approach to a child with hematuria
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TRANSCRIPT
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Approach to a child with Hematuria :
Sunil Agrawal
1st year
MD Pediatrics, IOM
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Contents:
• Introduction• Pathophysiology• Causes• History• Examination• Investigations• Management
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Introduction
Hematuria means blood in urine.It may be Gross or macroscopic and microscopic
hematuriaGross hematuria is seen by naked eyes while
microscopic hematuria needs microscope. Hematuria is defined as the presence of at least 5 red blood cells per HPF of centrifuged urine and/or 5 RBC per microliter in uncentrifuged specimen
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• Pathophysiology:
Structural disruption in the integrity of glomerular basement membrane caused by inflammatory or immunologic processes
Toxic disruptions of the renal tubules
Mechanical erosion of mucosal surfaces in the genitourinary tract
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Causes of Hematuria:
A) Glomerular hematuria
Isolated renal disease
-Postinfectious GN (Post streptococcal)- IgA nephropathy( Berger ds)- Alport syndrome( hereditary )- Thin Glomerular Basement membrane
disease- Membranoproliferative GN- Membranous nephropathy - Focal segmental glomerulosclerosis - Antiglomerular basement membrane
ds
Multisystem disease
-HSP nephritis -SLE nephritis-HUS-Wegener granulomatosis-Polyarteritis nodosa-Goodpasture syndrome-HIV nephropathy-Sickle cell glomerulopathy
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B) Extraglomerular hematuria
Upper Urinary tractTubulointerstitial
PyelonephritisInterstitial nephritisATNPapillary necrosisNephrocalcinosis
AnatomicHydronephrosisPolycystic kidney diseaseTumor (Wilms, Rhabdomyosarcoma, Angiomyolipoma)Trauma
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Vascular:• Arterial/venous thrombosis• Malformation (aneurysms, hemangioma)• Nutcracker syndrome• Hemoglobinopathy (Sickle cell trait/disease)Crystalluria: Calcium, Oxalate, Uric acidMedications: NSAIDs, anticoagulants
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Lower urinary tractInflammation- infectious and non infectious
CystitisUrethritis
UrolithiasisTraumaCoagulopathyHeavy exercise
Bladder tumorFactitious syndrome / by proxy
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Common causes of gross hematuria:
• Urinary tract infection• Meatal stenosis• Perineal irritation• Trauma• Urolithiasis/hypercalciuria• Coagulopathy• Tumor
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Glomerular cause of gross hematuriaIgA nephropathyAlport syndromeThin glomerular basement membrane diseasePost infectious glomerulonephritisHSP nephritisSLE nephritis
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Causes of Hematuria in the Newborn:
• Renal vein thrombosis (Asphyxia, dehydration, shock)
• Renal artery thrombosis • Autosomal recessive polycystic kidney disease • Obstructive uropathy• Urinary tract infection• Bleeding and clotting disorders• Trauma, bladder catheterization• Cortical necrosis (Hypoxic/ischemic perinatal
insult)• Nephrocalcinosis (Frusemide in premature)
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History:
• Age: 2-5yrs: Wilms tumor
5-12yrs: PSGN
• Sex: F>>M in >1-2yrs: UTI
F>>M: SLE nephritis
M>F : X-linked form of Alport syndrome
• Race: whites: Idiopathic hypercalciuria
blacks: Sickle cell disease
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Colour of urine:
Colour Causes
Dark yellow Normal concentrated urine
Dark brown or black
Bile pigmentsHomogentisic acid, melanin, tyrosinosis, methemoglobinuria
Cola coloured Glomerular hematuria
Red or pink urine
Extraglomerular hematuria, Hemoglobin, Myoglobin, Porphyrins, Chloroquine, Deferoxamine, Beets, blackberries, Rifampin, Red dyes in food, Urates
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Characteristics of urine:• Amount of urine: Reduced in AGN, ARF• Clots in urine: Extraglomerular• Frequency, Dysuria, recent enuresis : UTI• Frothy urine: Suggests Proteinuria seen in
Glomerular diseases• Timing: Initial stream – from urethra (Urethrorrhagia
– spotting in underwear); Terminal (with suprapubic pain, disturbance of micturition) – from bladder
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Associated Symptoms:• Fever: Infections, SLE, AGN• Facial puffiness, Oedema of legs, weight gain,
Shortness of breath: Acute Glomerulonephritis • Hypertension (Headache, visual changes, epistaxis,
seizures): AGN, ARF• Abdominal pain: Urolithiasis (Loin to groin), UTI,
clots, Nutcracker syndrome• Painless: Glomerular• Abdominal mass: Hydronephrosis, PKD, Wilm’s
tumour• Joint pain (HSP, SLE)• Rashes (HSP, SLE, PAN)• Neurologic – SLE, HUS (seizures, irritability)• Jaundice: Hemolysis, Obstructive jaundice
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• H/o exercise, menstruation, recent bladder catheterization or passage of a calculus
• Recent upper respiratory (1-2wks back), skin infection (3-6 wks): PSGN
• GI infection: HUS, HSP nephritis • Gross hematuria precipitated by URI: Alport
syndrome, IgA Nephropathy • H/o bleeding from other sites: Bleeding disorders,
Hemoptysis in Good Pasture syndrome• H/o Trauma, abdominal surgery, Child abuse (Social
factors - Munchausen), crush injury• H/o ingestion of drugs (ATT – Rifampicin, Ibuprofen,
Chloroquine, Metronidazole, Iron), i.v. contrast agents (Toxic nephropathy, RVT)
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• H/o Vision or hearing defects: Alport syndrome
• Family h/o: Hereditary glomerular diseases (Alport syndrome, Thin glomerular Basement Membrane Disease, IgA Nephropathy), Urolithiasis, Hypercalciuria, Sickle cell disease/trait
• H/o consanguinity or affected siblings in ARPKD, Metabolic disorders
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Examination:
• Vitals:– BP: in AGN, PKD– Temperature
• Oedema: in AGN• Pallor: Bleeding disorders, HUS, SLE, CRF• JVP: Raised in CHF• Per abdomen: Mass
– Kidney: Hydronephrosis (Urinary tract obstruction), Wilms tumour; B/L in ARPKD, hydronephrosis
– Bladder palpable: Distal obstruction – Tenderness: HSP
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• Skin lesions Purpura(HSP) Butterfly rash (SLE) Bruises (Trauma, Child abuse)• Abnormal external genitalia e.g. ambiguous genitalia
in WAGR syndrome (Wilms, aniridia, genital anomalies, mental retardation), Wilms tumour – hypospadias, cryptorchidism, Genital trauma
• Signs of Congestive cardiac failure, HTNsive encephalopathy: AGN
• Joint swelling, tenderness: HSP, SLE• Ophthalmologic: Alport syndrome (Anterior
lenticonus, macular flecks, recurrent corneal erosions), Aniridia (Wilms)
• Hearing assessment: Alport (B/L SNHL)
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General Approach to Investigate the child with
Hematuria
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Investigations:• Urine dipstick test: Based on the
peroxidase-like activity of hemoglobin
• It can detect trace amounts of hemoglobin and myoglobin.
• Can detect 5-10 intact RBC per mm3 of unspun urine
• False +ve: Urine pH >9, H2O2
• False –ve: High ascorbic acid, formalin
• Also for urine albumin
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Investigations:
Glomerular1. Brown, cola coloured or smoky2. RBC casts
3. Proteinuria 2+ or more 4. Deformed urinary RBCs
Non - glomerular1. Bright red, pink2.Terminal hematuria/ Passage of clots3. Proteinuria of < 2+4. Normal morphology of RBCs
Urine microscopy: Presence of RBCs and casts (> 5 RBCs per HPF) in centrifuged urine
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Study on Evaluation of hematuria using the urinary albumin-to-total-protein ratio to differentiate glomerular and nonglomerular bleeding
•N. Ohisa · R. Matsuki · H. Suzuki · H. Miura · Y. Ohisa · K. YoshidaDepartment of Clinical Laboratory, Tohoku University Hospital,Sendai, Japan•microscopy-based differentiation is not only tedious but the sensitivity and specificity may vary from one examiner to another. Furthermore, once
the specimen has been frozen, differentiation becomes difficult.•A total of 143 random urine specimens from patients seen at the Division of Nephrology, Endocrinology and Vascular Disease and the Urology Department at Tohoku University Hospital were included in the study. The inclusion criterion
for the study was a diagnosis of glomerular disease based on clinical features or histopathology with hematuria (5 or more RBCs per high-power fi eld). Of the 104 patients diagnosed with glomerular disease and 39 specimens from patients with nonglomerular disease, used as controls in the study.
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• With respect to the albumin-to-total-protein ratio, the mean value in the glomerular disease group was 0.72 } 0.10, whereas the mean in the nonglomerular �disease group was 0.35 } 0.17 (� P < 0.001). The distribution of the albumin-to-total-protein ratio in the glomerular and nonglomerular disease groups was clearly differentiated. Sensitivity and specificity as a function of the albumin-to-total-protein ratio. At a ratio cutoff of 0.59, sensitivity and specificity was maximized at 96.2% and 100%, respectively.
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Distribution of urinary albumin-to-total-protein ratio in glomerular and nonglomerular hematuria. The mean albumin-to-totalprotein ratio in the glomerular disease group was signifi cantly higher than that in the nonglomerular disease group. A cutoff of 0.59 excluded all nonglomerular disease cases, while detecting all but three glomerular disease cases. Gl, glomerular disease; non-Gl, nonglomerular disease; vertical axis, albumin-to-total-protein ratio; horizontal axis, glomerular disease, nonglomerular disease
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Urine albumin-to-total-protein ratio sensitivities and specifi itiesin differentiating glomerular and nonglomerular hematuria. At aratio of 0.59, sensitivity and specificity were 96.2% and 100%, respectively.
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Cola/ brown urine?Proteinuria(>30mg/dl)?
RBC cast?Acute nephritic syndrome?
Yes
Glomerular hematuria• CBC• Electrolytes,Ca• BUN/Cr• Serum protein/albumin• Cholesterol• C3/C4• ASO/Anti-DNase B• ANA• Antineutrophil antibody• Throat/ skin culture• 24-hour urine total protein
creatinine clearance
NO
Extraglomerular hematuriaStep 1• Urine cultureStep 2• Urine Ca/Cr• Renal/ bladder USGStep 3• Urinalysis: siblings, parents• Serum electrolytes, Cr, Ca• If crystalluria, urolitiasis or nephrocalcinosis: 24-hr urine for Ca, Cr, Uric acid, oxalate• If hydronephrosis/pyelocaliectasis: cystogram, renal scan
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Investigations:• Urine C/S • RFT: Blood urea nitrogen/serum creatinine, Na/K (↓Na in
AGN, ↑K in ARF)• Complete blood counts (CBC): Hb - ↓ in bleeding, HUS, SLE,
CRF; Abnormal TC, DC in infections, HUS, ↓ in SLE;• Platelet counts and Coagulation studies: (history suggestive
of bleeding disorder, HUS), Sickle cell (Hemoglobin electrophoresis)
• PBS: Microangiopathic hemolytic anemia• ESR, CRP - Infections• 24 hr urinary protein, Spot urinary protein: Creatinine ratio,
Serum albumin and cholesterol if associated proteinuria (Nephrotic syndrome)
• Urine calcium: Hypercalciuria is a relatively common finding in children. – 24-hour urinary calcium (>4 mg/kg/d), or– Spot urine calcium-creatinine ratio >0.21
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Investigations:• Imaging Studies
– Renal and bladder sonography: Urinary tract anomalies, such as hydronephrosis, hydroureter, nephrocalcinosis, tumor, and urolithiasis, Renal parenchymal disease
– X-Ray KUB: calculi– Doppler study of renal vessels and IVC: Renal vein
thrombosis– Intravenous urography– Spiral CT scan - Urolithiasis, Wilms tumor and polycystic
kidney disease, Renal trauma– Micturating cystourethrograms - Urethral and bladder
abnormalities (eg, cystitis), in recurrent UTI to r/o VUR, anomalies
– Radionuclide studies – Renal function and perfusion– Angiogram– Chest X-Ray (Pulmonary oedema, CHF)
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Investigations:• Renal biopsy:
Relative indications -• Significant proteinuria (3+ or more) or nephrotic
syndrome +• Recurrent persistent hematuria (Microscopic
>2yrs)• Abnormal renal function, Persistent HTN • Hematuria, Proteinuria, diminished renal function,
low C3 level persist beyond 2 mo of onset of AGN• Absence of evidence of streptococcal infection• Serologic abnormalities (abnormal ANA or dsDNA
levels) • A family history of end stage renal disease or
evidence of Chronic renal disease in patient
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Dx Histology Clinical LabIgA Nephro-pathy
IgA deposition in the mesangium, glomerular sclerosis, proliferative changes, crescents in severe cases
Gross, intermittent, painless hematuria
No specific changes, although increased serumIgA levels observed in some patients
HSP Same as IgA nephropathy Purpura, joint pains, abdominalpain, hematuria, etc
No specific laboratory data
SLE Mild glomerulitis, proliferative changes, immune complex deposition, crescents, immunoglobulin deposition
Hematuria, proteinuria, hypertension, joint pains, rashes, etc
Abnormal C3, C4, ANA, dsDNA, anemia, thrombocytopenia, etc
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Dx Histology Clinical LabAlport Syndrome
Some thinning of basement membranes, "basket weave" changes in the glomerular basementmembrane on electron microscopy
Sensorineural hearing loss, corneal abnormalities, hematuria, renal failure
No specific changes
Thin Basement Membrane disease
Average glomerular basement membranes thin (reported to be 100-200 nm)
Persistent microscopic or gross hematuria, significant family history
No specific changes
Mesangio-proliferative GN
Glomerular lobulations, thickening of the mesangial matrix and glomerular basement membranes, crescents, etc
Hematuria, proteinuria, hypertension
C3 levels may be low
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Investigations:
• Cystourethroscopy: Terminal hematuria, disturbances of micturition, suprapubic pain (Only if strong suspicion of bladder ulceration, tumours)
• Screening of first degree relatives in persistent hematuria
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Summary
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For Asymptomatic, isolated microscopic hematuria:
Isolated microscopic hematuria
Repeat urinalysis weekly x 2 (No exercise x 48hrs)
F/U Urine R/M with examination
Test parents for hematuria
Benign Familial Hematuria
Family h/o calculi
+Hearing test, +USG, +X-Ray KUB
Urine Ca/Cr ratio
Yearly Urine R/M, examination, BP
Negative
Positive
Yes
Normal
Persistent hematuria
No
No
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Management:
• According to cause:– Reassurance and F/U– Treat cystitis, pyelonephritis, AGN: Antibiotics– Supportive treatment: Diuretics, Fluid and salt
restriction, Antihypertensives– Monitoring – BP, I/O, weight, Urine R/M– Treat Hyperkalemia, ARF, CHF, acidosis, fluid
overload, HTN and its complications– ACE inhibitors useful in proteinuria– Immunosuppressive therapy: Depending on cause
(Steroids, cyclophosphamide)
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Management:
– Idiopathic Hypercalciuria: Hydrochlorothiazide, Potassium citrate, Sodium restriction
– Calculi: Plenty of water– ESRD: Dialysis, Renal transplantation– Correct thrombocytopenia, anemia, coagulation factor
deficiency– Renal vein thrombosis: Anticoagulant therapy or
thrombectomy may be needed– Surgical correction: Calculi, PUJ obstruction, Posterior
urethral valves, Wilms tumour
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References:
• Nelson Textbook of Pediatrics, 19th Ed• Nelson Essentials of Pediatrics, 6th Ed• O.P. Ghai Essential pediatrics, 7th Ed• Pediatric Nephrology, Shrivastava, Bagga,
4th Ed• Japanese Society of Nephrology 2007• Indian J Pediatrics 1999; 66 : 207-214• Various Websites
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