The document provides guidance on evaluating and managing hematuria in children. It begins by defining hematuria and describing diagnostic approaches. It then lists potential causes of hematuria originating from the upper and lower urinary tract, including various glomerular, tubular, and vascular diseases. Specific evaluation involves history, exam, urinalysis and potentially imaging or biopsy. It also discusses acute poststreptococcal glomerulonephritis in detail, covering etiology, pathogenesis, pathology, clinical manifestations, diagnosis, differential diagnosis, complications, and treatment. The overall document offers a comprehensive approach to a child presenting with hematuria.

1. APPROACH TO A CHILD WITH HEMATURIA
&
PSGN
Dr M SANJEEVAPPA
Designated Associate Professor
Dept of Pediatrics
GMC, Anantapuramu

2. APPROACH TO A CHILD WITH HEMATURIA
• Hematuria : defined as the persistent presence of
more than 5 RBCs/HPF in uncentrifuged urine.
• Qualitative estimation : Urinary dipstick method.
peroxidase chemical reaction between hemoglobin
(or myoglobin) and a colorimetric chemical
indicator impregnated on the dipstick.
• Significant hematuria > 50 RBCs/HPF.

3. APPROACH TO A CHILD WITH HEMATURIA
CAUSES OF RED URINE :
HEME POSITIVE : Hemoglobin , Myoglobin.
HEME NEGATIVE :
 Drugs : Chloroquine , Deferoxamine , Hydroxycobalamin,
Ibuprofen, Iron sorbitol, Metronidazole, Nitrofurantoin,
Phenothiazines, Phenytoin, Quinine, Rifampin.
 Dyes (Vegetable/Fruit) : Beets, Blackberries, Blueberries,
Food and candy colouring agents.
 Metabolites : Homogentisic acid, Melanin,
Methaemoglobin, Porphyrin, Tyrosinosis

4. APPROACH TO A CHILD WITH HEMATURIA
 Evaluation :
- Careful history.
- Physical examination.
- Microscopic urinalysis.
 Special consideration needed on :
- The family history.
- Identification of anatomic abnormalities.
- Malformation syndromes.
- Presence of gross hematuria.
- Hypertension, edema, heart failure.

5. APPROACH TO A CHILD WITH HEMATURIA
Determination of the level of hematuria :
- Upper urinary tract.
- Lower urinary tract.
 Upper urinary tract :
- Glomerulus.
- Tubular system.
- Interstitium.
 Lower urinary tract :
- Pelvocaliceal system,
- Ureter, Bladder, Urethra.

6. APPROACH TO A CHILD WITH HEMATURIA
 Hematuria from within the glomerulus :
- Brown, cola- or tea-colored.
- Proteinuria > 100mg/dL via dipstick.
- Urinary microscopy: RBC casts, and deformed
urinary RBCs (particularly acanthocytes).
 Hematuria originating within the tubular system :
- Associated with the presence of leukocytes.
- Renal tubular casts.

7. APPROACH TO A CHILD WITH HEMATURIA
 Hematuria originating from Lower urinary tract :
- Gross hematuria that is bright red or pink.
- Terminal hematuria (gross hematuria occurring at the
end of the urine stream).
- Blood clots.
- Normal urinary RBC morphology.
- Minimal proteinuria on dipstick (<100 mg/dL).

8. APPROACH TO A CHILD WITH HEMATURIA
CAUSES OF HEMATURIA IN CHILDREN :
 UPPER URINARY TRACT DISEASE
Isolated Renal Disease
 Postinfectious GN (poststreptococcal GN)
 Immunoglobulin (Ig) A nephropathy (Berger disease)
 Alport syndrome (hereditary nephritis)
 Membranous nephropathy
 Membranoproliferative GN
 Rapidly progressive GN
 Focal segmental glomerulosclerosis
 Anti–glomerular basement membrane disease.

9. APPROACH TO A CHILD WITH HEMATURIA
CAUSES OF HEMATURIA IN CHILDREN :
 UPPER URINARY TRACT DISEASE
Multisystem Disease
 Systemic lupus erythematosus nephritis
 Henoch-Schönlein purpura nephritis
 Granulomatosis with polyangiitis.
 Polyarteritis nodosa
 Goodpasture syndrome
 Hemolytic-uremic syndrome
 Sickle cell glomerulopathy
 HIV nephropathy

10. APPROACH TO A CHILD WITH HEMATURIA
CAUSES OF HEMATURIA IN CHILDREN :
 UPPER URINARY TRACT DISEASE
Tubulointerstitial Disease
 Pyelonephritis
 Interstitial nephritis
 Papillary necrosis
 Acute tubular necrosis

11. APPROACH TO A CHILD WITH HEMATURIA
CAUSES OF HEMATURIA IN CHILDREN :
 UPPER URINARY TRACT DISEASE
Vascular Disorders
 Arterial or venous thrombosis
 Malformations (aneurysms, hemangiomas)
 Nutcracker syndrome
 Hemoglobinopathy (sickle cell trait/disease)
 Crystalluria

12. APPROACH TO A CHILD WITH HEMATURIA
CAUSES OF HEMATURIA IN CHILDREN :
 UPPER URINARY TRACT DISEASE
Anatomic Disorders
 Hydronephrosis
 Cystic-syndromic kidney disease
 Polycystic kidney disease
 Multicystic dysplasia
 Tumor (Wilms tumor, rhabdomyosarcoma,
angiomyolipoma, medullary carcinoma)
 Trauma

13. APPROACH TO A CHILD WITH HEMATURIA
CAUSES OF HEMATURIA IN CHILDREN :
LOWER URINARY TRACT DISEASE
 Inflammation (infectious and noninfectious)
 Cystitis
 Urethritis
 Urolithiasis
 Trauma
 Coagulopathy
 Heavy exercise
 Bladder tumor
 Factitious syndrome, factitious syndrome by proxy

14. APPROACH TO A CHILD WITH HEMATURIA
 Tea- or cola-colored urine, facial or body edema,
hypertension, and oliguria are classic symptoms of
glomerulonephritis.
 Frequency, dysuria,and unexplained fevers suggest a
urinary tract infection.
 Hematuria associated with headache, mental status
changes, visual changes, epistaxis, or heart failure
suggests associated severe hypertension.
 Hematuria associated with unexplained perineal
bruising may indicate child abuse.

15. APPROACH TO A CHILD WITH HEMATURIA
 Hereditary glomerular diseases includes :
- Alport syndrome.
- Thin glomerular basement membrane disease.
- SLE nephritis.
- Hereditary angiopathy with nephropathy, aneurysms, and
muscle cramps (HANAC).
- IgA nephropathy (Berger disease).
- Autosomal recessive and autosomal dominant PCKD.
- Atypical hemolytic-uremic syndrome.
- Urolithiasis.
- Sickle cell disease/trait.

16. APPROACH TO A CHILD WITH HEMATURIA
PHYSICAL EXAMINATION :
 Thepresence of hypertension, edema, or signs of heart failure
suggests acute glomerulonephritis.
 Several malformation syndromes are associated with renal
disease. Eg : VATER syndrome.
 Abdominal masses may be caused by
- Bladder distention in posterior urethral valves.
- Hydronephrosis in ureteropelvic junction obstruction.
- Polycystic kidney disease
- Wilms tumor.

17. APPROACH TO A CHILD WITH HEMATURIA
PHYSICAL EXAMINATION :
 Hematuria associated with neurologic or cutaneous
abnormalities may be seen in syndromic renal disorders like
tuberous sclerosis, von Hippel-Lindau syndrome, and
Zellweger syndrome.
 Urethrorrhagia : urethral bleeding in the absence of urine, is
associated with dysuria and blood spots on underwear after
voiding.
 Recurrent episodes of gross hematuria suggest
IgA nephropathy, Alport syndrome, or thin glomerular
basement membrane disease.
 Dysuria and abdominal or flank pain are symptoms of
idiopathic hypercalciuria, or urolithiasis.

18. APPROACH TO A CHILD WITH HEMATURIA
 Renal and bladder ultrasonography : to rule out
structural lesions such as tumor, cystic disease,
hydronephrosis, or urolithiasis.
 A voiding cystourethrogram : may required in patients
with a urinary tract infection, renal scarring,
hydroureter.
Haematological features associated with hematuria :
 Anaemia : acute kidney injury, chronic kidney disease,
hemolytic-uremic syndrome, a chronic hemolytic anemia,
SLE,Goodpasture syndrome.
 Thrombocytopenia : malignancies ,SLE, ITP, HUS,
renal vein thrombosis, autosomal recessive polycystic
kidney disease.

19. APPROACH TO A CHILD WITH HEMATURIA
 Renal biopsy is indicated for some children with
persistent microscopic hematuria and for most
children with recurrent gross hematuria associated
with decreased renal function, proteinuria, or
hypertension.

20. ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
Etiology and Epidemiology :
 APSGN follows infection of the throat or skin by
nephritogenic strains of group A β-hemolytic streptococci
- throat infection : serotypes M1, M4, M25, and some
strains of M12.
- skin infections : serotype M49.
 97% of cases occur in less developed countries.
 New name for APSGN is post infectious
glomerulonephritis (PIGN)

21. ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
PATHOGENESIS :
 Morphologic studies and a depression in the serum C3 level
provide strong evidence that ASPGN is mediated by immune
complexes.
 Molecular mimicry : circulating antibodies elicited by
streptococcal antigens react with normal glomerular antigens
 In situ immune complex formation of antistreptococcal
antibodies with glomerular deposited antigen.
 complement activation by directly deposited streptococcal
antigens is also the mechanism of immunologic injury.

22. ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
PATHOLOGY :
 Glomeruli appear enlarged and bloodless and show a
diffuse mesangial cell proliferation, with an increase in
mesangial matrix.
 Polymorphonuclear leukocyte infiltration is common in
glomeruli.
 Immunofluorescence microscopy reveals a pattern of
“lumpy-bumpy” deposits of immunoglobulin and
complement on the glomerular basement membrane
and in the mesangium.

23. ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS

24. ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
CLINICAL MANIFESTATIONS :
 APSGN is most common in children ages 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 severity of kidney involvement varies from
asymptomatic microscopic hematuria with normal
renal function to gross hematuria with acute renal
failure.

25. ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
 CLINICAL MANIFESTATIONS :
 Common clinical features :
- Hematuria
- Generalized edema
- hypertension.
- oliguria.
 Patients are at risk for developing encephalopathy
and/or heart failure secondary to hypertension or
hypervolemia.

26. ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
 The acute phase generally resolves within 6-8 wk.
 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.
 Serum C3 levels returns to normal 6-8 wk after the
onset.

27. ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
DIAGNOSIS :
 Urinalysis : red blood cells, often associated with red
blood cell casts, proteinuria, and polymorphonuclear
leukocytes.
 A mild normochromic anemia due to hemodilution and
low-grade hemolysis.
 The serum C3 level is significantly reduced and returns
to normal 6-8 wk after the onset.

28. ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
DIAGNOSIS :
 Confirmation of the diagnosis requires clear evidence of
a prior streptococcal infection.
 A positive throat culture report might support the
diagnosis or might represent the carrier state.
 Serologic evidence for streptococcal infections :
- The antistreptolysin O titer(ASO) is commonly elevated
after a pharyngeal infection.
- the antideoxyribonuclease B level(AntiDNaseB)
elevated in skin infections.
- a positive streptozyme screen.

29. ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
DIAGNOSIS :
 MRI brain : posterior reversible encephalopathy syndrome.
 Chest x-ray is indicated in those with signs of heart failure.
 Renal biopsy : considered only
- in the presence of acute renal failure.
- nephrotic syndrome.
- absence of evidence of streptococcal infection.
-Normal complement levels.
-when hematuria and proteinuria, diminished renal
function, and/or a low C3 level persist more than 2 mo
after onset.

30. ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
DIFFERENTIAL DIAGNOSIS :
 IgA nephropathy
 Goodpasture syndrome
 Idiopathic rapidly progressive glomerulonephritis
 SLE nephritis.
 Endocarditis.
 Membranoproliferative GN.
 Acute exacerbation of chronic GN.

31. ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
COMPLICATIONS :
 Hypertension.
 Acute renal dysfunction.
 Heart failure.
 Hyperkalemia.
 Hyperphosphatemia.
 Hypocalcemia.
 Acidosis.
 Uremia.

32. ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
TREATMENT :
 Management is mainly symptomatic.
 Salt and fluid restriction.
 Diuretics.
 Hypertension treated with calcium channel antagonists,
ACE inhibitors
 10-day course of systemic antibiotic therapy with
penicillin to limit the spread of the nephritogenic
organisms.
 Acute renal failure may require treatment with dialysis.

33. ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
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.
 Chronic renal disease may be seen in < 2% of affected
children.

34. THANK YOU