Ch 20 Flashcards
1
Q
more hematuria**, usually sicker
- caused by glomerular disease
- RBC’s in urine, red cell casts on UA
- pt presents with acute post-streptococcal glomerulonephritis
A
Nephritic syndrome
2
Q
severe proteinuria** (>3.5 g/24 hours)
- low molecular weight proteins in urine (highly selective)
- hypoalbuminemia, hyperlipidemia, lipiduria
- subepithelial deposits**
A
Nephrotic syndrome
3
Q
rapid decline in GFR with concurrent dysregulation of electrolytes and fluid, retention of metabolic waste products
A
Acute Kidney Injury (AKI)
4
Q
diminished GFR that is persistently less than 60ml/min for at least 3 months and/or persistent albuminuria
- Major cause of death from renal disease
A
Chronic Kidney disease
5
Q
disorders in which the kidney is the only or predominant organ involved
A
primary glomerulonephritis
6
Q
when the glomerulus is affected by systemic immunologic disease such as SLE, vascular disorders such as HTN or metabolic diseases
A
secondary glomerulonephritis
7
Q
when there is no cellular inflammatory component
A
glomerulopathy
8
Q
- Antibody binding PLA2 receptor present in glomerular epithelial cell membrane, followed by complement activation
- immune complex deposition along the sub-epithelium of the basement membrane
- granular IF pattern
A
Nephrotic syndrome (membranous nephropathy)
9
Q
simultaneous lung and kidney lesions (hematuria and hemoptysis) due to anti-GBM Ab’s that cross react with other basement membranes (especially in lung alveoli)
- linear IF pattern
A
Goodpasture syndrome
10
Q
progressive fibrosis that leads to proteinuria and hematuria (stems from a loss of renal mass)
- often associated with systemic HTN
- nephrotic syndrome WITH nephritic syndrome
A
Focal Segmental Gloemrulosclerosis (FSGS)
- most common cause of nephritic syndrome in adults
11
Q
What is the treatment for FSGS?
A
Renin-Angiotensin System inhibitors
12
Q
fibrosis and inflammation of the tubules and interstitium (opposed to the glomerulus)
- results from either direct injury from proteinuria/cytokines, or tubules over-expressing adhesion molecules that stimulate inflammatory response
A
Tubulointerstitial Fibrosis
13
Q
1-4 weeks after untreated infection:
- formation of immune complex formation in situ/deposition of antibody against pyogenic exotoxin B (SpeB)
- “hump-like” deposits in subepithelial space
- diffuse proliferation of glomerular cells (enlarged and hypercellular) associated with influx of leukocytes
- granular IF deposits of IgG and C3
A
Post-Streptococcal Glomerulonephritis (PSGN)
14
Q
6-10 year old pt, with sudden/abrupt onset of malaise, fever, nausea, periorbital edema, mild-moderate HTN, oliguria, proteinuria, dysmorphic RBC casts and hematuria 1-2 weeks post-infection
- labs show elevated ASO, low serum complement levels
A
PSGN
15
Q
What can cause Non-streptococcal acute glomerulonephritis?
A
other infections: Staph endocarditis, P. pneumonia, meningococcemia, HepB, HepC, mumps, HIV, varicalla, mononucleosis, Toxoplasmosis, Malaria
16
Q
How does Non-strep acute glomerulonephritis differ from PSGN?
A
sometime it can produce immune deposits containing IgA rather than IgG
17
Q
anti-GBM antibodies that cross react with pulmonary alverolar BM, anti-collagen type 4
- antigen is alpha3 chain of collagen type 4
- associated with HLA-DRB1
- leads to renal failure in weeks-months if left untreated
A
Type 1 Rapidly Progressive Glomerulonephritis (RPcGN)
18
Q
How do you treat RPcGN type 1?
A
plasmapheresis (remove Ag/Ab from circulation)
19
Q
- immune complex deposition with granular pattern of immune complex formation
- cellular proliferation and crescent formation
- NOT helped by plasmapheresis
A
Type 2 RPcGN
- must treat the underlying cause
20
Q
- no anti-GBM complexes or immune complexes, but associated with anti-neutrophil cytoplasmic antibodies (ANCA**)
- idiopathic, manifestation of small-vessel vasculitis or polyangiitis (known to play a role in some vasculidities like granulomatosis with polyangiitis
A
Type 3 RPcGN
21
Q
- hematuria, red cell casts, proteinuria approaching nephrotic ranges
- variable edema and HTN
- rapid loss of renal function accompanied by oliguria
A
RPcGN
22
Q
What is the treatment for type 2 RPcGN?
A
steroids and cytotoxic drugs (anti-inflam)
- plasmapheresis only treats type 1
23
Q
child (or young adult) with massive selective proteinuria, though they have preserved renal function without hematuria or HTN
- normal glomerulus, but EM shows uniform/diffuse effacement in the visceral epithelial cells of foot processes
- effectively treated by corticosteroids**
A
Minimal Change Disease (MCD)
24
Q
What is the most common cause of nephrotic syndrome in children and can be challenged by steroid therapy?
A
MCD
25
What populations have an increased risk of MCD?
- patients with Hodgkin lymphoma, with T-cell mediated immune defects
- patients with certain HLA haplotypes associated with atopy
26
normal glomerulus, EM shows diffuse effacement of foot processes (extra epithelial damage and sclerosis under light microscopy)
- higher incidence of hematuria and HTN
- reduced GFR
- nonselective proteinuria
- poor response to corticosteroids
Focal Segmental Glomerulosclerosis (FSGS)
27
Podocin (NPHS2) mutation, chromosome 19q13
Finnish type FSGS
28
NPHS2 mutation, chromosome 1q25-q31 (AR)
| - steroid resistant pediatric form
Podocin FSGS
29
AD, insidious in onset with high rate of progression to renal insufficiency
Alpha-actinin 4 FSGS
30
Mutation associated with adult onset FSGS?
TRP6
31
chromosome 22, increases the risk of FSGS in African Americans
- also associated with increased resistance to trypanosome infection
Apolipoprotein L1
32
Adults and kids, usually African American
- retraction/collapse of the entire glomerular tuft, with or without additional lesions
- proliferation and hypertrophy of glomerular visceral epithelial cells
- significantly decreased GFR with azotemia, focal IgM and C3 in mesangial distribution, HTN
- does not respond to corticosteroids**
Collapsing glomerulosclerosis
33
What is the most characteristic lesion of HIV-associted nephropathy?
Collapsing glomerulosclerosis
34
35 year old male presents with nephrotic syndrome and microscopic hematuria, CD4 count >500.
What is he most at risk for infection from?
acute pyogenic infection (staph and strep pneumoniae), due to loss of Ig in the urine
35
adolescents and young adults
- nephrotic syndrome with a nephritic component, manifested by hematuria and mild proteinuria
- thickened GBM, showing "tram-track" appearance (splitting) d/t new basement membrane synthesis in response to subendothelial deposits of immune complexes
Membranoproliferative Glomerulonephritis (MPGN)
36
adult patient, mixed nephrotic/nephritic, deposition of iGG and complement
- associated with chronic antigenemia causing **immune complex deposition** (HepC, SLE, endocarditis, lymphomas)
Type 1 MPGN
37
sicker, nephritic patient
- alternative complement activation causes a **dense deposit**
- C3 found in the GBM, elaborates C3 Nephritic Factor (C3NeF)
- messangial proliferation with involvement of the basement membrane
Type 2 MPGN
38
immune complex deposition and activation of complement, mostly in adults
- associated with chronic immune complex disorders: SLE, HepB, HepC, endocarditis, HIV
- a1-AT deficiency
- malignant diseases like lymphoid tumors
Secondary MPGN (almost always Type 1)
39
excessive activation of alternative complement pathway and deposition in the glomerulus
- C3 nephritic factor (C3NeF) auto-Ab's bind C3 convertase, protecting it from INactivation -> promotes persistent C3 activation and subsequent HYPOcomplementemia
Dense deposit disease (MPGN Type 2)
40
What else can dense deposit disease be associated with other than C3NeF?
mutations in Factor H
41
- kids and yound adults, poor prognosis
- 50% progression to ESRD
- reoccurrence in 90% of transplant recipients
- **permeation of the lamina densa of the GBM by an extremely electron dense ribbon of material***
Dense deposit disease (MPGN Type 2)
42
What is the most common cause of glomerulonephritis worldwide?
Berger Disease (IgA nephropathy)
- IgA deposits found in the mesangium, detected by IF with recurring hematuria
- C3 commonly found in deposits, C1q and C4 are absent
43
affects any age, especially older kids and young adults
- pt presents with gross hematuria following an infection of the respiratory of GI tracts
- bleeding lasts a few days, then comes back every few months
- microscopic hematuria (30-40%)
- 5-10% develop acute nephritic syndrome
- prolonged progression to eventual renal failure (increased risk of progression with old age, heavy proteinuria, HTN and more glomerulosclerosis)
Berger Disease
44
pt presents with gross microscopic hematuria, red cell casts, slowly progressing proteinuria,
- auditory disturbances
- vision problems
- renal failure
- defective GBM (defect in *alpha-5 chain* of type 4 collagen synthesis)
Alport Syndrome
- X-linked inheritance 85%
NOTE: disease is onset at birth, but symptoms do not occur until later in life
45
What chromosomes are type 4 collagen genes found on?
2, 13, X
46
What is type 4 collagen crucial for?
function of GBM, lens of the eye, and the cochlea
47
common, asymptomatic hematuria, discovered by routine UA
- mild/moderate proteinuria, normal renal function, excellent prognosis
- defect in alpha-3/4 chain of type 4 collagen
- a5 chain of type 4 collagen IS present -> no ocular or auditory lesions
- no IgA immune deposition in mesangium
Thin Basement Membrane Disease
48
pt presents with loss of appetite, anemia, vomiting and weakness
morphology shows symmetrically contracted kidneys, diffuse granular cortical surfaces
- thinned cortex, with increase in peri-pelvic fat
Chronic Glomerulonephritis
| - the end point of all nephrotic and nephritic syndromes
49
Ab-Ag deposits in glomerular filtration barrier
- macrophage activation leads to injury and eventual fibrosis of the glomerulus
- **wire-loop appearance**
Lupus
50
What is the most common and severe form of Lupus?
Class 4
- >50% of all glomeruli involved "diffuse"
- proliferation of endothelial, mesangial and epithelial cells -> *lateral crescents* that fill Bowman's space
51
child presents with pruritic skin lesions on extensor surfaces of arms/legs and buttocks, abdominal pain, intestinal bleeding, arthralgia and renal abnormalities
- atopy and URI
Henoch-Schonlein Purpura
| - excellent prognosis in children, unless omnious clinical signs are present
52
What is Henoch-Schonlein Purpura most likely related to?
What are the main differences?
is probably a spectrum of disease related to IgA nephropathy (Bergers)
- Henoch-Schonlein Purpura is systemic, while Berger's is localized to the kidney
53
pt presents with nephrotic syndrome, hematuria (nephritic) and progressive renal insufficiency
- EM shows fibrillar deposits in the mesangium and glomerular capillary, that look like amyloid fibrils, but do not stain with Congo red
- selective deposition of polyclonal IgG (mostly IgG4) and C3 on IF
Fibrillary Glomerulonephritis
54
IgG-IgM complexes (cyroglobulins) induce cutaneous vasculitis, synovitis and proliferative glomerulonephritis
- associated with HepC
Essential Mixed Cryoglobulinemia
55
Where does Toxin ATI show focal, nonspecific necrosis?
straight portion of the proximal tubule and thick ascending limb
56
Eosinophilic hyaline and pigmented granular casts are common, especially in distal tubules and collecting ducts
- casts contain mostly **Tamm-Horsfall protein** (urinary glycoprotein normally secreted by the cells of the ascending thick limb and distal tubules)
Acute Tubular Injury/Necrosis (ATI)
57
What are 7 causes listed of ATI?
1. rhabdomyolysis (myoglobin is released -> nephrotoxic)
2. aminoglycosides (reserved for life-threatening gram- orgs)
3. mercuric chloride (large acidophillic inclusions)
4. carbon tetrachloride (lipid accumulation)
5. cisplatin and cyclosporine (chemotheraputic agents)
6. contrast dye (is hyperosmolar -> nephrotoxicity)
7. crystal deposition -> **ballooning of PCT**
58
What are the 3 phases of ATI?
1. initiation (36 hours, nephrotoxic insult has not yet caused acute renal failure)
2. maintenance (sustained decreases in urine output)
3. recovery
59
What is the diagnostic marker for ATI?
dirty brown granular casts aka renal failure casts
60
What is the difference between acute and chronic tubulointerstitial nephritis?
- acute: rapid clinical onset, interstitial edema, WBC infiltration of interstitium and tubules with tubular injury
- chronic: infiltration with mostly mononuclear WBC's, fibrosis, lots of tubular atrophy
61
What is the difference between tubulointerstitial nephritis and glomerular disease?
- absence of nephritic and nephrotic syndrome
| - presence of defects in tubular function
62
What are the common Gram neg bacteria that cause acute pyelonephritis?
E. coli, Proteus, Klebsiella, Enterobacter
| - Strep faecalis and staph saprophyticus called "honeyoon bugs" d/t likelihood to cause UTI in sexually active females
63
What organism can cause a caseating granulomatous inflammation?
mycobacterium
NOTE: funal infections are non-caseating
64
What is the Vesicoureteral Reflux (VUR)?
- congenital: malformed or incompetent valve
- acquired: atony of the bladder
They allow bacteria to gain access to the ureters
65
What is the intrarenal reflux?
infected bladder urine can be propelled up to the renal pelvis and deep into the renal parenchyma thru open ducts at the tips of the papillae
- most common at upper and lower poles of the kidney
66
morphological hallmarks are: patchy interstitial suppurative inflammation (focal abscesses or large wedge-like areas), intralobular WBC aggregates (WBD casts on UA) and tubular necrosis
acute pyelonephritis morphology
NOTE: affects the upper and lower poles most
67
What are the 3 complications of acute pyelonephritis?
1. papillary necrosis
2. pyonephrosis
3. perinephric abscess
68
seen in diabetics, sickle cell disease and those with urinary tract obstruction
- typically bilateral
- grey-white to yellow necrosis
- preservation of outlines of tubules with WBCs limited to the preserved and destroyed tissue
papillary necrosis
69
seen when there is a total or almost complete obstruction, particularly when it is high in the urinary tract
- severe infection that totally occludes the lumen and outflow with pus that fills the renal pelvis, calyces and ureter
pyonephrosis
70
suppurative inflammation that extends through the renal capsule into the perinephric tissue
perinephric abscess
71
50 year old male presents with dysuria/frequency with sudden onset of flank pain at the costovertebral angle (flank pain)
- culture shows pathogens, urine shows WBC's
Acute pyelonephritis
- associated with UTI, VUR, urinary tract instrumentation (catheters), **pregnancy** and DM
- more common in males <1 and >40
72
post-transplant (immunocompromised) pt with infection of tubular epithelial cell nuclei
- nuclear enlargement and intranuclear inclusions (viral cytopathic effect)
- inclusions arrayed in crystalline-like lattices
Pylomavirus nephropathy
73
What is the most common pyelonephritic scarring?
| - occurs early in childhood from superimposition of UTI on congenital VUR and intrarenal reflux
Reflux nephropathy
74
obstructions predispose pt to infections
- recurring inflammaition can lead to scarring and chronic pyelonephritis
- **defective posterior urethral valves bilateral**
- coarse, discrete corticomedullary scars overly dilated, blunted or deformed calyces -> flatten the papillae = **THYROIDIZATION**
Chronic obstructive pyelonephritis
- pt presents with back/flank pain, fever, pyuria, bacteremia
NOTE: pts receive medical attention late in disease course because onset is so slow
75
older pt presents with fever, rash, eosinophilia, and acute renal failure (increased serum creatinine and oliguria) approx 15 days after exposure to offending agent
- papillary necrosis with gross hematuria
Acute (Drug-Induced) Tubulointerstitial Nephritis
76
How do you treat Acute (drug-induced) tubulointerstitial nephritis?
removal of drugs leads to recovery and healing!
| - NSAID's, synthetic penicillins, other synthetic antibiotics
77
What are patients with analgesic nephropathy more likely to develop?
urothelial carcinoma of the renal pelvis
78
What is the earliest functional defect seen in hypercalcemia and nephrocalcinosis?
inability to concentrate urine
79
What does excess phosphate load lead to?
marked precipitation of calcium phosphate > presents as renal insufficiency several weeks later
80
Ig light chains form complexes with Tamm-Horsefall proteins under acidic conditions causing tubular obstruction and inflammation
Bence-Jones proteinuria and cast nephropathy
81
What is myeloma kidney?
light chain cast nephropathy
| - most of the kidney damage is restricted to the tubulointerstitial part
82
older African American pt with diabetes and HTN
| - inconspicious proteinuria, decreased GFR, increased risk towards chronic renal failure
Nephrosclerosis
83
When would you see hyperplastic changes in renal arteries?
Malignant Hypertension Nephrosclerosis
extreme BP -> endothelial cell damage -> increased permeability to fibrinogen -> fibrinoid necrosis -> intravascular thrombosis
84
African American male, DM, HTN, retinal hemorrhages, encephalopathy, CV abnormalities, renal failure
- early sx: d/t increased intracranial pressure (HA, NV, vision problems)
- proteinuria, maybe hematuria
- "flea-bitten" appearance of kidney
Malignant HTN Nephrosclerosis
85
What are the two demographics most likely to have Unilateral Renal Artery Stenosis?
1. old diabetic men -> cause by increase Renin production from ischemic kidney
2. women in their 20-30's -> fibromuscular dysplasia **sting of beads**
86
Pt looks like they have essential HTN, bruit can be head on affected kidney, elevated plasma renin, which shows response to ACE-I
Unilateral Renal Artery Stenosis
87
What is the definitive therapy for Unilateral Renal Artery Stenosis?
Arteriography (to find lesion, then surgery! (after pt has responded well to ACE-I or ARB)
88
What is they cause of Typical Hemolytic-uremia syndrome (HUS)?
Shiga-like toxin (E.coli hamburgers, raw milk, and person-person)
89
children and elderly pts, hematememesis and melena, following a flu-like prodrome
- oliguria/hematuria/ hemolytic anemia may follow
Typis HUS
| - acute setting resolves itself, long term is managed by dialysis, prognosis is poor
90
normal levels of ADAMTS13, inappropriate activation of complement
- neuro signs/symptoms
- endothelial injury
- defects in Factor H, 1 and CD46
Atypical HUS
| - can develop at any age
91
<40 year old pt presents with fever, **neurological symptoms**, microangiopathic hemolytic anemia, thrombocytopenia, and renal failure
- deficient in ADAMTS13 (normally regulates vWF)
Thrombotic Thrombocytopenic Purpura (TTP)
92
How is TTP treated?
plasmapheresis (provides functional ADAMTS13)
93
Subscapular petechiae, thickened capillary walls, mesangiolysis, fibrinoid necrosis and occlusive thrombi
HUS/TTP
94
Why should you avoid ACE-I and ARB's in Atherosclerotic Ischemic Renal Disease?
decrease in Ang II will dilate the efferent arteriole -> increasing RBF, but decreasing GFR = acute renal failure
95
What can prevent further decline in renal function in a pt with Atherosclerotic Ischemic Renal Disease?
surgical revascularization
96
African American male, with sickle cell and HTN
- flank pain
- excreting blood clots
- insidious onset of hematuria, followed by proteinuria, polyuria, HTN
- multiple expanding cysts of both kidneys
Autosomal Dominant Polycystic Kidney Disease (ADPKD)
97
Where is PDK1 expressed?
tubular epithelial cells, particularly those of distal nephron*
- involved in cell-cell and cell-matrix interactions
98
Where is PKD2 expressed?
integral membrane protein expressed in all segments of the renal tubules and many extrarenal tissues
- **is a Calcium permeable cation channel**
99
Where do Intracranial Berry Aneurysms arise from?
altered expression of polycystin in vascular smooth muscle
| - ***isolated, basilar subarachnoid hemorrhage in a young patient -> ADPKD***
100
highly fatal in infancy, obvious renal failure in all classes, childhood form shows smaller cysts at right angles
- mutations in **PKHD1** on chromosome 6 disrupt the collecting tubule
- tiny elongated cysts along the interior have a sponge-like appearance when cut
Autosomal Recessive Polycystic Disease
101
child pt presents with unexplained renal failure with familial history, large cysts at cortico-medullary junction (small cysts in cortex)
- polyuria, polydypsia, Na wasting and tubular acidosis
- renal failure in 5-10 years
Medullary Sponge Kidney
102
What is associated with renal cell carcinoma from the walls of cysts?
Acquired (dialysis associated) cystic disease
| - pts on hemodialysis for a long period of time have an increased incidence of RCC
103
When are calcium phosphate stones more common than calcium oxalate stones?
in the general population
104
What are calcium oxalate stones more common than calcium phosphate stones?
in pt's receiving renal dialysis
105
Which stone type is associated with hypercalciuria, with or without hypercalcemia?
Calcium Oxalate Stones
| - is a result of hyperparathyroidism, renal impairment of calcium reabsorption or hyper-absorptive intestinal tract
106
What is seen in diarrhea and metabolic acidosis?
hypocitraturia
| - may also lead to calcium stones
107
What type of stone is made from Magnesium ammonium phosphate
- caused by urea-splitting bacteria
- is the largest kidney stone
Struvite Stones
| - **Staghorn Calculi**
108
What type of stone mostly occurs unilaterally at the renal calyx, pelvis or the bladder
- vary in size (<5mm small, .7mm large)
- form staghorn calculi
- present in younger pt's (20/30's), show familial patterns
- cause renal colic, sharp flank pain that radiates to groin, and hematuria
Cystine Stones
109
Small (<5cm), pale, yellow-gray, well-circumscribed nodules within the cortex
- complex branching papillomatous structure with complex fronds
- cuboidal to polygonal in shape, with regular, small, central nuclei, little cytoplasm, and no atypia
Renal Papillary Adenoma (benign)
NOTE: potentially malignant at any size, but especially if greater than 3cm (consider all adenomas as potentially malignant)
110
benign neoplasm consisting of vessels, smooth muscle, and fat from the perivascular epithelioid cells
- likely to spontaneously hemorrhage
- associated with Tuberous Sclerosis**
- loss of function mutations in TSC1/2
- lesions of cerebral cortex that produce epilepsy, retardation, skin problems
Angiomyolipoma (aka Renal Fibroma, or Hamartoma)
111
epithelial neoplasm composed of large, eosinophillic cells with small, round benign-looking nuclei that have **large nucleoli**
- comes from intercalated disks of collecting ducts
- massive amounts of mitochondria
- tan/brown tumors well-circumscribed with a central scare
Oncocytoma
112
What is the greatest risk factor for Renal Cell Carcinoma?
smoking
- also HTN, obesity, unopposed estrogen therapy
- exposure to asbestos, heavy metals
113
AD inheritance
- mutations in FH gene (fumarate hydratase)
- cutaneous and uterine leiomyomata with an aggressive type of papillary carcinoma
Hereditary Leiomyomatosis/Renal Cell Cancer Syndrome
114
AD inheritance
- mutations in MET proto-oncogene
- many bilateral tumors with papillary histology
Hereditary papillary carcinoma
115
What is the most common type of renal cell carcinoma?
Clear cell carcinoma
- 98% caused by loss on chromosome 3 where VHL gene is
- inappropriate expression of genes turned on by HIF-1 promotes angiogenesis (VEGF) and stimulate grown IGF-1)
116
Nonpapillary, unilateral tumors
- large clear or granular cells
- bright yellow-white-grey tumors
- tumors are typically differentiated
- **likely to invade renal vein -> IVC -> heart**
- can cause a varicocele if located on LEFT
Clear Cell Carcinoma
117
multifocal origin tumor,
- sporadic: trisomies 7 and 17, loss of Y in males
- familiar: just trysomy 7
- cancer associated with dialysis-associated cystic disease
- not associated with chromosome 3p deletions (like VHL and clear cell are)
- cuboidal or columnar epitheliumm arranged in papillary pattern
Papillary Carcinoma
118
young pt
- translocations of TFE3 gene
- cells have clear cytoplasm with papillary architecture
Xp11 translocation carcinoma
119
often asymptomatic, discovered by CT/MRI for nonrenal cause
- may reach massive sizes before symptoms set in
- triad of symptoms: hematuria**, flank pain, and mass
Collecting duct (Bellini duct) carcinoma
120
What is the recommended treatment for a T1a tumor (<4cm) causing paraneoplastic syndromes?
partial nephrectomy
121
What are the 3 stages of paraneoplastic syndome?
Stage 1: only 1 kidney involved
Stage 2: kidney and far are involved
Stage 3: kidney and renal vein or lymph are involved
122
What is the main risk factor for urothelial carcinoma of the pelvis?
What other disorders are they associated with?
- smoking
| - Lynch syndrome and analgesic nephropathy
123
What tumors are typically found early, as they produce painless hematuria?
Urothelial carcinoma of the pelvis
NOTE: may block urine outflow and lead to hydronephrosis and flank pain
