Hematuria

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Hematuria

Definition

Hematuria is the presence of blood (red blood cells) in the urine. It is classified as:

Gross (macroscopic) hematuria - visible to the naked eye; urine appears red or brown
Microscopic hematuria - detected only on urinalysis; defined as ≥3 RBCs per high-power field (HPF) on properly collected midstream urine microscopy

Asymptomatic microscopic hematuria (AMH) may be detected by dipstick in up to 16% of screening populations, but dipstick alone is insufficient - urine microscopy must confirm true RBCs. - Henry's Clinical Diagnosis and Management by Laboratory Methods, p.551

Pseudohematuria

Before workup, exclude pseudohematuria - red/brown urine without RBCs on microscopy. Causes include:

Foods: beets, rhubarb, blackberries
Drugs: rifampicin, phenazopyridine, nitrofurantoin, chloroquine
Metabolites: myoglobinuria (rhabdomyolysis), hemoglobinuria (hemolysis)
Porphyria

The absence of RBCs on microscopy with a positive dipstick heme strongly suggests hemoglobinuria or myoglobinuria. - Campbell-Walsh-Wein Urology

Classification by Origin

1. Glomerular Hematuria

Feature	Finding
Urine color	Brown / "tea-colored" / "cola-colored"
RBC morphology	Dysmorphic / acanthocytes ("crenated" / Mickey Mouse cells)
RBC casts	Present - pathognomonic of glomerulonephritis
Proteinuria	Significant - often >500 mg/day
Clots	Absent

Causes:

IgA nephropathy (Berger disease) - most common; hematuria follows URTI by 24-48 hrs
Post-streptococcal glomerulonephritis (↑ ASO, ↓ C3)
Lupus nephritis (↑ ANA, ↓ C3/C4)
Goodpasture syndrome (hemoptysis + microcytic anemia)
Alport syndrome / familial nephritis (family history + sensorineural deafness)
Thin basement membrane disease
Membranoproliferative GN, membranous nephropathy

2. Nonglomerular Hematuria

Feature	Finding
Urine color	Bright red / pink
RBC morphology	Normal (circular, isomorphic)
RBC casts	Absent
Proteinuria	Minimal (if heavy, suggests parenchymal, not urologic)
Clots	May be present

a) Medical/Nonsurgical causes (renal parenchymal):

Tubulointerstitial disease (interstitial nephritis, analgesic nephropathy)
Papillary necrosis (diabetes, sickle cell disease/trait, analgesic abuse)
Polycystic kidney disease
Renal vascular disease: renal artery embolism/thrombosis, AV fistula, renal vein thrombosis, Nutcracker syndrome
Medullary sponge kidney
Sickle cell disease - typically unilateral, left-sided (4x more common left)

b) Surgical/Urologic causes:

Bladder cancer - most common cause of gross hematuria in patients >50 years
Renal cell carcinoma
Urothelial carcinoma (ureter, renal pelvis)
Urolithiasis (nephrolithiasis, ureteral calculi)
Benign prostatic hyperplasia (BPH)
Urinary tract infection (most common cause of gross hematuria in children)
Bladder/urethral trauma
Urethral stricture

Localization by Stream Pattern

Pattern	Location
Initial stream hematuria	Prostatic urethra or anterior urethra
Total (throughout stream)	Bladder, upper tract (kidney, ureter)
Terminal hematuria	Bladder neck, trigone, posterior urethra

Clot shape also helps: vermiform (worm-shaped) clots = upper tract (ureter molds the clot); cuboid clots = bladder origin.

Evaluation Flowchart (Glomerular)

Evaluation of glomerular hematuria - diagnostic pathway from history to diagnosis

Fig. 2.1 - Evaluation of glomerular hematuria (dysmorphic erythrocytes, RBC casts, proteinuria). - Campbell-Walsh-Wein Urology

Evaluation Approach

Step 1 - Urinalysis and Microscopy

Confirm RBCs (not pseudohematuria)
Check RBC morphology: dysmorphic = glomerular; isomorphic = non-glomerular
Look for RBC casts (= GN), WBCs/bacteria (= UTI), crystals (= stones)
Quantify proteinuria

Step 2 - History and Risk Stratification

High-risk features for malignancy:

Age >35 (especially >50)
Smoking history
Occupational exposure to industrial chemicals/dyes (benzidine, aniline)
Pelvic irradiation
Chronic cyclophosphamide exposure
Analgesic abuse
Chronic indwelling foreign bodies

Benign/low-risk features:

Young woman with dysuria, frequency → UTI
Recent vigorous exercise → exercise-induced hematuria (rule out IgA nephropathy)
Recent URTI + hematuria → IgA nephropathy vs. post-streptococcal GN
Family history of renal disease, deafness → Alport syndrome
Sickle cell trait/disease + left-sided flank pain

Step 3 - Laboratory Workup

For suspected glomerular disease:

Serum creatinine, BUN, electrolytes
CBC, serum albumin
C3, C4 (low in SLE, MPGN, post-strep GN)
ANA (SLE)
ASO / anti-DNase B titer (post-streptococcal)
ANCA (vasculitis)
Anti-GBM antibody (Goodpasture)
24-hour urine protein or urine protein:creatinine ratio

For suspected urologic/malignant cause:

Urine cytology
CT urogram (gold standard for upper tract evaluation)
Cystoscopy (mandatory to exclude bladder cancer - especially in adults >35 with gross hematuria)

Step 4 - Imaging

CT urogram (CTU): first-line for evaluating the upper urinary tract
Renal ultrasound: useful in children, pregnant women, renal failure
MR urography: contrast allergy, CKD, avoiding radiation
Retrograde pyelogram: for upper tract urothelial lesions

Step 5 - Cystoscopy

Indicated in all adults with gross hematuria and adults ≥35 with asymptomatic microscopic hematuria (per AUA guidelines). Bladder cancer is the most common cause of gross hematuria in adults >50. - Campbell-Walsh-Wein Urology, p.40

Special Situations

Anticoagulation

Anticoagulation at therapeutic levels does NOT independently cause hematuria (prevalence 3.2% vs. 4.8% in controls). Urologic disease was found in 81% of anticoagulated patients with >1 episode of microscopic hematuria. Do not attribute hematuria to anticoagulant therapy - full workup is required. - Campbell-Walsh-Wein Urology

Children

Causes include UTI (most common for gross), hypercalciuria, glomerulonephritis, IgA nephropathy, urolithiasis, Wilms tumor (rare). In isolated microscopic hematuria without proteinuria, test parents for hematuria and check urinary calcium:creatinine ratio. Cystoscopy is rarely indicated in children. - Campbell-Walsh-Wein Urology, p.3003

Sickle Cell Disease

Typically unilateral, left-sided (4x more common left due to longer left renal vein course and higher venous pressure). Treatment: bed rest, high urine output, urine alkalinization. For massive/persistent bleeding: epsilon-aminocaproic acid (EACA) or tranexamic acid (use with caution given thrombotic risk). Rarely, nephrectomy. - NKF Primer on Kidney Diseases, p.412

Renal Transplant Recipients

Add BK virus to the differential. Confirm by urine cytology (viral cytopathic changes) and urine BK virus PCR titers. - Campbell-Walsh-Wein Urology

AUA Asymptomatic Microhematuria (AMH) Guidelines

AMH = ≥3 RBC/HPF on properly collected urine in the absence of an obvious benign cause (after excluding UTI, menstruation, vigorous exercise, recent urologic procedure, trauma).

After confirming true AMH:

Renal function tests + urine protein
Upper tract imaging (CT urogram preferred)
Cystoscopy (in adults ≥35, or any risk factors)
Urology/nephrology referral as appropriate
Follow-up urinalysis if no cause found

Key Differentiating Points

Feature	Glomerular	Non-Glomerular
Color	Brown/cola	Bright red
RBC morphology	Dysmorphic	Isomorphic
RBC casts	Present	Absent
Proteinuria	Marked	Minimal
Clots	Absent	May be present
Pain	Usually absent	Colicky (stones), suprapubic

Sources: Campbell-Walsh-Wein Urology (3-Vol Set); Henry's Clinical Diagnosis and Management by Laboratory Methods; NKF Primer on Kidney Diseases, 8e; Brenner & Rector's The Kidney

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