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.
1
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. 2
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 3
persons become older.
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.

4
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 5
as with ARPKD.
Double ureters are seen exiting
from each kidney and extending to
the bladder that has been opened.
A small segment of aorta is seen
between the normal, smooth-
surfaced kidneys. A partial or
complete duplication of one or both
ureters occurs in about 1 in 150
persons. There is a potential for
obstructive problems due to the
abnormal flow of urine and the
entrance of two ureters into the
bladder in close proximity, but most
of the time this is an incidental
finding (except to a urologist).
6
Here is a "horseshoe" kidney. This is a congenital anomaly that most
often occurs in association with other anomalies or syndromes with
specific genetic defects such as trisomy 18. However, it can also
occur as an isolated anomaly. The possible problem here is that the
ureters take an abnormal course across the "bridge" of renal tissue
and this can lead to partial obstruction with hydronephrosis. 7
There is one relatively normal-sized kidney with a granular
surface and a few scattered, shallow cortical scars. The other
kidney shows atrophy because of renal arterial occlusion.
Such a situation can lead to hypertension (Goldblatt kidney).8
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. 9
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.

10
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.

11
This is an acute renal infarction. Note the wedge shape of this zone
of coagulative necrosis resulting from loss of blood supply with
resultant tissue ischemia that produces the pale infarct. The small
amount of blood supply from the capsule supplies the immediate
subcortical zone. The remaining cortex is congested, as is the
medulla. 12
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 lead13to
infarction.
This is the microscopic appearance of an acute renal infarct. At the far
right is normal kidney, then to the left of that hyperemic kidney that is
dying, then to the left of that pale pink infarcted kidney in which both 14
tubules and glomeruli are dead.
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.

15
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.

16
This is a normal glomerulus by light microscopy. The glomerular capillary loops
are thin and delicate. Endothelial and mesangial cells are normal in number.
17
The surrounding tubules are normal. Life is good.
This is an ascending bacterial infection leading to acute pyelonephritis.
Numerous PMN's are seen filling renal tubules across the center and right 18
of
this picture.
At high magnification, many neutrophils are seen in the tubules and interstitium
in a case of acute pyelonephritis. The neutrophils can collect in the distal 19
tubules and be passed in urine as WBC casts.
This PAS stain of a renal papilla with a portion of transitional lining epithelium at
the lower right demonstrates many budding cells and pseudohyphae of
Candida albicans. Fungal urinary tract infections are much less common than
bacterial infections, but both are likely to be ascending infections, having
originated in the lower urinary tract, typically bladder. 20
The large collection of chronic inflammatory cells here is in a
patient with a history of multiple recurrent urinary tract infections.
21
This is chronic pyelonephritis.
Both lymphocytes and plasma cells are seen in this case of chronic
pyelonephritis. It is not uncommon to see lymphocytes accompany just about
any chronic renal disease: glomerulonephritis, nephrosclerosis,
pyelonephritis. However, the plasma cells are most characteristic for chronic
22
pyelonephritis.
The tubular vacuolization and tubular dilation here is a result of the toxic
effect of ethylene glycol poisoning. This is representative of acute tubular
necrosis (ATN), which has many causes. ATN resulting from toxins usually
has diffuse tubular involvement, whereas ATN resulting from ischemia (as in
profound hypotension from cardiac failure) has patchy tubular involvement.23
At high power, the vasculitis is seen to involve a renal artery branch. This is a
necrotizing granulomatous vasculitis. In this case, the anti-neutrophil
cytoplasmic autoantibody (ANCA) serology was positive and a diagnosis of
Wegener granulomatosis was made. This patient also had pulmonary 24
involvement with this disease.
This is a renal biopsy at low magnification in which there is a focal lesion
centered around a blood vessel. Thus, a vasculitis is present. The one
glomerulus at the lower center appears normal. An adequate renal biopsy
should contain at least 6 glomeruli so that there is less chance that focal lesions
25
will be missed. Renal biopsies are often performed with ultrasound guidance.
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). 26
Malignant hypertension leads to fibrinoid necrosis of small renal arteries as
shown here. The damage to the arteries leads to formation of pink fibrin--hence
27
the term "fibrinoid".
Thickening of the arterial wall with malignant hypertension also is associated
with a hyperplastic arteriolosclerosis (hyperplastic arteriolitis). This arteriole has
an "onion skin" appearance. 28
This is nodular glomerulosclerosis (the Kimmelstiel-Wilson lesion) of diabetes
mellitus. Nodules of pink hyaline material form in regions of glomerular capillary
loops in the glomerulus. This is due to a marked increase in mesangial matrix
29
from damage as a result of non-enzymatic glycosylation of proteins.
This is a PAS stain of nodular glomerulosclerosis (Kimmelstiel-Wilson disease)
in a patient with long-standing diabetes mellitus. Note also the markedly
thickened arteriole at the lower right which is typical for the hyaline 30
arteriolosclerosis that is seen in diabetic kidneys as well.
The microscopic appearance of the "end stage kidney" is similar regardless of
cause, which is why a biopsy in a patient with chronic renal failure yields little
useful information. The cortex is fibrotic, the glomeruli are sclerotic, there are
scattered chronic inflammatory cell infiltrates, and the arteries are thickened.
Tubules are often dilated and filled with pink casts and give an appearance31of
"thyroidization."
This is chronic vascular rejection of a renal transplant, which has a poor
prognosis. Note the thickened arteries with intimal fibrosis and chronic
inflammation. These changes gradually occur over months in affected patients.
32
33
Chronic urate nephropathy leads to deposition of uric acid crystals in the interstitium,
forming tophi with surrounding foreign body inflammation, mononuclear cell infiltrates,
and fibrosis. The long, needle-shaped crystals form the pale mass shown here at high
magnification. Patients with hyperuricemia may also have nephrolithiasis with uric acid
stones. 34
Here is a vasculitis of a renal arterial branch. Lymphocytes are scattered in and around
the vessel. This happens to be the classic form of polyarteritis nodosa (PAN), a systemic
vasculitis that most often affects the kidneys. The ANCA serology is often negative.35
The microscopic appearance of xanthogranulomatous
pyelonephritis shows many pale to foamy macrophages from 36
breakdown of renal parenchyma with ongoing inflammation.
37
The hypercellularity of post-infectious glomerulonephritis is due to increased
numbers of epithelial, endothelial, and mesangial cells as well as neutrophils in
and around the glomerular capillary loops. This disease may follow several
weeks after infection with certain strains of group A beta hemolytic streptococci.
Patients who have had a strep infection typically have an elevated anti- 38
streptolysin O (ASO) titer.
This glomerulus is hypercellular and capillary loops are poorly
defined. This is a type of proliferative glomerulonephritis known as
post-infectious glomerulonephritis. This case followed a group A
beta hemolytic streptococcal infection of the pharynx 3 weeks 39
earlier.