At medium power, the urothelial carcinoma does resemble

urothelium, but the thickness is much greater than normal

urothelium, and the neoplastic cells show more pleomorphism.

The causative factors for urothelial carcinoma typically act upon

the entire extent of the transitional epithelium in the urinary tract,
and it is common for areas of neoplasia to arise multifocally. Seen
here is urothelial carcinoma in situ. The abnormal cells are
confined to the epithelium above the basement membrane.
This area was present in a random bladder biopsy in a patient
who also had a grossly visible lesion on cystoscopy.

Blade 060

:This bladder was removed surgically from a male who had a long
history of smoking. He had presented with hematuria. The
opened bladder reveals masses of a neoplasm that histologically
proved to be urothelial carcinoma (previously known as a
transitional cell carcinoma). Urothelial carcinoma can arise
anywhere in the urothelium lining the urinary tract from the
urethra to the calyces, but is most common in bladder. Urothelial
carcinoma is often multifocal and has a tendency to recur.

061
This bladder at autopsy has been opened to reveal areas of
hyperemia of the mucosa. This is acute cystitis

063

A urothelial carcinoma of the urothelium is shown here at low

power to reveal the frond-like papillary projections to the left of
the tumor above the surface. It is differentiated enough to
resemble urothelium, but it is producing a mass effect. No
invasion to the right is seen at this point.
064

At medium power, the urothelial carcinoma does resemble

urothelium, but the thickness is much greater than normal
urothelium, and the neoplastic cells show more pleomorphism.

069

In the bladder removed surgically and opened here can be seen

a large urothelial carcinoma. These neoplasms arise from the
urothelium. A presenting sign can often be hematuria. Cytologic
examination of urine can reveal malignant cells shed from the
surface of the neoplasm. Cystoscopy can be performed and
biopsies taken.

77

These fetal kidneys (from a gestation estimated at 25 weeks in

the second trimester) demonstrate a normal cut surface. Note
the pelvis and the calyces. Note the well-defined
corticomedullary junctions.

Renal 001
Here is a normal adult kidney. The capsule has been removed
and a pattern of fetal lobulations still persists, as it
sometimes does. The hilum at the mid left contains some
adipose tissue. At the lower right is a smooth-surfaced, small,
clear fluid-filled simple renal cyst. Such cysts occur either
singly or scattered around the renal parenchyma and are not
uncommon in adults

002
Here is a much larger simple renal cyst of the upper pole.
Other smaller cysts are also scattered around the kidney. The
ureter exits south on the left. Such a large renal cyst would be
seen on a radiographic imaging procedure, but could probably
be distinguished from a neoplasm by its uniform fluid density
and thin wall. Such simple cysts are unlikely to compromise
renal function.

005
There was a large renal calculus (stone) that obstructed the
calyces of the lower pole of this kidney, leading to a focal
hydronephrosis (dilation of the collecting system). The stasis from
the obstruction and dilation led to infection. The infection with
inflammation is characterized by the pale yellowish-tan areas
next to the dilated calyces with hyperemic mucosal surfaces.
The upper pole is normal and shows good corticomedullary
demarcations
The arrow points to the culprit in this case of hydronephrosis--
a ureteral calculus caught at the ureteropelvic junction. This
kidney demonstrates marked hydronephrosis with nearly
complete loss of cortex. Such a kidney would be non-
functional. If the other kidney had sufficient function, then renal
failure will not ensue. There is sufficient renal reserve capacity
that it is possible to survive with half of a normal kidney.
A long-standing obstruction (probably congenital) at the
ureteral orifice through which the metal probe passes led to
the marked hydroureter and hydronephrosis seen here. In the
intravenous urogram below, note the dilation of the right ureter,
compared to the normal left ureter. This patient had
vesicoureteral reflux. Such obstructive processes increase the
risk for urinary tract infection.
Acute renal arterial obstruction in this case led to massive
renal infarction in which the entire cortex is pale yellow, with
medullary hemorrhage.
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.
The end result of many renal diseases -- whether they are
renal vascular diseases, glomerulonephritis, or chronic
pyelonephritis--is end stage renal disease (ESRD). In ESRD,
the kidneys are small bilaterally, as shown here. This condition
is associated with chronic renal failure, and the patient's blood
urea nitrogen (BUN) and serum creatinine continue to
increase. Chronic renal failure can be treated by dialysis or by
kidney transplantation, as shown here
The surfaces of both kidneys demonstrate multiple
microabscesses from hematogenous spread of a bacterial
infection. The microabscesses have yellow centers and
prominent hyperemic borders.
The cut surface of the kidney reveals many small yellowish
microabscesses in both cortex and medulla. This type of
pyelonephritis is most typical for hematogenous dissemination
of infection to the kidney, rather than the more typical
ascending urinary tract infection.
In the lower pole of this kidney is a 1 cm pale yellow abscess.
Infections can reach the kidney either by ascending up the
urinary tract (from a bladder infection, for example) or by
hematogenous spread with sepsis. This lone abscess was
probably hematogenous in origin
Sometimes long-standing renal infection may be localized and
form a mass-like lesion. This is a disease known as
xanthogranulomatous pyelonephritis. It is uncommon, but may
mimic a neoplasm
In malignant nephrosclerosis, the kidney demonstrates focal
small hemorrhages. This is often due to an accelerated phase
of essential hypertension in which blood pressures are very
high (such as 300/150 mm Hg).
In this case, severe atherosclerosis in a patient with diabetes
mellitus led to severe aortic atherosclerosis with renal arterial
stenosis as well as nephrosclerosis and nodular
glomerulosclerosis of the kidneys. The end stage renal
disease was treated with renal transplantation. The transplant
kidney is placed in the pelvis because this is technically easier
and there is usually no point in trying to remove the native
kidneys. In this case, the patient developed chronic rejection
and that is why focal hemorrhages are seen in the kidney that
is slightly swollen. A radiographic study would show decreased
renal blood flow in the transplant kidney
This infant died soon after premature birth at 23 weeks
gestation from pulmonary hypoplasia as a result of
oligohydramnios. The oligohydramnios resulted from markedly
diminished fetal urine output as a consequence of polycystic
kidney disease. Note the bilaterally enlarged kidneys that
nearly fill the abdomen below the liver. The histologic
appearance in this case, coupled with the gross appearance.,
was consistent with autosomal recessive polycystic kidney
disease (ARPKD).
Here is a cut section of a kidney with autosomal recessive
polycystic kidney disease (ARPKD). Note that the cysts are
fairly small but uniformly distributed throughout the
parenchyma so that the disease is usually symmetrical in
appearance, with both kidneys markedly enlarged. The
recurrence risk for this disease is, of course, 25% because of
the autosomal recessive inheritance pattern. Affected babies
usually do not survive long. This disorder is linked to an
abnormal fibrocystin protein produced by the PKHD1 gene.
You're right, this isn't kidney, but remember that autosomal
recessive polycystic kidney disease also manifests with
congenital hepatic fibrosis, as seen here in which a portal area
is expanded with increased bile ducts radially arranged around
the perimeter. The abnormal fibrocysin protein product of the
mutated PKHD1 gene affects liver and pancreas as well as
kidney. The many dark clusters of cells in the hepatic
parenchyma are islands of extramedullary hematopoiesis
typical for fetal liver.
This is a multicystic dysplastic kidney. This condition must be
distinguished from ARPKD because it occurs only sporadically
and not with a defined inheritance pattern, though it is more
common than ARPKD. The cysts of multicystic renal dysplasia
are larger and more variably sized than those of ARPKD.
Often, multicystic renal dysplasia is unilateral. If bilateral, it is
often asymmetric. If bilateral, oligohydramnios and its
complications can ensue, just as with ARPKD.
A multicystic dysplastic kidney (also known as cystic renal
dysplasia) has been sectioned to reveal the variably sized
cysts that replace the renal parenchyma. In this case, the
disease was unilateral and presented in infancy as a mass
lesion which was removed surgically. Even with one kidney,
there is enough renal reserve capacity to live a normal life.

You may see references to polycystic kidney disease that

include Potter's classification. Type I is RPKD, type II is
multicystic dysplastic kidney, type III is dominant polycystic
kidney disease (DPKD), and type IV is cystic change with
congenital urinary tract obstructions
The cut surfaces of these kidneys in a patient with ADPKD
reveal that the parenchyma is replaced by large cysts. Note
how large these kidneys are in relation to the normal sized
transplanted kidney.
The contents of the chest and peritoneal cavity have been
removed at autopsy here to reveal markedly bilaterally
enlarged kidneys in the retroperitoneum in an adult who died
from complications of chronic renal failure. This patient had
autosomal dominant polycystic kidney disease (ADPKD).
This kidney in a patient with ADPKD weighed 3 kilograms! This
disease is inherited with an autosomal dominant pattern, so
the recurrence risk in the family is 50%. The cysts are not
usually present at birth, but develop slowly over time, so the
onset of renal failure occurs in middle age to later adult life.
These adult kidneys are about normal in size but have a few
scattered small cysts, none of which is over 2 cm in size. This
is cystic change associated with chronic renal dialysis.

The multiple irregular bilateral masses (many of which show

central indentations, or "umbilications", from necrosis) here
represent metastases of carcinoma to the kidneys. Kidney is
not a usual site for metastases.

This renal cell carcinoma is very large, as indicated by the 15

cm ruler. A portion of normal kidney protrudes at the lower
center. This patient was a physician himself and just didn't
have any early symptoms
Here is a renal cell carcinoma that on sectioning is mainly
cystic with extensive hemorrhage. Sometimes large simple
renal cysts may develop hemorrhage and mimic this
appearance.
Here is another example of urothelial carcinoma that is more
aggressive and is invading into the renal parenchyma, causing
obstruction of pelvis and calyces to produce hydronephrosis.
Hematuria is a frequent presenting symptom.
This small kidney from a 4 year old child contains a lobulated
tan-white mass. This is Wilms tumor of the kidney. Many are
now known to be associated with genetic defects on
chromosome 11. The children with Wilms tumor usually
present with abdominal enlargement from the mass effect.
Nowadays, treatment gives a better than 90% 5 year survival.
This is a Wilms tumor that is composed microscopically of
nests and sheets of dark blue cells at the left with compressed
normal renal parenchyma at the right

Wilms tumor resembles the fetal nephrogenic zone of the

kidney. The tumor shows attempts to form primitive glomerular
and tubular structures.
Renal cell carcinomas have a tendency to invade into the
renal vein, as shown here at the white arrow in a resected
kidney surrounded by adipose tissue. They may even crawl up
the vena cava and into the heart, but even these can be
removed! Here, the tumor extended up the vena cava and
occluded the adrenal vein, leading to hemorrhagic adrenal
infarction in the adrenal at the top of the specimen. Renal cell
carcinomas may invade through the renal capsule. Renal cell
carcinomas may metastasize to odd locations, and about a
fourth of them first present as metastatic lesions.
This is the classic histologic appearance of a renal cell
carcinoma: the neoplastic cells have clear cytoplasm and are
arranged in nests with intervening blood vessels. This
microscopic appearance is why they are often called "clear cell
carcinomas".
This is a renal cell carcinoma arising in the lower pole of the
kidney. It is fairly circumscribed. The cut surface demonstrates
a variegated appearance with yellowish areas, white areas,
brown areas, and hemorrhagic red areas. Though these
neoplasms are usually slow-growing, they can often reach a
considerable size before detection because there is a lot of
room to enlarge in the retroperitoneum, and there is another
kidney to provide renal function. Thus, presenting symptoms
and signs usually include flank pain, mass effect, and
hematuria
The cut surfaces of the kidney removed surgically here
demonstrate normal cortex and medulla, but the calyces show
focal papillary tumor masses of urothelial carcinoma.

This trichrome stain of a glomerulus in a patient with focal

segmental glomerulosclerosis (FSGS) demonstrates blue
collagen deposition. FSGS accounts for about a sixth of cases
of nephrotic syndrome in adults and in children
A silver stain of the glomerulus highlights the proteinaceous
basement membranes in black. There are characteristic
"spikes" seen with membranous glomerulonephritis seen here
in which the black basement membrane material appears as
projections around the capillary loops

Seen here within the glomeruli are crescents composed of

proliferating epithelial cells. Crescentic glomerulonephritis is
known as rapidly progressive glomerulonephritis (RPGN)
because this disease is very progressive. There are several
causes, and in this case is due to SLE. Note in the lower left
glomerulus that the capillary loops are markedly thickened (the
so-called "wire loop" lesion of lupus nephritis).

This is IgA nephropathy (Berger disease). The IgA is deposited

mainly within the mesangium, which then increases mesangial
cellularity as shown at the arrow. Patients with IgA
nephropathy usually present with hematuria.
This is a type of hereditary nephritis known as Alport syndrome in
which patients may also manifest nerve deafness and eye
problems. The renal tubular cells appear foamy because of the
accumulation of neutral fats and mucopolysaccharides. The
glomeruli show irregular thickening and splitting of basement
membranes.

This is a normal glomerulus by light microscopy. The

glomerular capillary loops are thin and delicate. Endothelial
and mesangial cells are normal in number. The surrounding
tubules are normal. Life is good.

Here is another glomerulus with epithelial crescents

squashing the glomerular tufts from all sides. RPGN may be
idiopathic or may result from SLE, post-infectious GN (as in
some cases of post-infectious GN), from various types of
vasculitis, and from Goodpasture syndrome.
This is the low power microscopic appearance of an
angiomylolipoma. There is normal renal parenchyma at the
left. The tumor has a strip of adipose tissue (the "lipoma" part)
that then blends in with interlacing bundles of smooth muscle
(the "myo" component) in which are scattered vascular spaces
(the "angio" component).

This kidney was removed because of acute transplant

rejection. Note the swollen and hemorrhagic appearance of
this entire kidney

These are normal term infant kidneys. Note the presence of

fetal lobulations and the smooth cortical surfaces with some
attached adipose tissue.
This rare neoplasm of the kidney is called angiomyolipoma.
Note that it is solid and has a tan to yellowish-tan cut surface.
It is also multifocal (a smaller nodule appears in the upper
pole. Most of these tumors are incidental findings, but persons
with a rare condition known as tuberous sclerosis often have
these tumors. [Image contributed by John Nicholls, MD, Hong
Kong University
In cross section, this normal adult kidney demonstrates the lighter
outer cortex and the darker medulla, with the renal pyramids
into which the collecting ducts coalesce and drain into the
calyces and central pelvis.

This is chronic urate nephropathy with pale yellowish tan

tophaceous deposits in the medulla. There is also an acute
urate nephropathy that can occur with a "lysis" syndrome
reulting from massive cellular necrosis of leukemia or
lymphoma cells with chemotherapy. The metabolic breakdown
of the cell nuclei yields large amounts of urate which, when
excreted, plug renal tubules

Simple renal cysts, as seen here, can also be multiple, but

they are never as numerous as with polycystic change, and
they do not predispose to chronic renal failure or to neoplasia.
Such simple cysts become more common as persons become
older.
The small bumps seen here over the ureteral mucosa are
called ureteritis cystica and represent cystic areas of glandular
metaplasia resulting from inflammation. They are more
commonly seen in the bladder, where they are called cystitis
cystica

Cystic change resulting from long-term renal dialysis may

rarely give rise to renal cell carcinoma. A large variegated
mass is seen here on sectioning of a kidney that has large
cysts arranged around the mass.

This small round white nodule in the medulla is an incidental

autopsy finding known as a medullary fibroma, also called a
renomedullary interstitial cell tumor, a designation larger in
size than its importance. They are generally 0.5 cm in size or
less and are not associated with any renal diseases.
This silver stain demonstrates a double contour to many
basement membranes, or the "tram-tracking" that is
characteristic of membranoproliferative glomerulonephritis
(MPGN) type I that results from basement membrane
reduplication.

The pale white areas involving some or all of many renal

papillae are areas of papillary necrosis. This is an
uncommon but severe complication of acute pyelonephritis,
particularly in persons with diabetes mellitus. Papillary
necrosis may also accompany analgesic nephropathy. [Image
courtesy of Dr. John Nicholls, Hong Kong University

Sometimes a very large calculus nearly fills the calyceal system,

with extensions into calyces that give the appearance of a stag's
(deer) horns. Hence, the name "staghorn calculus". Seen here is
a horn-like stone extending into a dilated calyx, with nearly
unrecognizable overlying renal cortex from severe
hydronephrosis and pyelonephritis. Nephrectomy may be
performed because the kidney is non-functional and serves only
as a source for infection.
And finally, if all else fails, call it "chronic glomerulonephritis".
Seen here are atrophic kidneys with a thin cortex from a
patient at autopsy with chronic renal failure (CRF). About a
third to half of patients with CRF slowly reach end stage
without significant signs or symptoms along the way, and at
the end stage renal disease (ESRD) there are no diagnostic
features and, therefore, no point in performing a renal biopsy.
A steadily rising serum creatinine and urea nitrogen are clues.
Most patients will also be hypertensive. (Some simple cysts
are also seen here.)
There is scarring of this kidney from chronic obstruction and
pyelonephritis. The renal pelvis is markedly dilated, but the
ureter is not, indicating that the point of obstruction is the
ureteropelvic junction.