urine or >5 RBC per high power field (HPF) of 10 ml of fresh urine, centrifuged at 2,000 rpm.

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• Macroscopic (gross) hematuria refers to urine that is visibly bloody (bright red to brown or tea (cola) colored). The color depends on the amount of blood, the
source of bleeding, and urine acidity.

• Microscopic hematuria (microhematuria) refers to the presence of RBC without urine discoloration, detected by microscopy or chemical (dipstick) analysis.

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Common causes of “dark urine” mimicking hematuria

• Drugs: rifampin, nitrofurantoin, metronidazole; methyldopa, levodopa
• Pigments: hemoglobin, myoglobin, bilirubin; urate
• Nutrients: beets, blackberries

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Glumerulonephritis

Glomerulonephritis (GN) is the term used for a group of primary or secondary immune-mediated renal diseases characterized by inflammation of the glomeruli or small blood vessels in the kidneys.

GN has many different causes ranging from post-infectious glomerulonephritis to systemic diseases such as Henoch- Schönlein purpura and systemic lupus erythematosus.

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Glomerulonephritis may present as :

asymptomatic haematuria
or proteinuria,
acute nephritis,
rapidly progressive glomerulonephritis (RPGN),
a mixed nephritic/nephrotic syndrome,
or nephrotic syndrome

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Aetiology
The cause may be post-infectious or non-infectious.
A) Post-infectious glomerulonephritis
Streptococcal
Post-streptococcal GN usually develops 1–6 weeks after infection with nephritogenic strains of Group A B-haemolytic streptococcus (GAS).
The incidence is 5–10% in patients with pharyngitis and 25% after skin infection.
Deposits of IgG and C3 are found in glomeruli and serum C3 is low.
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Non-streptococcal

Bacterial: infective endocarditis, typhoid, pneumonococcal pneumonia, meningococcaemia
Viral: hepatitis B, Epstein–Barr virus, varicella, coxsackie virus
Parasitic: malaria, toxoplasmosis.

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B) Non-infectious

Primary glomerular diseases
Membranoproliferative GN (MPGN)
IgA nephropathy (Berger disease)
Mesangial proliferative GN
Focal and segmental glomerulosclerosis (FSGS).
Secondary to multisystem systemic disease( Systemic lupus erythematosus,Henoch–Schönlein purpura ,Goodpasture syndrome)
Drugs: penicillamine

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Acute post streptococcal GN

Group A β-hemolytic streptococcal (GAS) infections are common in children and can lead to acute glomerulonephritis (GN).
Acute poststreptococcal glomerulonephritis (APSGN) is a classic example of the acute nephritic syndrome characterized by the sudden onset of gross hematuria, edema, hypertension, and renal insufficiency.

It is one of the most common glomerular causes of gross hematuria in children.

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Etiology and Epidemiology

APSGN follows infection of the throat or skin by certain “nephritogenic” strains of GAS.
97% of cases occur in less-developed countries.
Poststreptococcal GN commonly follows streptococcal pharyngitis during cold-weather months and streptococcal skin infections or impitigo during warm-weather months.
Although epidemics of nephritis have been described in association with throat (serotype 12) and skin (serotype 49) infections, this disease is most commonly sporadic.

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Pathogenesis
a depression in the serum complement (C3) level provide strong evidence that ASPGN is mediated by immune complexes.
Precise mechanisms by which nephritogenic streptococci induce immunologic injury continue to be elucidated.
Mechanism include circulating immune complex formation with streptococcal antigens and subsequent glomerular deposition, molecular mimicry whereby circulating antibodies elicited by streptococcal antigens react with normal glomerular antigens, in situ immune complex formation of antistreptococcal antibodies with glomerular deposited antigen, and complement activation.

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Clinical Manifestations

Poststreptococcal GN is most common in children aged 5-12 yr and uncommon before the age of 3 yr.

The typical patient develops an acute nephritic syndrome 1-2 wk after an antecedent streptococcal pharyngitis or 3-6 wk after a streptococcal pyoderma.

The history of a specific infection may be absent or mild.

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APSGN Spectrum ranges from microhematuria to nephrotic syndrome, severe renal failure, and encephalopathy or seizures due to hypertension

Acute glomerulonephritis is characterized by the abrupt onset of hematuria, proteinuria, hypertension, and edema.

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The hematuria is often grossly visible as tea-colored or cola-colored urine. In some children, however, the hematuria may be microscopic only.

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Patients will usually have oliguria and, in rare cases, anuria.

Fluid retention leads to edema that is usually periorbital and, rarely, severe.

Intravascular overload caused by salt and water retention can lead to signs of congestive heart failure.
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Summery of clinical presentation of APSGN

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INVESTIGATIONS

• General Urine examination
a- Grossly cola (tea) colored urine
b - Dipstick analysis
Hematuria, proteinuria
C- Urine microscopy
Red blood cell (RBC) casts
Dysmorphic RBCs
Leukocytes (sterile pyuria)
D- urine for protein
Proteinuria <2 g/l in 85 % of cases (U protein/creatinine <2 g/g)
Nephrotic presentation may herald poor renal outcome
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COLA COLORED URINE

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RBC CASTS

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2) Complement

Reduced plasma C3 in >90 % of cases
Normalize within 6–12 weeks after presentation
Plasma C4 generally normal
3) Bacterial/viral identification
Pharyngeal swab for Index patient and siblings (opportunity of preventing spread of nephritogenic strain)
Culture of beta-hemolytic steptococci
Rapid streptococcal antigen test
Skin swab (Suspected pyoderma)
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4 ) Serology

a) Antistreptolysin O titer (ASOT)
Elevated in 70–80 % of APIGN cases 1–5 weeks after infection,
Unreliable for streptococcal pyoderma
b) Streptozyme test
Simple, sensitive hemagglutination assay detecting antibodies against several streptococcal antigens (streptolysin O, DNaseB, hyaluronidase,streptokinase, anti-nicotinamide adenine dinucleotidase (NADase))

c) Anti-Dnase B (ADB)
Elevated in 80–90 % of cases of pyoderma-associated APSGN
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5) Blood tests:

renal function: creatinine, urea and electrolytes (With severe oliguria, azotemia and acidosis may be present )
FBC (MILD Normocytic normochromic ANEMIA , CRP, ESR (usually elevated)
The plasma volume is usually expanded, causing a decline in serum protein, hemoglobin, and hematocrit levels by dilution
6 ) Cardiovascular status:
ECG, echocardiogram
7 ) Imaging:
CXR, (with significant HTN & fluid retention may show cardiomegaly ,pulmonary edema ,plueural effusion)
renal ultrasound(is nonspecific, usually revealing bilaterally enlarged echogenic kidneys)

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8) Kidney biopsy

Indications (rare):
Alternative diagnosis (e.g., MPGN, IgA Nephropathy)
Normal serum C3
Persistently low serum C3 (>12 weeks after onset)
Persistent GN /deteriorating renal function
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Histopathological finding in APSGN
• Bright- field microscopy
Endocapillary proliferative glomerulonephritis with diffusely increased cellularity, occasionally with abundant polymorphonuclear neutrophils
Enlarged, bloodless glomeruli secondary to capillary occlusion
B. Immuno fluorescence
Discrete deposits of C3, IgG, and IgM in the mesangium
and in the glomerular basement membrane
C. Electron microscopy
Subepithelial electron-dense deposits (“humps,” a lesion of APSGN) containing mainly C3 and IgG/IgM and streptococcal antigens
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TREATMENT OF APSGN

Hospitalization for patients who have this disease needs to be determined individually
When to Admit ???

1) Severe hypertension
2) Renal failure with significant electrolyte disturbances
3) Congestive heart failure from volume overload
4) Oliguria or anuria
5) Rapidly progressive renal failure

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General measures:

a) Monitor: twice daily weight, fluid balance, BP
b) Fluid restrict to urine output plus insensible losses
c) Diet: Na restriction for fluid retention

A 10-day course of penicillin is usually given to eradicate any remaining GABHS and thus prevent the spread of the organism to others. No evidence has been found that such treatment affects the course of nephritis in the patient. Close contacts should be screened for streptococcal infection and treated if present.

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Management is directed at treating the acute effects of renal insufficiency and hypertension

Loop diuretics: furosemide for edema and volume-related hypertension
Antihypertensive agents: e.g. nifedipine or captopril

Control of severe hypertension will often require the use of intravenous sodium nitroprusside or labetalol

The signs of congestive heart failure usually resolve with control of the hypertension.

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Occasionally a patient develops acute renal failure severe enough to require dialysis

Every child should be monitored regularly until the hypertension, electrolyte and creatinine abnormalities, and serum complement values return to normal.

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Complications of APSGN

Acute complications result from hypertension and acute renal dysfunction.
Hypertension is seen in 60% of patients and is associated with hypertensive encephalopathy in 10% of cases.
Other potential complications include heart failure, hyperkalemia, hyperphosphatemia, hypocalcemia, acidosis, seizures, and uremia.

Acute renal failure can require treatment with dialysis

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Course of APSGN

The acute phase generally resolves within 6-8 wk.

Although urinary protein excretion and hypertension usually normalize by 4-6 wk after onset, persistent microscopic hematuria can persist for 1-2 yr after the initial presentation

Proteinuria should resolve by 3 months, and complement levels should normalize by 6 to 8 weeks
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Prognosis

Complete recovery occurs in >95% of children with APSGN.

Recurrences are extremely rare.

Mortality in the acute stage can be avoided by appropriate management of acute renal failure, cardiac failure, and hypertension.

Infrequently chronic renal disease in <2% of affected children.

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Henoch-Schonlein purpura (HSP)

is the most common form of vasculitis in children.
This small-vessel vasculitis is mediated by immunoglobulin A (IgA)-containing immune complexes and is characterized by:-
1) nonthrombocytopenic purpura,
2) abdominal pain,
3) arthralgias,
4) and renal disease.
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EPIDEMIOLOGY

HSP mainly affects young children, with a peak incidence at 4 to 6 years of age

a 1.5:1 male-to-female ratio.

HSP appears to be more prevalent during the winter and spring

in at least 30% of cases, an upper respiratory infection precedes the onset of symptoms

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Clinical features of HSP

Cutaneous manifestations are the most common clinical features of patients with HSP.

Commonly a macular-petechial rash is present. This rash is symmetric, sometimes purpuric(palpable purpura) , localized predominantly in the extensor surface of the lower extremities, forearms, and buttocks and tends to spare the trunk.
Nonpitting edema of the scalp, hands, and feet may be present in 30% to 70% of young children
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Joint manifestations occur in 60% to 80% patients, with knees, ankles, wrist, and fingers most commonly affected.

The joints involved are usually tender and swollen, but these symptoms resolve without any residual deformity.

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Gastrointestinal manifestations develop in 50% to 70% of patients with HSP

Intermittent colicky abdominal pain, vomiting, or gastrointestinal bleeding are most common
up to 5% of the patients develop complications such as intestinal infarction, perforation, or intussusception
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Renal involvement occurs in 20% to 50% of cases and is responsible for the long-term morbidity in affected patients.
The spectrum of renal involvement in HSP is broad and may include microscopic hematuria (transient or persistent), macroscopic hematuria , proteinuria, nephritic syndrome, and nephriticnephrotic syndrome.
HSP nephritis when mild tends to resolve without any particular intervention.
However, 2% to 5% of patients with renal involvement progress to end-stage renal disease.

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Testicular swelling and tenderness may be present in up to 35% of male patients with HSP.

Other serious complications such as pulmonary hemorrhage and central nervous system involvement have also been described
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Evaluation of HSP

The diagnosis of HSP is based on clinical findings.

In general, complete blood count, platelet count, coagulation studies, and complement levels are normal.
The serum albumin and renal function are normal in the majority of patients but vary according to the degree of renal involvement.

IgA levels may be transiently elevated in 50% of the patients with HSP.

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Urinalyses obtained at various times in the disease process may reveal hematuria and various degrees of proteinuria.

A renal biopsy is not indicated in all patients with a diagnosis of HSP; however, it should be considered in patients with significant proteinuria for more than 1 month, renal insufficiency, hypertension, or nephrotic syndrome
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Ultrasound is often used in the setting of gastrointestinal complaints to look for bowel wall edema or the rare occurrence of an associated intussusception.

Although often unnecessary in typical HSP, biopsies of skin and kidney can provide important diagnostic information, particularly in atypical or severe cases, and characteristically show IgA deposition in affected tissues.

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Treatment of HSP
Treatment of HSP is supportive, with an emphasis on assuring adequate hydration, nutrition, and analgesia.

Controversy continues concerning the appropriate use of glucocorticoids in the management of HSP, but steroids are most often used to treat significant gastrointestinal involvement or other life-threatening manifestations.

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Empiric use of prednisone (1 mg/kg/day for 1 to 2 wk, followed by taper) reduces abdominal and joint pain but does not alter overall prognosis nor prevent renal disease.

In some cases, chronic HSP renal disease is managed with a variety of immunosuppressants ( e.g azathioprine)

End-stage renal disease develops in up to 8% of children with HSP nephritis.

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Prognosis of HSP

Overall, the prognosis for childhood HSP is excellent, and most children experience an acute, self-limited course.

About 30% of children with HSP experience one or more recurrences, typically within 4-6 mo of diagnosis.

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The prognosis of HSP nephritis for most patients is excellent. Spontaneous and complete resolution of the nephritis typically occurs in those with mild initial manifestations (isolated hematuria with insignificant proteinuria)

Chronic renal disease develops in 2-5% of children with HSP, and approximately 8% of those with HSP nephritis go on to have end-stage renal disease.