APPROACH TO

HEMATURIA

UNDER THE SUPERVISION AND Presented by : Alka rani (15)

GUIDANCE OF : Anindya bisht (18)
Anisha malik (19)
PEDIATRICS DEPARTMENT Ankit kumar (20)
CASE

• A previously healthy 10-year-old girl is seen in paediatric department complaining of a 3-

day episode of "red urine," which has now resolved. His parents are scared because this
has never happened to her before.
• What are the common causes of “Red Urine” ?

• How to make a diagnosis based on History Examination & Laboratory investigations?

• How to approach a case of hematuria?

• How to manage?
HEMATURIA

• Definition: presence of blood in the urine

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.
• The passage of blood in the urine is always alarming and investigation is warranted.
COMMEN CAUSE OF RED URINE
[MIMICS]
• Hematuria
• Hemoglobinuria, myoglobinuia
• Anthrocyanin in beets and blackberries.
• Chronic lead and mercury poisoning
• Phenolphthalein (in bowel evacuants)
• Phenothiazines (compazine).
• Rifampicin.
 TYPES OF HEMATURIA
• According to the amount of the RBCs in the urine

1. Gross(Macroscopic):The presence of blood in the urine in sufficient quantity to be visible to the naked eye

2. Microhematuria:3 red blood cells per high-power field on urine microscopy

• According to timing:

1. EARLY(Initial): Urethral origin, distal to external sphincter.

2. TERMINAL : Bladder neck or prostate origin.

3. DIFFUSE(total): Bladder or upper urinary tract.

 CAUSES OF HEMATURIA
• Urological causes(90% cases)

• Renal causes (9% cases)

• Hematological causes(1% cases)

DIAGNOSIS OF HEMATURIA
HISTORY[CLUE]

1. Age & Sex: commen causes of hematuria by age & sex-

• 0-20 yr
Acute glomerulonephritis
• Acute UTI
• Congenital UT anomalies with obstruction

• 20-40 yr
• Acute UTI
• Stones
• Bladder cancer
• 40-60 yr (men)
bladder tumor
• Stones
• Acute UTI

• 40-60 yr (women)
• Acute UTI
• Stones
• Bladder tumor
Characteristics of urine:

•Amount of urine: Reduced in AGN, ARF

•Clots in urine: Extraglomerular causes.
• Increased 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
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
•H/o exercise, menstruation, recent bladder catheterization or
passage of a calculus
•Recent upper respiratory (1-2wks back)
skin infection (3-6 wks): PSGN
•Gl 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, crush injury
•H/o ingestion of drugs (ATT - Rifampicin, Ibuprofen,
Chloroquine, Metronidazole, Iron), i.v. contrast agents (Toxic
nephropathy, RVT)
•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

ARKD, Metabolic disorders
EXAMINATION

Vitals
•BP: increased in AGN, PKD
•Temperature
General examinations
•Oedema: in AGN
•Pallor: Bleeding disorders, HUS, SLE, CRF
•Skin rashes and arthritis: HSP, SLE

CVS
•irregular cardiac rhythm, murmur or hypertension
•JVP: Raised in CHF
Per abdomen: Mass
•kidney: hydronephrosis (urinary tract obstruction), wilms tumor,
B/L ARPKD, hydronephrosis
•bladder palpable: distal obstruction

•Tenderness: HSP
External genitalia: meatal stenosis, phimosis, urethral discharge
General Approach to Investigate the child with
Hematuria
•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 mm'
of uncentrifuged urine
•False +ve: Urine pH >9, H202
•False -ve: High ascorbic acid,
formalin
•Also for urine albumin
Investigations:

•Urine C/S
•RFT: Blood urea nitrogen/serum creatinine, Na/K (decrease Na in
AGN, increased K in ARF)
•Complete blood counts (CBC): Hb decreases in bleeding, HUS, SLE,
CRF; Abnormal TC, DC in infections, HUS, decreases 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
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 cysto-urethrograms - 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)
RENAL BIOPSY:
INDICATIONS

1. Age below 12 months (genetic/congenital causes)& >16 yrs >12 years with persistent microscopic
hematuria, low C3 & steroid resistant.
2. Gross or persistent microscopic hematuria
3. Low blood C3
4. Persistent Hypertension
5. Impaired renal Function
6. Failure of steroid therapy (Steroid Resistance)
7. Before starting Calcineurin Inhibitors (Cyclosporine A & Tacrolimus) ,also after prolonged therapy(>30-
36 months) & Reduced Kidney function with decline in Estimated GFR that persists after reduction in CNI
doses.
8. Fever, Rash & Arthralgia(Systemic symptoms)
9. Acute Kidney injury not related to Hypovolemia
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.
MANAGEMENT
Hematuria is a sign and not itself a disease, thus, therapy should be directed at the process causing
it.

IMMUNOGLOBULIN A NEPHROPATHY
• It is characterized by a predominance of IgA within mesangial glomerular deposits in the
absence of systemic disease.
• Focal and segmental mesangial proliferation and an increased mesangial matrix are seen in
the glomerulus. Renal histology demonstrates mesangial proliferation that may be associated
with epithelial cell crescent formation and sclerosis. IgA deposits in the mesangium are often
accompanied by C3 complement.
• IgA nephropathy is an immune complex disease initiated by excessive amounts of poorly
galactosylated IgA1 in the serum, causing the production of IgG and IgA autoantibodies.
Management
• The primary treatment of IgA nephropathy is appropriate blood pressure control and
management of significant proteinuria.
• Angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists are
effective in reducing proteinuria and retarding the rate of disease progression when used
individually or in combination.
• Fish oil, which contains antiinflammatory omega-3 polyunsaturated fatty acids, may
decrease the rate of disease progression in adults.
• If a renin-angiotensin system (RAS) blockade proves ineffective and significant proteinuria persists, then
addition of immunosuppressive therapy with corticosteroids is recommended. Corticosteroids reduce
proteinuria and improve renal function in those patients with a glomerular filtration rate > 60 mL/min/m2.
• Patients with IgA nephropathy may undergo successful kidney transplantation. Although recurrent disease
is frequent, allograft loss caused by IgA nephropathy occurs in only 15–30% of patients.
POST-STREPTOCOCCAL GLOMERULONEPHRITIS

• Group A β-hemolytic streptococcal infections are common in children and can lead to the
postinfectious complication of acute glomerulonephritis (GN).
• The severity of kidney involvement varies from asymptomatic microscopic hematuria with
normal renal function to gross hematuria with acute renal failure. Depending on the severity of
renal involvement, patients can develop various degrees of edema, hypertension, and oliguria.
• Patients are at risk for developing encephalopathy and/or heart failure secondary to
hypertension or hypervolemia. Hypertensive encephalopathy must be considered in patients
with blurred vision, severe headaches, altered mental status, or new seizures.
Treatment
• Management is directed at treating the acute effects of renal dysfunction and hypertension.
• Although a 10-day course of systemic antibiotic therapy with penicillin is recommended to limit the
spread of the nephritogenic organisms, antibiotic therapy does not affect the natural history of
APSGN.
• Sodium and fluid restriction, diuretics, and pharmacotherapy with calcium channel antagonists,
vasodilators, or angiotensin-converting enzyme inhibitors are standard therapies used to treat
hypertension.
HENOCH-SCHÖNLEIN PURPURA NEPHRITIS

• Henoch-Schönlein purpura (HSP) is an idiopathic systemic immune complex–mediated

vasculitis associated with IgA deposition within small-vessel walls.
• The classic tetrad of HSP nephritis includes a palpable purpura, arthritis or arthralgia,
abdominal pain, and evidence for renal disease. These may develop over a period of days to
weeks and may vary in their order of presentation. Notably, not all of the tetrad are present in
all patients.
• The nephritis associated with HSP usually follows the onset of the rash, often presenting
weeks or even months after the initial nonrenal manifestations' have resolved
Treatment
• No convincing randomized clinical studies or evidence-based guidelines exist for treatment
of HSP nephritis.
• Mild HSP nephritis does not require treatment, because it usually resolves spontaneously.
• Aggressive therapy which includes high-dose and extended courses of corticosteroids with
azathioprine, mycophenolate mofetil, or cyclophosphamide with careful monitoring may be
reasonable in those with the most severe HSP nephritis
• One common approach in children with severe clinical renal involvement is the use of oral prednisone (1
mg/kg per day for 3 months), along with angiotensin-converting enzyme inhibitors, followed by
azathioprine or mycophenolate mofetil if severe clinical involvement persists.
• For children with severe histologic manifestations, treatment with intravenous methylprednisolone pulses
for 3 days, followed by a combination of oral prednisone (for 3 months) and azathioprine or
mycophenolate mofetil may be considered.
• For children with the most severe histology and progressive renal failure, intravenous steroids plus
plasmapheresis may be considered.
• If progression to end-stage renal disease occurs, renal transplantation is the treatment of choice.
MEMBRANOPROLIFERATIVE
GLOMERULONEPHRITIS
• Also known as mesangiocapillary glomerulonephritis, most commonly occurs in older children or
young adults. MPGN can be classified into primary (idiopathic) and secondary forms of glomerular
disease. Secondary forms of MPGN are most commonly associated with subacute and chronic
infection, including hepatitis B and C, syphilis, subacute bacterial endocarditis, and infected shunts,
especially ventriculoatrial shunts (shunt nephritis).
• Patients present in equal proportions with nephrotic syndrome, acute nephritic syndrome (hematuria,
hypertension, and some level of renal dysfunction), or persistent asymptomatic microscopic
hematuria and proteinuria. Serum C3 complement levels are low in the majority of cases
Treatment
• No definitive therapy exists, but several reports, including a randomized controlled trial,
indicate that extended courses of alternate-day prednisone (for years) provide benefit.
• The apparent pathophysiology of C3GN promises that treatments targeting the interruption of
complement activation pathways, such as complement factor H replacement or shutting down
the terminal complement cascade by blocking C5 activation with eculizumab (anti–C5
antibody), could be beneficial in preventing the progression of renal disease.
IDIOPATHIC HYPERCALCIURIA

• Idiopathic hypercalciuria, which may be inherited as an autosomal dominant disorder, can

clinically present as recurrent gross hematuria, persistent microscopic hematuria, dysuria,
crystalluria, or abdominal pain with or without kidney stone formation.
• Hypercalciuria is diagnosed by a 24-hr urinary calcium excretion >4 mg/kg.
• A spot urine calcium:creatinine ratio (mg/dL:mg/dL) > 0.2 suggests hypercalciuria in an
older child. Normal ratios may be as high as 0.8 in infants < 7 months of age.
Treatment
• Oral thiazide diuretics can normalize urinary calcium excretion by stimulating calcium reabsorption
in the proximal and distal tubules. Such therapy can lead to the resolution of gross hematuria or
dysuria and can prevent nephrolithiasis.
• In patients with persistent gross hematuria or dysuria, therapy is initiated with hydrochlorothiazide at
a dose of 1-2 mg/kg/24 hr as a single morning dose. The dose is titrated upward until the 24-hr
urinary calcium excretion is < 4 mg/kg and clinical manifestations resolve.
• After 1 year of treatment, hydrochlorothiazide is usually discontinued, but it may be resumed if
gross hematuria, nephrolithiasis, or dysuria recurs.
• During hydrochlorothiazide therapy, the serum potassium level should be monitored
periodically to avoid hypokalemia.
• Potassium citrate at a dose of 1 mEq/kg/24 hr may also be beneficial, particularly in
patients with low urinary citrate excretion, a low urine pH, and symptomatic dysuria or
crystalluria.
• Sodium restriction is important because urinary calcium excretion parallels sodium
excretion. Importantly, dietary calcium restriction is not recommended because calcium is a
critical requirement for growth, and no evidence supports a relationship between decreased
calcium intake and decreased urinary calcium levels
RENAL CALCULI

• Most spontaneous stones are composed of calcium, oxalate, or phosphate crystals; others
are caused by uric acid, cystine, ammonium crystals, or phosphate crystals, or a
combination of these substances.
• Children with urolithiasis usually have gross or microscopic hematuria. If the calculus
causes ureteral or renal pelvic obstruction, then severe flank pain or abdominal pain
occurs.
• The pain typically radiates anteriorly to the scrotum or labia. Often the pain is intermittent,
corresponding to periods of obstruction of urine flow, which increases the pressure in the
collecting system
Treatment
• In a child with a renal or ureteral calculus, the decision whether to remove the stone
depends on its location, size, and composition (if known) and whether obstruction and/or
infection is present.