Pathology of the kidney and urinary tract - Course

Course content
RENAL DISEASES
1. Glomerular nephropathies - GN
2. Tubulo-interstitial nephropathies (NTl)
3. Vascular NPs-vascular kidney damages in HTA
4. Renal Tumors
DISEASES OF LOWER URINARY TRACT
1. Infections of lower urinary tract
2. Obstructive Uropathy (hidronephrosis)
3. Renal lithiasis (Urolitiasis)
4.Tumors of LUT
5. Malformations of the kidney and urinary tract

Anatomy Reui*t*t

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'Kidneys

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'Shdder
 Nephropathies (NP)
NP=bilateral renal Etlfl*rl G:*rrtlr
diseases with varied Aa'fntill nlnt,:la

clinical picture and SlJrl6r{:ils

morphological
substrate
depending on the
location of primarY
lesions - 3 categories Anatomy of the
of NPs: Irl*phrcn
- glomerular
- tubular
- interstitial
Main functional unit of the kidney =nephron

GLOMERULAR NPS

renal diseases that

have in common the
location of the primarY
lesion at the level of
glomerulus
 Rw*l R**p*$ Frncst$*R$
Diagnosis (biopsy-
PBR):
- optical microscopy L:tu 1\ ,/ \ r'*,,,*
(Mo) t
PAS-show
glomerular basal L:1;:Illl ,1,,
memDranes
argentic
-rmpregnalon
0rawrng gromerurar
and tubular basal
Fr*:!n I
$*:li*nr
I
rG-]
,f+*-t*
r;;Rr;K
membranes
FlLr*r*srtrt*
[l:fi ti!,]Ff
- immunofluorescenc I
I
e (lF) releaves
locafion of antigens, lg*, 16A. l1r,! t
I
t
complement and i:1, {r;1. Cf C
imunglobulines f l*{:t'!.n Llrr:lll
Frbri*:1;*r: lYlicrr'tilli)
- electron microscopy
(r,\rE)
KixBf s. L:nlr*r llirrtlr rry

glomerurar
ultrastructural
H&E :liir
cnanges lAS :l:;n
lln*r:llir
lrir:ir.:!$",P slrl;

Glomerular NPs
After degree of glomerular damage ) 4 types of glomerular diseases:
(a) global: entire glomerulus is affected;
(b) segmental: glomerulus is partially affected (1-2 segments);
(c) diffuse: all glomeruli are affected;
(d) focal: only some glomeruli are affected.
 Clinical picture of glomerular NPs
renal disease clinical picture

Nephritic syndrome - Sn Hematuria, Oliguria, Azotemia,

Hypertension

Nephrotic syndrome - SN Massive proteinuria,

Hypoalbuminemia, Edema,
Hyperlipidemial-uria
Mixt syndrome Association of Sn and SN

Acute renal failure: oliguria uremta

(weeks/months)

Chronic renal failure: prolonged uremia

uremia (years)

Glomerular NPs

Clinicall! + 2main tYPes:

. primary GNPs or glomerulonephfritis --- initial
involvement of glomerulus
. systemic (secondarY) GNPs or
glomerulonephfritis - systemic diseases affecting
secondary glomeruli
 Glomerular diseases
Primary GD
- Nephrotic syndrome niob$y sf Slam$ular S.**eals,
. Minimal change disease
. Membranous
nephropathy or GN ,,rrryr,r,.h€.qrlr

Nephritic syndrome
epr'he'il*il' " '
-
. Postinfectious
flenlfili:31.b ot 6ES

glomerulonephritis-GN Nyd$dybnhi.rr€1,,5,
. Crescentic GN ,.,1.,.
rl
- Primary hematuria ,,' I '.
. Membranoproliferative
glomeruloneph ritis-G N
. lgA nephropathy

Glomerular NPs with nephritic syndrome

. diffuse proliferative glomerulonefritis

. rapidly progressive glomerulonefritis (with

crescents)
 Diffuse proliferative glomerulonefritis

immune complication wlth diffuse

involvement of olomeruli that occurs
at 2-4 weeks afier an infection with
B haemolytic streptococcus group A
any age, most frequently in children
(6-10 years)
is manifested with Sn

oranular deposits of immune

Eomplexes in the capillary walls

larqe electron-dense nodular

deFosits of immune complexes
disoosed on the external surface of
GBM

Diffuse proliferative
glomerulonefritis rrrut,rr,;rr,ut\'i!i!i!i'il
ill

MO
. diffuse olomerular lesion: all qlomeruli
are affeited simultaneously, 6ilaterally
. qlomerulus is increased in volume-
hipercellularity
. endothelial and mesangial cell
oroliferation
. influx of neutrophils in capillary lumen,
with obliteraration of capillary lumen
. renal tubules are normal
ME
. nodular deposits of immune
comolexes arranqed
surfdce of GBM
- on the external
Evolution
. (95%) completely healing at children
. (5o/o). recovery is reduced at adults -
RPG
 RPG-Rapidly prog ressive
glomerulonefritis
(epithel ial crescents)
. RPG = rapid and
progressive loss of renal u.**'"*Y3*--**]
function in several
months and death by
CRF
. different etiology and
pathogenic mechanisms
MO
. proliferation of parietal
epithelial cells of Bowman
capsule ) with
obstruction of Bowman
space and compressing
of the glomerular
capillaries

Primary glomerular NPs with nephrotic syndrome

. Minimal change disease (llpoid nephrosis)

. Membranous nephropathy
 Minimal change disease (lipoid nephrosis)

. the most common cause of

nephrotic syndrome in children (1- .l-t
4 years)
. etiology
l

- primary or idiopatic: cause is not

Known
j

- a secondary to respiratory
infections or immunization
i

EM :
I

. orimarv lesion is qlomerular ) 1

tusion bf e>,tracap-i lary epithel ial I

cell orocesses ,... J

. eoithelial cells come into direct !

contact with the GBM, which I
becomes permeable with loss of !

lipoproteins, which are reabsorbed :

:

at the level of renaltubules

IMF does not show the presence of
complement or lgs

Minimal change disease (lipoid nephrosis)

MO
. glomeruli are normal
. oroximal tubular epithelial cells
bre loaded with lipids ) old
term of lipoid nephrosis reflects
the oresence of numerous fat
droos into renal tubules
MA
. kidnevs are increased of
volunie, the renal cortex being
pale-yellow (by accumulation
of lioids in the tubular
epithelium) and with smooth
external surface
. Evolution:
- good in children
- unfavorable in adults

-*...,i
 M e m b ra n o us G I o m e_rp I gne_pht ifi_q
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. the most common cause of

nephrotic syndrome in adults
Etiology
. primary or idiopathic (80-90%)
. secondary to systemic
diseases (10-20%)
EM
. early, immune complex
deposits on the external
surface of GBM with GBM
expansion between these
deposits looking as radiary
spikes (aspect of wheel)
. late, the spikes fuse and
include immune deposits
resulting a lacy appearance

M.E. - thickened GBI\4 by deposition of immune cx Ag-Ac on

the extemal epithelial surface of MB

Mem branous G lomeru loneph ritis

.MO
(a) early-normal
appearance of glomerular
capillary walls;
(b) late-diffuse thickeni ng
of GBM.
. lmmunofluorescence -
granular deposits of lg G
and complement on the
external surface of GBM

MO - metenamin - silver stain:

deposition of new matrix of GBM around
immune complexes
 Glomerular NP with mixt sYndrome
(nephritic Ai nephrotic syndromes)

memb ranoproliferative G N
- is manifested with mixt syndrome (Sn and SN)
- etiology
. primary or idioPathic
. secondary to some systemic diseases: LES and lE

Me mb ranop rol iferative g I omeru oneph riti s-2 types

I

ME
. Type I

- mesangial cell. proliferation with

mesanglum Interposlng
between the external and
internal laver of GBM
(appeararice of double contour)
. Type ll
- marked thickening of GBM bY
immune dePosits tnto GBM
(immune complex dePosit
disease) **,*"--
MO
. type I

- mesanqial cell proliferation and

increasbd mesangial matrix -
(Sn) )
lobular appearance ot
glomerulus
. type ll
- thickening of GBM (SN)

10
 Secondary glomerular diseases
and complications

Secondary glomerular disease

- Diabetic glomerulosclerosis-GS
- Renal amyloidosis

Complications
. Chronic glomerulonephritis-GNC

Diabetic nePhroPathY
- ls manifested as:
. diabetic diffuse (Bell) or nodular (Kimmelstiel-Wilson)
glomerulosclerosis
. papillary renal necrosis- papillary vessel thrombosis with removing
of papillary necrotic area into ureter ureter obstruction and ARF
. ''
acute suppurative pielonephritis-predisposition to bacterial interstitial
infections

11
 Diabetic glomeru losclerosis
manifestation of diabetic
m icroangioPathY: reti noPathY,
ischemic heart dtsease ano
peripheral vascular insuffi ciency
MO-3 types of glomerular lesions
- GBM thickening is the most earlY
form of diabetiC microangioPathY
= PAS (+) deposits
- diffuse GS (Sdr. Bell) consists of
diffuse dePosits of PAS (+)
material into glomerular
mesanglum
- nodular GS (Kimmelstiel-Wilson
sdr) consists of nodular dePosits
of PAS (+) material into
glomerular mesangium
Evolution-deposits i ncrease with
obliteration cif capillary lumen and
development of CRF

Amyloid nePhropathY
renal amyloidosis
Kidney - is a target organ in
systemic reactive amYloidosis
Clinically - nePhrotic sYndrome
MA
- kidneys are normal or slightlY
increased in size, looking as
translucent, waxY structure
having elastic, rubberry
consistencY
Ml - amyloid dePosits occur on
-
mesangium and GBM
- blood vessels
-tubular BM
ln advanced disease occurs entire -'
obliteration of glomeruli )CRF t*t*'l

lz
Chronic g lomerulonePhritis
end siage of renal disease

. end stage of glomerular-nelropathies .

and is the main cause ol chronlc renal
failure
Morphology
MA
. both kidneys are atrophied, pales with
an adherent capsule and fine granular
external surface
. On the cut section, the cortex is
atrophied with hilar adipose tisuue
hyperplasia
MI
. Glomeruli are hvalinized and
corresponding tirbules are replaced by
connective tissue
. A reduced number of glomeruli and
tubules are hypertrophied, (increased
in volum but i/ith a riormal function)
giving the appearance of cortical
microgranulararity
. There is a marked interstitial fibrosis
associated with chronic inflammation

Small kidney with microgranular external surface

13
 Tu bu lar-interstitial neph ropathies
. lmpairement of renal tubules and interstitium
represents an imporlant cause of renal
failure

. NTI Classification:
(1) acute tubular necrosis
(2) tubulo interstitial nephritis
(3) pielonephritis

Acute tubular necrosis -NTA

. Morphology
- tubular epithelial necrosis ) is manifested clinically by acute
renalfailure (lRA)
. etiology - 2 main groups
- lschemic
- Toxic
. ischemic tubular necrosis - insufficient kidney perfusion
caused by
- hypovolemic shock or acute bleeding
- severe burns
. toxic tubular necrosis - nephrotoxic substances:
- Endogenous: myoglobinuria
- exogenous: heavy metals (Pb, Hg), organic solvents (CHC|3'
CCl4), drugs (Ab, NSAIDS)

t4
 Acute tubular necrosis -NTA
MA
. kidneys are enlarg.ed,, pale,.friable
(appearance ot Dolleo meal);
. on cut section - the renal cortex is
pale, and medulla is congested.
MI
. toxic acute tubulonecrosis
the lesions are located in proximal
epithelial tubules )tubular epithelial
necrosls
- necrotic epithelial cells have
uniform appearance, acidoPhilic,
without nuclei, some are
detached and fall in the lumen
(epithelial cylinders or casts).
- tubular BM is intact, forming the
support for ePithelial remaining .',]
cell regeneration . r, :;1.,,'; 1'
.,:i,,j; l,'I
,,
,;1 '
- normal glomeruli ,..- ,';i,1i1r;fl'-
, -i-i.i ,: . .,..i '

BM=basement membrane

Tu bu lo-i nterstitial neph ritis

. deqenerative tubular lesions and
int6rstitial inflammatory infiltrate
. acute and chronic
tubulo-interstitial nephritis (NTIA)
. 2-3 weeks after exPosure to a
causative agent - cirugs ) allergic
manifestations
.Ml
- edema and interstitial
inflam matory infiltrate with
lymphocytes and eosinoPhils
- degenerative tubular lesions (focal
tubular necrosis)
. Evolution
reversible - stoPPing drug
administration
- rapidly progressive renal failure

Drug-induced interstitial nephritis

15
 Pyelonephritis

Urinary catheter colonized by E coli or Proteus

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Macroscopy
ascending PNA - SS
- Hvperaemic pielocaliceal mucosa
is'covered bY a Purulent exudate
- Suppurative medularY lines
radiatin g toward cortex
- Cortical large abscesses, Yellow,
irregular, surrounded bY an area
of hyperaemia;
- laroe areas of suPpuration
coifluenting with'wedge shaPe
descending PNA (PYoemic
abscesses)
- affected kidneYs are swelled and
conqested and Presents
dissbminated microabscesses on
the external renal surfaces.
- microabscesses aPPear as Yellow
nodules, 2 mm in diameter, under
tension, surrounded bY an
hyperaemlc area.
Acute pyelonephritis with abscesses

T6
 Microscopy
MI
. interstitial microabscesses
containing occasional microbial
colonies
. tubular damage
. PMNs form leucocitarY casts or
cylinders in renal tubules
. glomeruli are normal
Evolution:
(a) favorable: healing by connective
' ' organization (cortical fibrosis
leaves deep scars);
(b) unfavorable:
. renal papillary necrosis in
diabetics
. perinephriticabscess
. PNC - recurrent infections
. septicemia with BGN and shock

Chronic pyelonePh ritis

Cronic renal disease, that occurs after repeated
renal infections followed by healing
Clinically, disease is manifested through HTA
and cRF
Diagnosis
- affected kidneys are contracted asymmetrically
- deformation of pielocaliceal system
Etiology
infection)
- indistinctive patogens (non-specific
- specific patogens: Mycobacterium tuberculosis

I7
 Unspecific chronic pyelonephritis
Macroscopv:
- rerial oelvis is dilated and
deformed with thickened mucosa
- kidnev - is diminished and
asvminetric (deep scars in the
foim of wedge, with iregular,
decreased cortex and atrophled
medulla).
Microscopy
. chronic inflammation and
interstitial fibrosis in the renal
pelvis ) papillary atroPhY and
fibrosis
. dilated tubules, bounded bY an
atrophied epithelium, contain a
prot'einaceous, eosi noPhilic
inaterial giving. a histologic thyroid
apperance ot me Kloney
. qlomeruliare hvalinized (HTA)
5nd vessel walls are marked
thickened
+

Specific chron ic pyelonePhritis

(tuberculous PNC)
Etiology-mycobacterium tuberculos is
Pathogeny
- blood dissemination from a primary
pulmonary localization
- ascending infection from genital foci
Diagnosis
- morphology - evidence of tuberculous
oranuloma
- iricrobiotogy - evidence of mycobacterium
tuberculosis in the urine
Macroscopy-2 forms:
- Nodular: multiple cazeous nodules of 0,5-2
cm in diameter
- Ulcerative: destructive renal parenchyma
through caseous materlal removed by urine
Complications:
- ln the unilateral lesion the extension of
inflammation reaches the bladder with
secondary affectton of the other kidney
- Bilateral lesions progress to the chronic renal
failure and death

l8
 RENAL TUMORS
. Primary Tumors
- Benign Tumors
. Adenoma
. Fibroma

- Malignant Tumors
. Renal clear cell carcinoma
. Nephroblastoma
. Secondary tumors (rare)
Benign tumors - are without clinical significance ) in 20% - incidental aspects
at postmortem examination

hrtrallgnant tumons

. Primary
- Renal adenocarcinoma (Grawitz T)
- Nephroblatoma ( Wilms T)
. Secondary - multiple nodules - rare

t9
 Renal clear cell carcinoma or renal
adenocarcinoma (G rawitz Tl

the most common malignant kidney tumor

in adults (50 - 60 years old)
90o/o of malignant kidney tumors
most frequent in men (2 | 1)
origin-renal tubular epithelium (proximal
and distal contort tubules)
clinically-hematuria, lumbar pain and
abdominal tumor mass

Macroscopy

SE-polar tumoral masses

with false encapsulation,
proiemining from the
kidney cortex
SS- characteristic
appearance, yellow-g ray,
with areas of necrosis
and hemorrhage

20
 hill-ranal
adenocarcinor-n&
Tumoral architecture:
various types of growth
- Tubular-adenocarcinoma
- Papillary
- Solid
Cytology Rrnrl tcll t*rtlnome
- tumoral parenchyma-clear
polygonal cells with distinct
cell membranes, central
and hypercromatic nuclei
and clear cytoplasm
containing glycogen or fat
- delicate stroma very well
vascularized

Renal clear cell carcinoma - CCR

Dissemination
- hematogenous way (cords of tumor cells are present in the renal vein
and inferior vena cava)
- lymphatic pathway
- direct way (to the renal Pelvis)
The most affected organs are lung, brain, bones, liver, adrenal,
lymph nodes and controlateral kidney.
Prognosis
- Reserved - RS at 10 Years is 20%
- Unfavorable prognosis - aggressive tumor has a tendency to be silent
until it reaches large dimensions, often being metastatic at diagnosis.
Treatment
- surgical resection of the tumor

2l
 Nephroblastoma (Wilms T)
. the most common malignant tumor in childhood
i*ith mlximum frequeri'cy between 1- 4 years)
equal incidence at both sexes
. embryonic tumor derived from remaining
nefroblastema in the renal Pelvis
. mixed neoplasm compg.sqd of metane.phric
blastema dnd its epithelial and stromal
Oerivitives in varyi'ng stages of differentiation
. clinical Picture
-abdominaltumoralmass,observedin90%ofcases
- hematuria, HTA

MacroscoPY

tumor clearlY defined

and encaPsulated
.SS
- white-graY, lobular
with areas
appearance,
of necrosis and
hemorrhage
- tumor is bounded bY a
rim of normal renal
parencnyma
- renal Pelvis is
comPressed

22
 Microscopy
=>the tumor has a triphasic
structure
- epithelial component
(immature glomerular
and tubular structures)
- stromal component
looking as
sarcomatous tumor
- primitive blastema
composed of small
cells (metanephric
blastema)

Dissemination and prognosis

Dissemination
- lymphatic pathway in hilar, and para-aortic lymph nodes
- hematogenous way - in the lung, liver, adrenal, diaphragm,
retroperitoneum and bones
Prognosis - microscopic appearance:
- marked glomerular and tubular differentiation is associated with
a good prognosis
- nuclear pleomorphism and presence of abnormal mitotic figures
are associated with a worse prognosis
The treatment consists of surgical resection and
systemic chemotherapy, associated with radiotherapy of
the affected area

23
 Diseases of lower urinary tract - LUT

1. Infections of lower urinary tract

2. Obstructive uropathy (hidronephrosis)
3. Renal lithiasis (Urolithiasis)
4.Tumors of lower urinarY tract
5. Malformations of the kidney and urinary
tract

1. Infections of lower urinary tract

. are favored by obstruction of LUT and
secondary urinary stasis;
. are caused by BGN of the the colon: E.coli,
Proteus, etc.
. LUT infections are presenting different names
after location:
- pelvic mucosa (Pielitis)
- ureteral mucosa (uretheritis)
- bladder mucosa (cYstitis)
- urethral mucosa (urethritis)

Cystitis
. inflammation of the bladder mucosa of bacterial cause
. types. acute and chronic
. Acute exudative cystitis: differenttypes dependi!9 o.n the
type of inflammatory exudate: catharal, haemorrnagtc'
suppuratlve
. Chronic non-sPecific cYstitis
- recurrentinflammation
infections of UTI
and fibrosis in the bladder wall
- chronic
. Chronic specific cystitis (tuberculosis)
- secondary to a tbc PNC or genital tuberculosis
- Macroscopy: ulcerative lessions of the mucosa
- Microscopy: the caseous granuloma (tuberculous granuloma)

24
 2. Renal lithiasis
(Urolithiasis)
renal disease characterized by abnormal
precipitation of urinary salts with formation of
solitary or multiple, uni or bilateral calculi
(calcium oxalate, calcium phosphate, etc )
Causes:
(a) the increased concentration of urinary salts
(dehydration, stasis);
(b) low solubility of salts in the urine due to a
changed pH (renal diseases, metabolic
diseases)

Renal lithiasis
Locations (2)
- pielo - caliceal system
. small and multiple calculi
through mobilization produce
lumbar oain
. laroe calculi cause
ob5truction and urinary stasis
(hidronephrosis and
iecondary infections)
- bladder
. calculi coming from ureter
. local calculi secondary
formed by urethral obstruction
Complications
- persistent infections: PNC,
ilyonephrosis, peri nephric
abscess
- scuamous metaplasia and
LJDU

25
 3. Obstructive uroPathY
(hydronephrosis)
. Hydronephrosis = renal pelvis dilation caused
by chronic obstruction of the urinary tract of
different causes
Causes:
- nodular prostate hyPerPlasia
- calculi
- malignant tumors (cervical or bladder carcinoma)
Consequences:
- urinary dilatation tract
- atrophy by compression of the renal parenchyma
(accumulation of urine above the obstacle).

Morphology
Macrosco py (2 evolutive
forms):
- primary hydronePhrosis
. moderate dilatation of the
renal pelvis, with a slight
wallthinning
. normal renal ParenchYma
(without kidneY damage)
- secondary
hydronephrosis
. massive dilatation of the
renal pelvis, with very thin
wall
. irreversible atroPhY and
fibrosis of renal
parenchyma

Hidronefroza - Dilatarea sistemului pelvicalicial

26
 4.Tumors of UT
Origin: urothelial mucosal epithelium
(transitional);
a Location: bladder and pielo-caliceal system;
a Types
- Benign tumors: transitional papillomas
. pediculated papillary tumor (2 cm);
Macroscopy:
.Microscopy:connective-vascu|araxiscoveredbytransitiona|
epithelium-with normal histology and cytology
. Evolution: tendencY to reccure
- Malignant
.
tumors
Carcinomas-transitional carcinomas

Transitional
. Oriqin: urothelial mucosal
epiihel i um (transitional) ;

. favoring factors:
- smoking cigarettes
- mechanical irritation by calculi
- chronic infection
. the most common location is the
region of bladder trigon
. Ma- vegetative tumor
. Microscopy.
- atvpical transitional epithelium )
incieased number of cell laYers
. Prognosis.- histological grade and
stage ot olsease
- differentiated - good Prognosis
- undifferentiated - reserved
prognosis
. Treatment - lesion resection (local
or total cYstectomY) followed bY
irradiation.

^n
 5. Malformations of the kidneY
and urinary tract

A Malformations of the B. Malformations of urinarY

tract
kidney
1. Horseshoe kidney 1. Double ureter uni or
2. Ectopic kidney bilateral
2. Congenital stenosis of
3. Policystic kidney the urether

Malformations of the kidney

1. Horseshoe kidney
. the fusion by connective tissue
of the 2 kidrievs at the level of
inferior or sup'erior poles
. the ureters are located on the
front aspect of the kidneYs
. the renalfunction is not
affected
2. Ectopic kidnev = lack of
ascdndinq kidnev to the renal
lodge) t-he kidn'ey is located
in the oelvis
3. Policystic kidney
. the presence of cysts in the
kidney
. 2 types: adult and infantil tYPes

28
 Policystic kidney
Adult type
. Autozomal dominant disease
. p- abnormal cell differentiation
) renal tubular ePithelial
hyperplasia ) secondary
tubular obstruction;
the cystic changes develoP
after birth.
. MA-enlarged and irregular
kidneys (4 kg), comPosed of
various sized cysts, (5-6 cm)
containing a serous or bloodY
fluid, separated from normal
renal parenchYma

Policystic kidneys
Infantil type
. Autozomal recessive disease;
. P-lack of junction between
nephron and collector tubule ->
fusiforne ectasia of the
collector channels; the cYstic
changes are Present at birth.
. MA-kidneys are enlarged and
have a preserved shaPe; theY
are spongious on the cut
surface due to the Presence of
cystic fusiforme dilatation that
extend radiary to the cortex
and medulla.

29
7-

b. Malformations of the urinary tract

1 . Uni or bilateral double ureter
- the 2 ureters can fuse to a point above the
bladder junction or they may have entire
separate courses with different bladder
entrances

2.Congenital stenosis of the ureter

- the ureter lumen is congenital narrowed

30