ANNALYN S. DA-ANOY , M.D. , R.M.T.

Azotemia vs. Uremia

 Biochemical abnormality  Azotemia

 Elevated BUN +
 Elevated creatinine clinical signs &
symptoms
Nephrotic Syndrome

1. Massive proteinuria (3.5 gms or

more/day)

2. Hypoalbuminemia (less than 3 gm/dl)

3. Generalized edema

4. Hyperlipidemia & lipiduria

Nephritic vs.
Nephrotic
 Hematuria  Heavy proteinuria
 Mild to moderate  Hypoalbuminemia
proteinuria  Severe edema
 Hypertension  Hyperlipidemia
 Lipiduria
Diabetes Mellitus

1. Capillary basement membrane thickening

2. Diffuse mesangial sclerosis
- diffuse increase in mesangial matrix
3. Nodular glomerulosclerosis Syn:
intercapillary glomerulosclerosis
Kimmelsteil-Wilson lesion
- ball-like deposits of laminated matrix 
enlarge & compress capillaries  renal ischemia
& tubular atrophy
4. Renal atherosclerosis/arteriosclerosis
5. Pyelonephritis, necrotizing papillitis
DM: Nodular Glomerulosclerosis
ADPKD

 Bilateral; adults
 Mutations in:
 PKD1 (polycystin-1)
 PKD2 (polycystin-2)

 Cysts & anomalies in other organs:

 Liver, spleen, pancreas
 Intracranial berry aneurysm
 Mitral valve prolapse
ADPKD

 Enlarged kidneys made up of cysts

 PKD1 mutation more common, with earlier
onset of renal failure
Slide# 81 Polycystic Kidney Disease (Adult
type)
Tubulointerstitial Nephritis

 ACUTE  CHRONIC
- Rapid clinical onset - Mononuclear leukocytes
- Interstitial edema - Interstitial fibrosis
- Neutrophils & eos in - Widespread tubular atrophy
interstitium & tubules
- Focal tubular necrosis
Pyelonephritis & UTI

 Gram-neg bacilli (>85%)

 E. coli, Proteus, Klebsiella, Enterobacter
 from fecal flora in most patients

 Routes of Infection
1. Hematogenous
2. Ascending (more common)
Papillary Necrosis
Acute Pyelonephritis -
Complications
1. Papillary necrosis
 In diabetics & those with urinary tract obstruction
 Usually bilateral
 Necrosis of tips or distal 2/3 of the pyramids
2. Pyonephrosis
 Pus is not drained & fills the renal pelvis, calyces &
ureters

3. Perinephric abscess
 Suppurative inflammation extends through the renal
capsule into the perinephric tissue
Chronic Pyelonephritis

 Chronic tubulointerstitial inflammation &

scarring with involvement of the pelvis &
calyces

 2 types:
1. Reflux nephropathy
- Renal involvement occurs during childhood
2. Chronic obstructive pyelonephritis
- Effects are due to infection and obstruction
Chronic Pyelonephritis -
Morphology
 Gross:
 Asymmetric involvement
 Irregular scars – coarse, discrete, corticomedullary scars
overlying blunted or deformed calyces

 Microscopic:
 Tubular atrophy with dilatation & hypertrophy in others
 Thyroidization
 Chronic interstitial inflammation
 fibrosis
Slide#161 Acute and Chronic
Pyelonephritis
RIGHT LEFT 70 GRAMS
60 GRAMS
Slide# 61 Hydronephrosis with severe
acute
and chronic pyelonephritis
Slide#172 Tuberculous Pyelonephritis
 Slide#172 Tuberculous
Pyelonephritis
Diseases of the Blood
Vessels
1. Benign nephrosclerosis
2. Malignant nephrosclerosis
3. Renal artery stenosis
4. Thrombotic microangiopathies
5. Others
Benign Nephrosclerosis

 Medial & intimal thickening

 Hyaline deposition (protein extravasation &

increased deposition of basement membrane
matrix)

 Vascular narrowing  patchy ischemic

atrophy
HYALINE ARTERIOLOSCLEROSIS
HYALINE ATHEROLOSCLEROSIS
Slide#214 Chronic Pyelonephritis with
arterio and arteriolonephrosclerosis
AKI

 Destruction of tubular epithelial cells

 Acute diminution or loss of renal

function

 Most common cause of ARF

ACUTE TUBULAR
NECROSIS

Necrotic & detached tubular

epithelial cells

Swollen, vacuolated epithelial cells

SLIDE 62 Renal infarction
Slide#62 Renal Infarction

Infarcted area
Slide# 34 Wilm’s Tumor
(Nephroblastoma)
Slide# 34 Wilm’s Tumor
(Nephroblastoma)
Slide# 34 Wilm’s Tumor
(Nephroblastoma)
Tumors – Malignant

1. Renal cell carcinoma

- adenocarcinoma of the kidneys -
hypernephroma

2. Urothelial Carcinoma
Renal Cell Carcinoma:
Risk Factors
1. Cigarette-smoking
2. Obesity
3. Hypertension
4. Unopposed estrogen therapy
5. Exposure to asbestos, petroleum products &
heavy metals
Renal Cell Carcinoma:
Major Types

1. Clear cell carcinoma (70% - 90%)

2. Papillary carcinoma (10% - 15%)
3. Chromophobe renal cell carcinoma (5%)
4. Collecting duct carcinoma (<1%)
Renal Cell Carcinoma:
Morphology
 Gross:
 Poles (upper > lower)
 Solitary, spherical mass
 Bright yellow to gray-white
 Areas of ischemic necrosis, hemorrhagic
discoloration, and softening
 Tendency to invade renal vein
 Papillary Carcinoma:
 Multifocal
 Hemorrhagic & cystic
Slide# 27 Clear cell Carcinoma,
Kidney
Renal Cell Carcinoma:
Clinical Features
 costovertebral pain, palpable mass,
hematuria (10%)
 paraneoplastic syndromes – mimic
 Tends to metastasize widely before giving
rise to local s/sx
 Lungs (>50%)
 Bones (33%)
 5 yr SR = 45%
Urothelial Carcinoma

 From the urothelium of the renal pelvis

 May be multiple (pelvis, ureter, bladder)
Urothelial
Carcinoma
 Histology of the normal
bladder.
•The lumen of the bladder
(L) is on the left.
•Lining the bladder wall is
the epithelium (Ep).
•The loose connective
tissue beneath the
epithelium is the lamina
propria (LP).
•The bladder musculature
is labeled (Mus).
NORMAL UROTHELIUM
 a resected bladder which
has been opened to reveal
the mucosal surface.
 There is a large , irregular,
nodular, and hemorrhagic
surface
 contrasts with the normal
smooth, glistening tan
mucosa with regular folds
seen in the center of the
specimen
Slide#181 Urothelial Carcinoma, Low
grade
Slide#181 Urothelial
Carcinoma, Low grade
HIGH GRADE UROTHELIAL
CARCINOMA , BLADDER
Slide# 248 Urothelial Cell Carcinoma,
High Grade
High grade papillary urothelial
carcinoma. At low
magnification there is focal
necrosis, a feature not seen
with lower grade lesions.
Slide# 248 Urothelial Cell
Carcinoma, High Grade
 This acute renal infarction is
pale, typical of coagulative
necrosis. It is roughly
wedge-shaped. Renal
infarctions usually result
from embolization of
cardiac valvular vegetations
or a portion of cardiac
mural thrombus.
Sometimes a renal arterial
vasculitis can lead to
infarction.
 This gross photograph is of
a resected bladder which
has been opened to reveal
the mucosal surface. There
is a large invasive
transitional cell carcinoma
which can be recognised by
its irregular, nodular, and
hemorrhagic surface which
contrasts with the normal
smooth, glistening tan
mucosa with regular folds
seen in the center of the
specimen
High grade papillary urothelial
carcinoma. At low
magnification there is focal
necrosis, a feature not seen
with lower grade lesions.
 Urothelium: formerly called
transitional epithelium
since intermediate between
nonkeratinizing squamous
and pseudostratified
columnar epithelium; 5-7
cell layers thick in
contracted bladder, 2-3
cells thick in distended
bladder; lines renal pelvis,
ureters, bladder, most of
urethra but not terminal
urethra
 Histology of the normal
bladder.
•The lumen of the bladder
(L) is on the left.
•Lining the bladder wall is
the epithelium (Ep).
•The loose connective
tissue beneath the
epithelium is the lamina
propria (LP).
•The bladder musculature
is labeled (Mus).
 The enlarged prostate
gland seen here not only
has enlarged lateral lobes,
but also a greatly enlarged
median lobe that obstructs
the prostatic urethra. This
led to obstruction with
bladder hypertrophy, as
evidenced by the
prominent trabeculation of
the bladder wall seen here
from the mucosal surface.
Obstruction with stasis also
led to the formation of the
yellow-brown calculus
(stone).
 Obstruction from nodular
prostatic hyperplasia has
led to prominent
trabeculation seen on the
mucosal surface of this
bladder with hypertrophy.
The stasis from obstruction
predisposes to infection.
The obstruction can also
lead to bilateral
hydroureter and
hydronephrosis.
NORMAL UROTHELIUM
 This gross photograph
shows the cut surface of a
kidney which has been
longitudinally bisected.
There is a large renal cell
carcinoma in the upper pole
with a typical variegated
appearance with bright
yellow areas, areas of
hemorrhage, and tan and
white areas. The bright
yellow color is related to
the lipid content in these
tumors.
 The typical "clear cell"
appearance of many renal
cell carcinomas is illustrated
in this photomicrograph.
The malignant cells have
abundant clear or empty
appearing cytoplasm, and
the delicate lobular growth
pattern is a result of the
numerous capillaries
between clusters of cancer
cells.
RENAL PRE-LAB ACTIVITY
1 A. AND B.

 DEFINE AZOTEMIA AND UREMIA

2. A AND B.

2A.GIVE THE
DIAGNOSIS
2B.GIVE THE MOST
COMMON
HISTOLOGIC
SUBTYPE OF THIS
TUMOR.
3A. AND 3.B.
3.A.GIVE THE
DIAGNOSIS.

3.B. TRUE OR FALSE

This tumor produce
noticeable hematuria.
4.A and B.
CASE OF A 1 YO INFANT
,RENAL MASS
4.A and B.

 A. GIVE THE DIAGNOSIS

 B. TRUE OR FALSE
THIS TUMOR HAS A GOOD
PROGNOSIS.
5.A AND B.
5. A AND B.

A. GIVE THE DIAGNOSIS

B. GIVE THE MOST COMMON ROUTE OF
INFECTION.
6. A AND B.

 DIFFERENTIATE NEPHRITIC AND

NEPHROTIC SYNDROME?