ANATOMY OF URINARY TRACT HEMATURIA - Presence of blood in urine

2 TYPES:

- Gross: saat blood yang ada di urine dapat

dilihat langsung
o Urine: pink/red/brown
o Biasanya do not have other sign and
symptoms
o If + blood clots: may have bladder
pain/pain in the back
- Microscopic: saat blood yang ada di urine tidak
dapat dilihat secara langsung, tapi dapat
dilihat di mikroskop

ETIOLOGY (BASED ON LOCATION)

KIDNEY
Glomerular Extraglomerular
- Glomerulonephritis - Benign/malignant
- IgA nephropathy renal tumor
- Thin basement - Polycystic kidney
membrane dz dz
- Alport’s syndrome - Sickle cell dz
- Pyelonephritis
- Stones/Renal cyst
- Renal Ca
- Renal papillary
necrosis
- Trauma
URETER
- Tumor/Carcinoma
- Stones
- Urethral stricture
- Infection
- Trauma
BLADDER
- Benign/malignant tumor
- Carcinoma
- Stone
- Infection: Cystitis
- Chronic irritation
- Trauma
URETHRA
- Infection: urethritis
- Traumatic catheterization
- Stone
- Stricture
URINARY TRACT PROSTATE
- Benign prostatic hyperplasia (BPH)
- Body’s drainage system for removing wastes - Prostatitis
and extra fluid - Prostate Ca
- Urinary tract includes: 2 kidneys, 2 urethers, - Trauma
bladder, urethra NON-URINARY TRACT HEMATURIA
- Hepatitis
KIDNEYS - Sexual activity
- Menstruation
- Setiap hari nya kidney filter 120-150 quarts (1
- Endometriosis
quarts = 0.94 liter)  produce 1-2 quarts of - Vigorous exercise
urine DRUGS CAUSE RED URINE
- Rifampicin
- Chloroquin
 - Ibuprofen DIAGNOSTIC APPROACH TO MACROSCOPIC HEMATURIA
- Nitrofurantoin
- Phenytoin

CAST IN URINE SEDIMENT

DIAGNOSTIC APPROACH TO MICROSCOPIC HEMATURIA
CAST

- solidification of material (protein) in the lumen

of kidney tubule (nephron)
- if present = indicate renal dz (rather than
lower urinary tract dz)

HYALINE CAST

- most difficult to visualise, least important

- result of solidification of Tamm-Horsfall
mucoprotein (secreted by renal tubular cell),
may be present w/o sig. Proteinuria
- a few may be seen in healthy person
- may be seen in: kegiatan/exercise berat; renal
dz

CELLULAR CAST

- composed of: RBCs/WBCs/renal tubular

epithelial cell
- result from: clumping/conglutination of cells
yg tergabung dgn protein matrix

RBC CAST

- may be a result of: leakage of RBCs through

glomerular membrane/bleeding to tubules
- indicate: dz affect glomerulus
(glomerulonephritis, IgA nephropathy, Lupus
nephritis), subacute bacterial endocarditis,
renal infarction, rarely in severe pyelonephritis
- Blood cast, Haemoglobin cast: orange-
yellow/red-brown color – indicate: urinary
statis, chronic condition
WBC CAST

- Composed of: neutrophils LUTS (Lower Urinary Tract Symptoms)

- Indicate: tubulointerstitial dz (acute
pyelonephritis: WBC + bacteria in urine)
- May also seen in: acute interstitial nephritis,
lupus nephritis, acute papillary necrosis
- WBC cast indicate kidney dz rather than lower
urinary tract dz

BACTERIAL CAST

- Composed of: bacteria in a protein (hyaline)

matrix
- May be misinterpreted as granular/cellular
cast
- Identified by: gram-staining dried
(cytocentrifuged) sediment
- Indicate: acute pyelonephritis/intrinsic renal
infection

EPITHELIAL CAST

- Composed: renal epithelial cells

- Indicate: acute tubular necrosis, viral infection:
cytomegalovirus, exposure to nephrotoxic
(mercury or drugs)

GRANULAR CAST

- Degeneration of cells in cellular cast

- Indicate: stasis in nephron, tubulointerstitial
dz

WAXY CAST

- Final stage of degeneration of cell (cellular 

granular  waxy) History Taking
- Indicate: stasis renal, nephron obstruction
(ass. with chronic renal dz) Pain associated with infection/ inflammation

FATTY CAST Painless associated with tumor or TB

- Contain globules of fat (triglyceride/natural Loin pain  Kidney disease

fat) Colic pain  stone
- Ass. with: massive proteinuria (300 mg/dL) –
nephrotic syndrome Suprapubic pain + dysuria + frequency  cystitis
- May be found in: diabetic nephropathy, toxic
Initial hematuria  suggest bleeding from urethra and
renal poisoning prostate

Terminal hematuria  prostate and bladder

Total hematuria  Upper urinary tract

History of familial polycystic kidney dz, TB

Travelling  schistosomiasis

History of catheterization

Check for prostatism

Pelvic injury and fracture

Medication anticoagulant, other drugs

Any history of blood malignancies, malaria and sickle cell RISK FACTOR/ETIOLOGY
disease, hemolysis
- Smoking
Strenuous exercise, muscle injury  myoglobinuria - Obesity
- Hypertension
History of renal biopsy
- Occupational exposure to certain chemicals
Abdominal pain with purplish urine  Acute (e.g trichloroethylene, benzene, dll)
intermittent porphyria - Prolonged use of NSAIDs
- Long term renal dialysis  acquired cystic dz
of kidney  RCC
Physical Examination - Chronic hepatitis C infection
- Kidney stones (in males)
 Anemia, weight loss  CKD, malignancies - Genetic: von Hippel-Lindau syndrome,
 Palpable abdominal mass  Hypernephroma, hereditary papillary renal carcinoma, Birt-
distended bladder Hogg-Dube syndrome, hereditary renal
 DRE Smooth enlargement of prostate  BPH carcinoma
DRE hard craggy prostate  Prostate Ca
 Bone tenderness  Bone meta
CLASSIFICATION – histological classification penting utk
tentuin prognosis and treatment
Laboratory

 FBC : Decreased Hb in gross hematuria,

malignancy. Increased HB in polycythemia
associated with hypernephroma. Increased
WCC in infection. Low platelet in blood
dyscrasia. High ESR in TB, malignancy.
 Urine microscopy : RBC indicates Hbnuria,
ingestion of substance, high WCC in infection
 Ureum, Creatinine and electrolyte : Renal
failure
 Clotting screen : Anticoagulant therapy, blood
dyscrasia
 CXR : Metastasis, TB
 KUB radiograph : Renal calculus
- CLEAR CELL CARCINOMA (ccRCC)
o Mascroscopic: solid, yellowish lesion
Specific Investigation
w/ variable degree of internal
 PSA : prostate ca, BPH, prostatitis necrosis, hemorrhage & cystic
 Sickling test : Sickle cell disease degeneration
 IVU : Stone, tumor, TB o Fast-growing tumors
 US : cystic vs solid, stone, urinary tract o Histologically: lesions present clear
obstruction cell bcos lipid- and glycogen-rich
 CT : tumor, cyst, obstructive uropathy cytoplasmic content
 Cystoscopy : infection, tumor, stone - Papillary
 Ureteroscopy : tumor, obstruction - Chromophobe
 Renal angiograph : vascular - Collecting duct
malformation,tumor - Translocation associated
 Biopsy : glomerular disease and tumor - Tubulocystic
- Unclassified

SIGN & SYMPTOMS

RENAL CELL CARCINOMA (RCC)
- ↓BB
- Kidney cancer (renal mass) that originates
- Fatigue
epithelial cells in proximal convoluted tubule
- Anemia
- Most common kidney cancer in adults
- Fever
- VHL gene: Von Hippel-Lindau tumor
- Hypertension
suppressor gene
- Hypercalcemia
- Night sweats
 - Varicocele – usually left sided – due to T3c Tumor extends to
obstruction of testicular vein renal veins/vena cava
above diaphram
CLASSIC TRIAD T4 Tumor invade beyond Gerota
fascia
- Hematuria
N Nx Can’t be assessed
- Flank pain N0 No regional lymph node
- Palpable mass in the flank/abdomen – non metastasis
tender, moving with respiration N1 Metastasis in regional lymph
nodes
PF – dilakukan utk melihat apakah ada metastasis:
M M0 No distant metastasis
- Lung (75%) M1 Distant metastasis
- Soft tissue
- Bone
AJCC STAGING
- Liver
- Cutaneous site Stage T N M
- Central nervous system I T1 N0 M0
II T2 N0 M0
ROBSON STAGING III T1-2 N1 M0
Stage I Tumor within kidney capsule T3 Nx,N0,N1 M0
Stage II Tumor invade perinephric fat but IV T4 Any N M0
still contained in Gerota fascia Any T Any N M1
Stage III A Tumor invade renal
vein/inferior vena cava
DD OF RENAL MASS
B Regional lymph node
C Both - Abscess
Stage IV Tumor invae adjascent viscera - Angiomyolipoma (benign neoplasm)
(exclude ipsilateral - Metastasis from distant primary lesion
adrenal)/distant metastasis - Metastatic melanoma
- Oncocytoma (benign adenoma)
- Renal cyst
- Renal infarction
- Sarcoma

DD RCC

- Acute pyelonephritis
- Bladder cancer
- Chronic pyelonephritis
TNM STAGING - Non-hodgkin lymphoma
- Wilms tumor
T Tx Pri tumor can’t be assessed
T0 No tumor DIAGNOSIS
T1 ≤ 7 cm, limited to kidney
T1a ≤ 4 cm LAB
T1b 4 – 7 cm
- Urinalysis (UA)
T2 >7 cm, limited to kidney
- Urine cytology
T2a 7 – 10 cm
- CBC with differential
T2b >10 cm
- Electrolyte
T3 Tumor extend to major
- Renal profile
veins/adrenal
gland/perinephric tissue (not - Liver function test (LFT: AST, ALT)
beyond Gerota fascia) - Serum calcium
T3a Invades adrenal
IMAGING
gland/perinephritic
tissue (not beyond - CT scan (Pelvic CT) - utk diagnosis + liat staging
Gerota fascia) - MRI (if venous involvement suspected/patient
T3b Tumor extends to ga bs terima contrast)
renal veins/vena cava
- USG (useful for cystic renal lesions)
below diaphram
- Chest CT/X-ray
 - Bone scan (suspect bone metastasis/ALP↑)
- Brain CT (suspect brain metastasis)
- PET scan (for distant metastasis) MONITORING

THERAPY Stage I & HT, PF Every 6m (for

II Chest CT/X-ray 2y) annually
- Surgery BUN, creatinine (for 5 y)
o Partial Nephrectomy (remove tumor Calcium levels
and save the kidney) Abd CT scan Once 4-6m
 For: T1a renal mass Stage III PF Every 4m (for 2y)
 T1b: bisa radical/partial Chest CT/X-ray  every 6m (for
nephrectomy LFT,BUN,creatinin 3y)  annually
 Thermal ablation – higher e (for 5 y)
risk for local tumor Calcium levels
recurrence Abd CT scan At 4-6m 
annually/indicate
o Radical nephrectomy (complete
d
removal of kidney)
End-stage USG
o Laparoscopic nephrectomy
Renal dz CT scan
o Palliative nephrectomy (utk mrk yg
↑ALP Bone scan
udh metastasis – utk mengurangi Low risk Chest X-ray Annually (for 3y)
symptoms nya aja) patient
- Molecular-targeted therapy (for treatment of (T1N0Mx)
metastatic kidney cancer) –
managed
surgically
Moderate Abd CT/MRI 3-6m stlh surgery
-high  imaging every
patient 6m (for 3y) 
annually (for 5y)
After Cross-sectional 3-6m stlh ablation
Ablation CT/MRI (w/ or w/o  annually (for
contrast) 5y)

PROGNOSIS 5-YEAR SURVIVAL RATE

Stage I >90%

Stage II 75-95%

Stage III 59-70%

Stage IV <10%, median survivor of 16-20 months

- Immunotherapy
- Radiation therapy (for palliative)
- Chemotherapy
AKI, CKD, ACKD
Bladder Cancer (Transitional Cell Carcinoma) Etiology

Present as painless visible hematuria in older male  IgA deposition in glomerular mesangium
smoker. Other symptoms dysuria, blood clots and  No evidence of a role for any specific antigen
obstructive symptoms. 90% urothelial cancer.

Risk factor Diagnostic

 Male  Immunofluorescence and immuneperoxidase

 Smoker studies for IgA deposits
 Age >40 o Benign if absence of proteinuria,
 Preexisting urothelial cancer (RCC, ureteral, hypertension or decreased GFR.
prostate) o Severe if proteinuria >500-1000
 Chronic UTI mg/day, elevated serum creatinine,
 Chemical/ toxin exposure hypertension.
Therapy
Diagnostic tools
 If benign  monitor every 6-12 mo for sign of
 Cystoscopy with biopsy : gold standard progression
 Hexaminolevulinate fluorescence cystoscopy :  If severe  primarily aid at reducing
for detection of CIS proteinuria and optimizing BP
 Multiphasic CT Urograph : improve sensitivity o ACEi or ARB optimizing BP and
of cystoscopy reducing proteinuria
 US : sensitivity 63%, specificity 99% o Fish oil
o Very severe  Immunosuppressive
Therapy agents
o Renal transplant if already
 Transurethral resection if minimally invasive progressed to CKD
 Intravesicular chemotherapy after operation
 Radical cystectomy + cisplatin

Prognosis 10 years survival is 65-72%

IgA Nephropathy

Present with hematuria within 12-72 hours of a (usually)

Upper Respiratory Tract Infection (synpharingitic
hematuria). Visible/ non visible hematuria with
proteinuria.

Peak incidence is between 20s-40s, leads to CKD in 25

years. Hypertension and heavy proteinuria may occur in
advance state.
Thin Basement Membrane Nephropathy have sign of volume overload (increased JVP,
S3, edema, pulmo crackles)
Hematuria with normal renal function, no or minimal  Biopsy is recommended in adult
proteinuria. Thinned GBM on electron microscopy.
Therapy
Most common cause of persistent hematuria in children
and adult.  Children  Supportive
 Adults
o Treat underlying infection
o Antihypertensive, diuretics and
sodium restriction for managing
nephritic complication
Prognosis

 Complete recovery in children

 Adult  CKD

Etiology Nephrolithiasis

 Defect in type IV collagen Rapid onset of excrutiating back and flank pain radiate
to abdomen and groin. Increasing pain with movement,
associated with nausea, vomiting, dysuria and urinary
Diagnostic
frequency.
 Renal biopsy if proteinuria 200-300 mg/ day
Etiology
 Electron microscopy if no proteinuria, normal
renal function Stones because of supersaturation in urine 
 Immunohistochemical to distinguish TBMN precipitation and crystallization
with early Alport syndrome
 Calcium oxalate 75% (hypercalcemic,
hyperPTH, excess sodium intake)
Therapy  Calcium phosphate (sama kayak Ca oxalate)
 Uric acid (excess dietary purines, MPD,
 BP goal <130/80 mmHg
uricosuric agents, metabolic syndrome)
 ACEi if proteinuria >1 g/ day
 Proteus mirabillis  struvite formation

Prognosis : excellent Complication

 Ureteral obstruction
 Pyelonephritis
Infection related GN  Sepsis
 Renal failure
New onset of Nephritic syndrome (hematuria, Diagnostic
proteinuria, edema, hypertension), AKI and infection.
 CT scan non contrast
Epidemiology  US for pregnant woman
 Hematuria
 Post streptococcal GN occurs in children
Therapy
 Immunocompromising comorbidities DM,
alcoholism.  Pain control NSAID/ Opidoid
Etiology  Hydration oral/ IV
 Uncontrolled pain, nausea and vomiting, AKI
 Mostly associated with Streptococcal
 hospitalize
pharyngitis and impetigo
 Sepsis : Broad spectrum Abx and drainage via
 In children 1-2 wks after pharyngitis and 2-4
nephrostomy
wks after impetigo
 Stone passage
Diagnostic
o Nifedipine and tamsulosine
 ASTO for streptococcal infection o Lithotripsy
 Hypocomplementemia C3 and C4  Prevention
 Adult may have nephrotic range proteinuria, o Reducing phosphate containing soft
hematuria RBC cast, while older adult may drinks
o Stop thiazide, citrate
supplementation, allopurinol
BPH  Ecoli, kleb, proteus, pseudomonas
 STD  chlamidya
Urgency frequency, nocturia, urge incontinence, stress Diagnostic
incontinence, hesitancy, poor flow, straining, dysuria
 DRE, urinalysis and culture, PSA.
Diagnostic using DRE  If abscess occur  CT, MRI, TRUS.
 Renal function
Therapy
Therapy
 Diuretics
 First line Fluoroquinolone, TMP SMX 3-4 wks
 Moderate to severe : Alpha bloker (terasozin,
 Supportive : pain reliever and stool softener
doxasozin) + 5alpha RI (finasteride), or
 Abscess  drainage
phosphodiesterase inhibitor (tadalafil)

Alport Syndrome
Prostatitis
Hematuria with strong family history of renal disease
Abdominal pain, recent UTI, fever, chills, urinary
and sensory neural hearing loss
retention, recent prostate biopsy
Diagnostic urinalysis with microscopy, SrCr, family
Ascending infection through reflux of urine to prostate
history and biopsy.
through ejaculatory/ prostate ducts.

Eti