Definitions of glomerular

pathology
Diffuse: more than 50% of sampled
glomeruli are abnormal
Focal: less than 50% of sampled glomeruli
are abnormal
Segmental: Only a portion of an individual
glomerulus is abnormal
Global: The entire individual glomerulus is
abnormal.
Review of the biopsy specimen
• Glomerulus: Diffuse/focal. Segmental/global.
• Endothelium, glomerular basement
membrane, podocyte, mesangium (cells and
matrix), urinary space, Bowman’s capsule.
• Interstitium: Tubules, casts, fibrosis,
inflammatory infiltrate, arterioles
• Light, immunofluorescence, and electron
microscopy constitute a full biopsy
 DT
PT

P DT
T

e
MD PT
DT
Proliferative pattern
Membranous pattern
Membranoproliferative pattern
Crescentic (RPGN) necrosis
Sclerotic pattern
Minimal Change Disease
Normal light microscopy
Fig 2. The glomerular basement membrane is of normal thickness without deposits in this case of
minimal change disease. The visceral epithelial cells show diffuse effacement of foot processes. An
area of microvillous transformation is also present, representing the irregular epithelial-cell surface that
occurs in proteinuric states. Foot-process effacement is generally quite extensive in minimal change
disease, although the degree of foot-process effacement cannot be used to definitively distinguish
minimal change disease from unsampled FSGS
One of the two glomeruli shown contains two small peripheral foci of segmental sclerosis with
intracapillary foam cells and prominence of overlying visceral epithelial cells. This is
representative of an early segmental sclerosing lesion in focal segmental glomerulosclerosis
(FSGS). There is also surrounding mild interstitial fibrosis, and the glomerulus that is sclerosed
is mildly enlarged. Of note, significant glomerular-size increase, even without segmental
sclerosis, is an indicator of possible unsampled or evolving FSGS. (Jones' silver stain, X100).
In this biopsy, the segmental sclerotic lesion on the right with FSGS is composed of
obliteration of capillary lumens and increased mesangial matrix. The remaining portion of
the glomerular tuft appears unremarkable, without basement membrane changes or any
apparent deposits. The visceral epithelial cells overlying this early sclerotic lesion appear
activated. (Jones' silver stain, X400).
Immunofluorescence studies in cases of FSGS may show immunoglobulin (Ig) M in mesangial
areas or in areas of hyalinosis (smooth, globular staining on right).
The mesangial matrix is mildly increased without deposits in this case of FSGS.
Endothelial cells are unremarkable, and visceral epithelial cells show extensive blunting
and effacement of foot processes with early microvillous transformation. Occasional
vacuolization and blebbing is also present in the visceral epithelial cells. No immune
complexes are present.
The collapsing pattern in collapsing glomerulopathy is evident here, with an
accentuation of each lobule due to the collapse of the tufts. There is also overlying
glomerular visceral epithelial cells.
The localized sclerotic lesion that only involves the proximal tubular pole of the
glomerulus has been classified as the tip lesion, with some evidence suggesting
a better prognosis than typical FSGS .
The sclerotic lesion here is sharply localized to the proximal tubular pole, with adhesion and
continuity of the capillary loop to Bowman's capsule, and intercapillary foam cells localized to
this area, characteristic of the so-called tip lesion variant of FSGS
Glomeruli may show normal appearance, have varying mesangial proliferation, or even
segmental sclerosis by light microscopy in C1q nephropathy. This glomerulus shows mild
mesangial hypercellularity with minimal increase in the matrix.
Immunofluorescence shows mesangial or even paramesangial staining for C1q in
C1q nephropathy, typically with lesser intensity staining for immunoglobulin (Ig)
and C3. The immunofluorescence findings in C1q nephropathy are crucial in
making the diagnosis and ruling out possible IgA nephropathy .
Electron microscopic studies in C1q nephropathy confirm mesangial deposits
underlying the basement membrane as it traverses over the mesangial area.
There are no reticular aggregates present, a feature useful in distinguishing this
from possible lupus nephritis
The thickened capillary wall shows numerous "holes" in tangential sections, indicating deposits.
(Deposits do not take up the silver stain.) Well-developed spikes around the deposits are not
present in this early stage II membranous glomerulonephritis, but segmental, small nubs of
silver-stained basement membrane material protruding from the basement membrane contour
on the epithelial side can be seen (Jones' silver stain, original magnification x400).
High-power oil-immersion view of the markedly thickened capillary wall in (A) stage II-III and (B) stage III
membranous glomerulonephritis. Well-developed spikes of basement membrane silver-staining material
protrude from the basement membrane. In tangential sections, holes are seen, indicating the presence of the
silver-negative deposits. In stage III, some of the deposits are completely surrounded by basement
membrane, and the basement membrane appears split in these areas (Jones' silver stain, original
magnification x1,000).
Diffuse finely granular capillary wall IgG deposits in stage I
membranous glomerulonephritis (immunofluorescence with
anti-IgG, original magnification x200).
Diffuse coarsely granular capillary wall IgG deposits in stage II-III
membranous glomerulonephritis (immunofluorescence with anti-IgG,
original magnification x100).
Medium-sized dense deposits on the epithelial side of the basement membrane
(subepithelial) with occasional early basement membrane reaction, late stage I
membranous glomerulonephritis (transmission electron microscopy, original
magnification x10,200).
Stage II-III membranous glomerulonephritis with thickened capillary wall resulting from numerous medium to
large subepithelial dense deposits and basement membrane reaction. Basement membrane–like material
surrounds some of the deposits, a feature of stage III membranous glomerulonephritis, whereas most of the
deposits still only have basement membrane reaction around the side (stage II lesion)(
Secondary membranous glomerulonephritis with numerous subepithelial deposits
(stage II) and mesangial deposits. In this case, the likely underlying etiology was
hepatitis B infection (see Fig 5 above)
Extensive double contours of the glomerular basement membranes, stained by silver, in
membranoproliferative glomerulonephritis type 1, caused by mesangial interposition and new basement
membrane formation in response to subendothelial immune complex deposits. The deposits are PAS
positive and globular-to-sausage shaped (Jones' silver stain; original magnification, x400).
Segmental, coarsely granular-to-globular or elongated capillary wall
IgG deposits in membranoproliferative glomerulonephritis type 1
Membranoproliferative glomerulonephritis type 1 with multiple,
large subendothelial deposits
Dense deposit disease is also called membranoproliferative glomerulonephritis type 2 based on the
similar light microscopic findings in the two conditions. Mesangial proliferation, double countours of the
glomerular basement membrane, and mesangial interposition are evident in this figure. No obvious
deposits, which typically appear pink on this PAS-methenamine silver stain, are visualized. The refractile,
ribbon-like appearance of the basement membrane is a clue to the correct diagnosis of dense deposit
disease, which is confirmed by immunoflurorescence and electron microscopy (Jones' silver stain;
original magnification, x400).
Dense deposit disease also may show large, globular mesangial staining for C3, in
addition to the capillary wall staining (immunofluorescence with anti-C3; original
magnification, x400).   
Dense deposit disease with dense transformation of the glomerular basement
membrane, endocapillary proliferation and large, globular mesangial densities
(transmission electron micrograph; original magnification, x4600). 
Dense deposit disease showing dense transformation of virtually the entire width
of the glomerular basement membrane (transmission electron micrograph;
original magnification, x8000).  
Fibrillary glomerulonephritis has varying appearances by light microscopy, with mild to
extensive mesangial proliferative and membranoproliferative appearance being the
most common. In this case, there was a distinct membranoproliferative and even
nodular appearance
Fibrillary glomerulonephritis may have varying degrees of mesangial proliferation or
membranoproliferative pattern by light microscopy. In this case, there was moderate
mesangial proliferation and occasional basement membrane splitting. Additional
studies confirmed the diagnosis of fibrillary glomerulonephritis with typical electron
microscopy appearance, negative Congo red stain, and IgG staining by
immunofluorescence
In approximately one third of cases seen in our series of fibrillary glomerulonephritis,
crescents were present, as in this case. In some of these, confluent deposits caused
immunofluorescence to have a pseudolinear appearance, which could give rise to
diagnostic confusion until electron microscopy is examined
Immunofluorescence studies in fibrillary glomerulonephritis are striking and
characteristic with smudgy positivity in mesangial and capillary loop areas. The
mesangial staining most commonly is more extensive than the capillary loop staining,
and the typical smudginess allows suspicion of fibrillary glomerulonephritis. The most
common staining is IgG, with IgG4 subtype typically being most prominent (anti-IgG
immunofluorescence; original magnification x400).
The diagnosis of fibrillary glomerulonephritis is ultimately made by electron microscopy,
which shows randomly arranged fibrils in mesangial and capillary loop areas with an
intramembranous, subepithelial, and/or subendothelial location. Negative Congo red
stains are necessary to specifically exclude the possibility of amyloid (transmission
electron microscopy; original magnification x25,625).
High-power view of fibrils in fibrillary glomerulonephritis, illustrating slightly coarser
diameter than in amyloid. The fibrils are randomly arranged in the loose background. A
negative Congo red stain is necessary to definitively rule out amyloid deposits,
although fibrillary glomerulonephritis can be suspected from the characteristic
immunofluorescence microscopy and the slightly larger fibril size
Immunotactoid glomerulopathy typically shows mesangial proliferation or a
membranoproliferative pattern by light microscopy, as in this case. There is widespread
splitting of the glomerular basement membrane and increased mesangial matrix, with
thickened Bowman's capsule and adhesions of the tuft to Bowman's capsule
Immunotactoid glomerulopathy shows positivity for IgG and rarely other
immunoglobulins, along with complement. The positivity is in a segmental capillary
loop distribution, along with mesangial positivity, mirroring the distribution of deposits
by light microscopy. Deposits more typically are polyclonal, although there may be
predominance of one light chain, as in this case, where there was predominant IgG
kappa staining, but with concomitant lambda staining (anti-kappa antibody, x 400).
Immunotactoid glomerulopathy is defined, in our view, by the presence of organized
deposits by electron microscopy, which show stacking in parallel arrays and/or
microtubular substructure. This morphology may be seen in immunotactoid
glomerulopathy, or be associated with paraproteins such as cryoglobulin (see
Cryoglobulinemic Glomerulonephritis section). In this case there are massive mesangial
and subendothelial deposits with deposits organized in parallel arrays, some cut
longitudinally and some cut in cross-section. The microtubules are quite large, close to 50
nm in diameter (transmission electron microscopy, x 4,000).
Immunotactoid glomerulopathy deposits show organized structure by electron microscopy,
either organized in parallel arrays, and/or with microtubular substructure. Some deposits
are cut in cross-section, clearly revealing the microtubular substructure, whereas others,
stacked in adjacent parallel arrays, are cut longitudinally. These deposits permeate the
glomerular basement membrane; there is complete overlying effacement of foot processes
on the left
Nephritic syndrome
Glomeruli show diffuse hypercellularity due to mesangial and
endothelial cell increase and a large number of
polymorphonuclear neutrophils (PMNs). These light microscopic
findings are typical of diffuse proliferative acute postinfectious
glomerulonephritis
Diffuse proliferative acute postinfectious glomerulonephritis with
numerous PMNs with PAS-positive cytoplasm and endocapillary
proliferation
The large number of PMNs typical of acute poststreptococcal glomerulonephritis is
evident in this high-power silver stain. The glomerular basement membrane does not
show splitting or spikes. There is endocapillary proliferation, ie, proliferation of
endothelial and mesangial cells and infiltrating cells in addition to filling and
distending capillary loops. The large number of PMNs is characteristic of
postinfectious glomerulonephritis, with the prototype being poststreptococcal
glomerulonephritis
Crescents may occasionally be found in diffuse proliferative acute postinfectious
glomerulonephritis, particularly in those patients who undergo renal biopsy when
spontaneous resolution does not occur. The crescent in this case has ruptured
Bowman's capsule, and there is an intense lymphoplasmocytic interstitial infiltrate
surrounding the glomerulus
Acute postinfectious glomerulonephritis by immunofluorescence
typically shows irregular capillary loop deposits staining for IgG,
seen here, or C3
Large, subepithelial, hump-like scattered deposits in acute postinfectious
glomerulonephritis. The deposits are irregularly spaced and frequently mottled, and they sit
on top of the basement membrane with little, if any, basement membrane reaction
IgA nephropathy with minimal increase in mesangial matrix and cells (normal is less than
or equal to 3 cells/mesangial area). The diagnosis must rely on additional
immunofluorescence and electron microscopic studies ([A] periodic acid-Schiff, original
magnification x200; [B] Jones' silver stain, original magnification x400 ).
IgA nephropathy with moderate mesangial expansion with increased matrix and cells ([A]
periodic acid-Schiff; [B] Jones' silver stain; original magnification for each x200).
IgA nephropathy may have superimposed segmental sclerosis in addition to variable mesangial
increase. (A) A small peripheral sclerotic lesion with adhesion is present; (B) more advanced
segmental sclerosis is shown
The diagnosis of IgA nephropathy rests on the finding of dominant or codominant IgA
mesangial deposits, as shown here. Staining may also be present for IgG and IgM, but not
in greater intensity than for IgA. C3 is also often present in the mesangial areas, usually
equal to or less than IgA staining
Mesangial electron dense deposits and increased mesangial matrix
and cellularity in IgA nephropathy
Marked increase in mesangial cellularity and matrix with massive mesangial dense
deposits, with some extension of deposits to paramesangial areas. (Left) There is also
interposition of cells in the glomerular basement membrane with new basement membrane
formation on the endothelial aspect of the interposed cells
Fibrillary glomerulonephritis has varying appearances by light
microscopy, with mild to extensive mesangial proliferative and
membranoproliferative appearance being the most common.
striking and characteristic with smudgy positivity in mesangial
and capillary loop areas. The mesangial staining most commonly
is more extensive than the capillary loop staining, and the typical
smudginess allows suspicion of fibrillary glomerulonephritis. The
most common staining is IgG
The diagnosis of fibrillary glomerulonephritis is ultimately made by
electron microscopy, which shows randomly arranged fibrils in mesangial
and capillary loop areas with an intramembranous, subepithelial, and/or
subendothelial location. Negative Congo red stains are necessary to
specifically exclude the possibility of amyloid .
The fibrils are randomly oriented and somewhat larger than in
amyloid, 12 to 15 nm. A negative Congo red stain is necessary to
definitively rule out amyloid deposits, although fibrillary
glomerulonephritis can be suspected from the characteristic
immunofluorescence microscopy and the slightly larger fibril size
Immunotactoid glomerulopathy is defined by the presence of
organized deposits by electron microscopy, which show stacking in
parallel arrays and/or microtubular substructure. This morphology
may be seen in immunotactoid glomerulopathy, or be associated
with paraproteins such as cryoglobulin. The microtubules are quite
large, close to 50 nm in diameter
 Glomerular Diseases That
Cause Hematuria Or Nephritic
Syndrome
PIGN; IgA; H-S Purpura
Diffuse proliferative acute postinfectious glomerulonephritis
with numerous PMNs with PAS-positive cytoplasm and
endocapillary proliferation
Crescents may occasionally be found in diffuse proliferative acute
postinfectious glomerulonephritis, particularly in those patients
who undergo renal biopsy when spontaneous resolution does not
occur.
PIGN: immunofluorescence typically shows
irregular capillary loop deposits staining for IgG,
seen here, or C3. (Lumpy-bumpy/starry sky)
Large, subepithelial, hump-like scattered deposits in acute
postinfectious glomerulonephritis.
 IgA

IgA nephropathy with Mild (left) and moderate

mesangial expansion with increased matrix and cells
The diagnosis of IgA nephropathy rests on the finding of
dominant or codominant IgA mesangial deposits
Mesangial electron dense deposits and increased mesangial matrix
and cellularity in IgA nephropathy
Henoch-Schönlein purpura (HSP) also has mesangial IgA
deposits, and thus it appears morphologically like IgA
nephropathy. Clinicopathological correlation is required to
distinguish HSP from IgA nephropathy, but crescents, shown
here, are more frequent in biopsied HSP than in IgA
 Amyloid

Acellular eosinophilic material is typical of amyloid deposits and may be

found in mesangial areas or peripheral capillary loops within the
glomerulus. In a severe case of amyloidosis, massive distention of
mesangial areas and distortion of peripheral capillary loops. (Shown on
right)
Congo red stain is viewed under polarized light, areas of
amyloid show apple green birefringence.
By electron microscopy, amyloid appears as randomly
oriented thin fibrils, 10 to 12 nm in diameter, with a loose,
flocculent background.
 LCDD

A nodular glomerulosclerosis, which strongly resembles diabetic nephropathy

Glomerular capillary loop, mesangial staining, and linear
tubular staining are characteristic of light chain deposition
disease. Either kappa or lambda light chain paraprotein may
cause light chain deposition disease, although kappa more
commonly is the culprit
The granular, amorphous deposits typical of light chain deposition
disease are seen as silt-like material on the endothelial aspects of the
glomerular basement membrane
 HIVAN

The most common lesion in patients with HIV infection-related renal

disease is so-called HIV associated nephropathy (HIVAN). This
manifests as glomerulosclerosis in a focal and segmental pattern with
collapse of the glomerular tufts and disproportionate cystic changes of
the tubules.
 Lupus nephritis

Mesangial lupus nephritis (WHO Class IIb) shows mild mesangial

expansion by light microscopy, without evidence of endocapillary
proliferation. If mesangial immune complexes are present but no
mesangial increase is detected by light microscopy, WHO Class IIa
is diagnosed
Immunofluorescence shows mesangial staining in WHO Class IIb
lupus nephritis, without peripheral capillary loop deposits
Very mild endocapillary increase of cells is also present, and occasional
subendothelial deposits were present by electron microscopy, indicating a
combination of lupus WHO Class V and very early proliferative changes.
WHO Class Vb, with diffuse granular capillary wall and mesangial positivity
Diffuse subepithelial dense deposits and lesser mesangial deposits
in this field in membranous lupus nephritis.
Cryoglobulinemic glomerulonephritis with membranoproliferative
and mesangial proliferative features. In this biopsy, strongly PAS-
positive small cryoglobulin plugs are present within capillary
loops.
Acute cryoglobulinemic glomerulonephritis with mesangial
proliferation, occasional interposition, inflammatory cells, and
strongly PAS-positive glomerular material, characteristic of
cryoglobulinemic deposits within capillary lumens
The very segmental nature of deposits in cryoglobulin-related
glomerulonephritis is evident in this case with strong,
discontinuous, segmental deposits, corresponding to large
deposits seen by light microscopy (see slides above).
Complement typically co-localizes with immunoglobulins in
cryoglobulinemic glomerulonephritis
Early segmental fibrinoid necrosis with early cellular crescent
formation without endocapillary proliferation or evidence of immune
complexes in the remaining glomerular tuft. This light microscopic
finding is that of a pauci-immune necrotizing glomerulonephritis, with a
specific diagnosis of anti-GBM antibody-mediated glomerulonephritis
made by immunofluorescence
Smooth, linear staining of glomerular basement membranes with
antibody to IgG and crescent formation in the glomerulus on the
left, diagnostic findings of anti-GBM antibody-mediated
glomerulonephritis
Segmental fibrinoid necrosis with nuclear debris and glomerular
basement membrane disruption, typical of early stage of pauci-
immune crescentic glomerulonephritis
Well-developed cellular crescent with collapse of small amount of
remaining glomerular tuft with segmental fibrinoid necrosis and
extracapillary fibrin and necrosis in pauci-immune crescentic
glomerulonephritis
Electron microscopy shows the absence of deposits along the capillary
wall in a case of pauci-immune crescentic glomerulonephritis, consistent
with Wegener's granulomatosis.
 DM Nephropathy

Diabetic nephropathy is characterized by light microscopy by mesangial

expansion, sometimes with nodule formation, mesangial hypercellularity,
and a thickened glomerular basement membrane. In this case, there is
diffuse mesangial hypercellularity and expansion with only small nodule
formation.
Diabetic nephropathy is one of the causes of nodular
glomerulosclerosis, illustrated here, with large nodules of matrix within
mesangial areas with lesser increase in mesangial cellularity. The
glomerular basement membrane is thick without apparent deposits.
There is diffuse mesangial matrix expansion and increased mesangial
hypercellularity and prominent glomerular basement membranes in
diabetic nephropathy.
This case shows nodular glomerulosclerosis and linear
accentuation of the glomerular basement membrane with IgG,
which is typical of diabetic nephropathy. There are no immune
complexes in diabetic nephropathy
Direct immunofluorescence study showing ribbon-like linear deposition of
IgG along the glomerular basement membrane. The glomerular tuft is
slightly compressed by cellular proliferation, forming a crescent. AntiGBM
Disease.
The lesion consists of fibrin thrombi within glomeruli, which
may extend to arterioles. In this patient with hemolytic uremic
syndrome, the thrombotic microangiopathy was confined to
glomeruli, with extensive fibrin thrombi and platelet plugs filling
up the capillary loops.
In thrombotic microangiopathy, no deposits are seen by
electron microscopy or immunofluorescence. In more
chronic stages, new basement membrane may be formed
after the endothelial injury and early interposition with
expansion of the lamina rara interna can occur, as
illustrated in this case.
Hyalinosis is evident in the arteriole and interlobular
artery in hypertensive nephrosclerosis, along with mild
medial thickening caused by both hypertrophy and
hyperplasia of vascular smooth muscle cells. The hyalin
material is the result of insudation of plasma proteins,
and is pink and glassy-smooth in appearance (ie, hyalin).
Long-term cyclosporine
toxicity is associated with
interstitial fibrosis and tubular
atrophy.

Obstructive arteriolopathy with

ischemic glomerulosclerosis is
observed in cyclosporine
nephropathy. The arterioles
and small arteries show
hyalinization
Vacuolization of the renal tubules is observed in association with
interstitial fibrosis in a patient with hypokalemic nephropathy.
Myeloma kidney. Many dilated tubules are obstructed by densely
eosinophilic hard casts, with giant cell reaction and inflammatory cell
infiltrates. There is also vacuolation and degeneration of tubules.
Hyperacute rejection showing glomerular and peritubular capillary
infiltration and thrombosis with tubular injury and cast formation.
 Chronic transplant rejection.
Interstitial fibrosis and tubular
atrophy. Fibrosis of the interstitium
is depicted in blue.

Chronic transplant rejection. Fibrous

intimal thickening. Pronounced
thickening of the intima leads to almost
complete occulsion of the vascular
lumen (left).
Chronic calcineurin nephrotoxicity. Biopsy specimen of a rat with chronic
cyclosporine nephrotoxicity showing characteristic arteriolar hyalinosis (a)
(arrows). Other findings (not shown) include tunulointerstitial fibrosis
Type I acute rejection is manifested by interstitial mononuclear cell
infiltration (arrow) with invasion of the tubules
Type II rejection, called acute vascular rejection, is manifested by
endothelialitis with mononuclear cell infiltration beneath the arterial
endothelium
Type III acute cellular rejection. Severe small-vessel vasculitis with transmural
mononuclear cell infiltration, fibrinoid necrosis (arrows), and very swollen
endothelial cells
Acute antibody-mediated
rejection. a, Peritubular and
glomerular capillaries contain
numerous polymorphonuclear
leukocytes and mononuclear cells.

b, Numerous polymorphonuclear
leukocytes are observed in a
peritubular capillary. Interstitial
edema is noted
 Acute antibody-mediated rejection.

Immunohistochemistry
demonstrating peritubular capillary
staining of C4d

Immunofluorescence staining of
peritubular capillaries with C4d
Hyperacute rejection. Hyperacute rejection refers to immediate rejection of
the kidney due to preformed antibodies to alloantigens of the endothelium.
a, Hyperacute rejection is associated with massive platelet accumulation
within a glomerular capillary (by electron microscopy). b, This is followed by
further endothelial damage, resulting in capillaries filled with sludged red
blood cells and fibrin
BK polyoma virus infection. a, Prominent intranuclear viral inclusions are
present within tubular epithelial cells (arrows)
Tubulointerstitial nephritis with diffuse intranuclear polyomavirus
inclusions (arrows)
Immunohistochemistry staining highlights intranuclear polyomavirus
inclusions (SV40 immunoperoxidase stain, original magnification ×200).
chronic allograft nephropathy. a, Interstitial fibrosis, glomerulosclerosis,
and tubular atrophy (trichrome).
CAN: Fibrointimal proliferation in an intrarenal artery
Electron microscopic
appearances in chronic
allograft nephropathy.
Note the multiple layers of
peritubular capillary
basement membranes.
CAN/Transplant glomerulopathy with mesangial matrix expansion and
thickening of capillary loops (hematoxylin and eosin).
Transplant glomerulopathy showing membrane reduplication in
capillary loops (between arrows)
Urinalysis
Dysmorphic glomerular
erythrocytes. The
dysmorphism consists
mainly in irregularities of
the cell membrane.
Neutrophils. Note
their typical
lobulated nucleus
and granular
cytoplasm.
Different types of renal
tubular cells.
Three cells from the superficial layers of the uroepithelium.
A high-power (×100)
examination of urine
demonstrates singlets and
yeast (blastospores), budding
yeast (arrows), and
pseudohyphae in a patient with
Candida albicans infection.
Hyaline cast
Finely granular cast.
Erythrocyte cast. The
arrows indicate the
erythrocytes
embedded in the
matrix of the cast
RBC cast: think glomerular ds.
Hemoglobin cast with
its typical brownish
Leukocyte cast. The
polymorphonuclear
leukocytes are identifiable
due to their lobulated
nucleus
Epithelial cast. Renal
tubular cells are identifiable
thanks to their large
nucleus. : Early ATN
Established ATN: Muddy brown cast
What should you do now ?
Uric acid crystals.
This rhomboid
shape is the most
frequent.
Uric acid crystals:
complex crystals
suggestive of acute
uric acid
nephropathy or uric
acid nephrolithiasis.
Bihydrated
calcium oxalate
crystals with their
typical
appearance of a
“letter envelope.”
Oxalate crystals: a
pseudocast of
calcium oxalate
crystals accompanied
by crystals of calcium
oxalate dihydrate
Different types of
monohydrated
calcium oxalate
crystals.
A starlike calcium
phosphate crystal.
Triple phosphate
crystal, on the
background of a
massive amount of
amorphous
phosphate particles.
Coffin Lid
Coffin-lid crystals
of magnesium
ammonium
phosphate
(struvite).
Cystine crystals heaped
one on the other
Amoxicillin crystal
resembling a branch of a
broom bush.
A large crystal of
indinavir.
Spiral CT scan showing a single
stone in the right renal pelvis.

Struvite stones: left staghorn

calculus and a single bladder
stone.
Decoy cells as seen
by phase contrast
microscopy. Note
the enlarged
nucleus of the lower
cell that contains a
large inclusion body

BK nephropathy
A decoy cell as seen
by Papanicolaou
stain. Again, note the
large nuclear
inclusion body
A decoy cell as seen
by transmission
electron microscopy
(original
magnification
×30,000), whose
nucleus is engorged
with virus particles.
Also note various
chromatin granules
close to nuclear
membrane (=
chromatin
margination).
Images
Normal kidney on US
Enlarged echogenic kidneys: HIVAN
Column of Bertin, a normal finding on US
Hydronephrosis on US
Sagittal ultrasound showing an upper pole renal calculus (arrow). Note the
acoustic shadowing
Sagittal ultrasound
showing a large
hyperechoic mass arising
from the lower pole. Mass
shown on CT.
Sagittal renal ultrasound showing a complex cyst
Normal renal arterial
tracing showing the
rapid systolic upstroke
and early systolic peak
velocity (~100 cm/s).

Tardus parvus
waveform
demonstrating the
slow systolic
upstroke
(acceleration) and
decreased peak
systolic velocity (~20
cm/s) associated
with renal artery
stenosis. Note
different scales on
vertical axis.
Large central renal cell cancer
Plain film showing bilateral medullary nephrocalcinosis in a patient
with distal renal tubular acidosis.
Noncontrast computed tomography (CT) scan in a patient with hereditary
oxalosis and dense bilateral renal calcification (arrows). The left kidney is
atrophic.
CT scan showing cortical nephrocalcinosis in the right kidney (arrows)
following cortical necrosis.
Normal parenchymal enhancement and normal renal excretion. Early
postcontrast tomogram in intravenous urography.
The IVU was performed in a
previously asymptomatic
adult to investigate
nonspecific right loin pain.
There is unilateral (right
side) dilation of the
pelvicalyceal system. The
ureter has not been
visualized.
A retrograde pyelogram shows the tumor
is within and obstructing the ureter
(arrows). Above the tumor, there is dilation
of the ureter, but below it, the ureter is of a
normal caliber.
Diuretic isotopic renography.
Idealized tracings for normal,
obstructed, and dilated kidneys
without obstruction of the upper
urinary tract. In obstruction,
there is delayed excretion of
99mTc-MAG3 despite
administration of furosemide.
When there is dilation of the
upper urinary tract without
obstruction, the isotope is
retained but is rapidly excreted
after the administration of
furosemide.
Retrograde pyelogram showing
idiopathic retroperitoneal
fibrosis. Dilation of the
pelvicalyceal system. The ureters,
however, are not dilated and the
left ureter can be seen being pulled
medially as a result of being
encased in thick fibrous tissue.
Gross vesicoureteral
reflux (VUR) and
intrarenal reflux. A voiding
cystourethrogram showing
bilateral grade V VUR and
intrarenal reflux into several
renal lobes in an infant
presenting with urinary tract
infection.
Renal pathology of reflux nephropathy. Light microscopy of a
glomerulus showing segmental glomerulosclerosis and
hyalinosis.
Microscopic changes in reflux nephropathy. Low-power view of renal cortex
showing sclerosed glomeruli, chronic cellular infiltrate, and dilated, atrophic
tubules, with eosinophilic casts and thick-walled blood vessels.
Emphysematous pyelonephritis. Contrast-enhanced computed tomography
scan showing gas (arrowheads) within an enlarged left kidney and marked
enhancement of Gerota’s fascia (G) and the posterior perirenal space (P)
indicative of inflammatory involvement.
Emphysematous pyelonephritis. A plain radiograph in this febrile diabetic
subject revealed diffuse gas formation throughout both kidneys and
retroperitoneum
 Acute pyelonephritis.
Ultrasound demonstrates an
enlarged echogenic kidney.
Bipolar length of kidney is 12.9
cm.

Computed tomography scan

with contrast obtained 24 hours
later demonstrates multiple
nonenhancing abscesses
(arrowheads).
 Magnetic resonance angiography.
Coronal three-dimensional image following
contrast administration showing normal
renal arteries

Fibromuscular dysplasia of the

proximal right renal artery.
Fibromuscular dysplasia. Selective right renal arteriogram demonstrating
typical beaded appearance.
 Aortogram demonstrating a tight
left renal artery stenosis

Postangioplasty image with marked

improvement of the stenosis
Renal vein thrombosis
Post-transplantation
lymphocele. a, Ultrasound
appearance. A large
echolucent lymphocele can
be seen inferior to the
transplanted kidney. b,
Computed tomography
appearance. A 5 × 5-cm
lymphocele (arrowheads) is
present under the
transplanted kidney (arrows).
 Membranoproliferative
glomerulonephritis type II. Partial
lipodystrophy; note the absence of
subcutaneous fat from the face.

Drusen bodies in the retina.

The rash is a palpable purpuric vasculitis on the lower limbs spreading on
extensor surfaces to the buttocks and occasionally to the upper limbs.
Histology shows leukocytoclastic vasculitis with IgA deposits in blood vessel
walls.
Renal angiogram in
polyarteritis nodosa.
Angiogram shows patchy
renal perfusion defects
and aneurysms
Markedly enlarged polycystic kidneys from a patient with ADPKD in
comparison to a normal kidney in the middle.
Angiokeratoma in Fabry’s disease. Note the multiple periumbilical
angiokeratomas.
Nail-patella
syndrome. Clinical
(a) and radiologic
(b) appearance of
absence of the
patellae.
Ocular abnormalities in Alport’s
syndrome. a, Anterior lenticonus shown by
slit-lamp ophthalmoscopy. b, Perimacular
flecks.
Papillary necrosis in sickle cell disease. Intravenous urography shows
abnormal calyces with filling defects
Life cycle of schistosomes.
Schistosomal infection:
a. Pseudotubercles in bladder
b. Mesangioproliferative GN
c. Stool sample with ova
Maculopapular rash in a patient with
drug-induced acute interstitial nephritis
(AIN). Such cutaneous lesions occur in
about 40% of patients with drug-
induced AIN
Drug-induced acute interstitial nephritis. On light microscopy, the
characteristic feature is of an interstitial infiltration with mononuclear cells and
normal glomeruli. It is usually associated with interstitial edema and with tubular
lesions.
Interstitial nephritis in a patient with analgesic nephropathy associated with
marked mononuclear cellular infiltrate including eosinophils (arrows).
 Light microscopic section
demonstrating cholesterol clefts with
giant cell reaction and recanalization in
the lumen of a medium-sized renal
vessel.
Livedo Reticularis

Cholesterol emboli: “2 wks post procedure”

Another example of Cholesterol emboli
a, Normal cortical renal tubules. b and
c, ATN: note the flattened epithelium,
bare basement membranes, and
intraluminal cellular debris.
Prurigo Nodularis: a finding in HD patients
Porphyria cutanea tarda. Tense bullae, erosions, and
crusts of the dorsal hands.
Calcific Uremic Arteriolopathy

Calf calcification in a patient with
gross ulcerations in both legs from
the popliteal fossae to the ankles.
Medial calcification and intimal
hyperplasia of an arteriole at the dermal-
subcutaneous junction. Note
calcification of interlobular capillaries in
the subcutaneous tissue.
Nephrogenic fibrosing dermopathy. a, Peau d’orange appearance. b, Swelling of
the hands, accompanied by palmar erythema, blisters, and contracture of the fingers.
Haphazardly arranged dermal collagen bundles with surrounding clefts and a
strikingly increased number of similarly arranged spindled and plump fibroblast-like
cells.
There may also be degeneration and frank necrosis of individual
cells or tubular segments in acute tubular necrosis, or flattened,
regenerating type epithelium with degenerated cells in the lumen
(middle left)
More extensive intratubular polymorphonuclear neutrophils (PMNs)
are present in this case of acute pyelonephritis. The PMNs are
easily recognizable by their multilobed irregular nuclei. There is
associated tubular degeneration and necrosis, but only minimal
interstitial changes
Chronic pyelonephritis is suggested when tubulointerstitial
fibrosis and glomerular scarring are present in a so-called
geographic pattern. This refers to irregular zones of scarring,
with intervening preserved areas, fitting together like jigsaw
pieces or like a map of countries bordering on each other.
In acute interstitial nephritis, there is edema associated with an
interstitial lymphoplasmocytic infiltrate.
Close-up of intratubular refractile casts with surrounding
syncytial giant cell reaction with chronic tubulointerstitial
nephritis and fibrosis, characteristic of myeloma cast
nephropathy
Right: Cytomegalovirus infection is diagnosed by the appearance of
large cells with basophilic enlarged nuclei with inclusions. There is
frequent tubular injury and degeneration. Cytomegalovirus infection
most commonly affects tubular epithelial cells and occurs most
commonly in the transplant.
Left: The marked enlargement of the tubular epithelial cells with
markedly enlarged nuclei and degeneration is evident in this case of
cytomegalovirus infection in the transplant
Cytomegalovirus can also be seen by electron microscopy. The virus
has a typical bull's eye appearance when present in the cytoplasm,
where it has picked up an extra layer of the nuclear membrane.
Right: There is a pleomorphic interstitial infiltrate composed of lymphocytes
and plasma cells with occasional admixed PMNs and characteristic viral
inclusions in tubular epithelial cells, as shown here. The infected tubular
cells often are enlarged, and in some cases may even resemble the
inclusions of cytomegalovirus infection. The viral inclusions are
intranuclear, basophilic and smudgy.
Left: The enlarged, basophilic, smudgy viral inclusions typical of BK
polyoma virus nephropathy are seen in the tubular epithelium in this renal
transplant case.
Immunostaining is a useful diagnostic tool for suspected cases of
BK polyoma virus nephropathy, as shown here with positive
staining of an enlarged nuclear inclusion with antibody to the
related simian kidney virus SV40.
Right: Antibody-mediated rejection is very strongly correlated with the
presence of type III vascular rejection with fibrinoid necrosis of the vessel
wall
Left: C4d is a breakdown product of complement, and its presence in
peritubular capillaries correlates strongly with the presence of anti-donor
antibodies. This immunofluorescence test is thus used as an adjunct to
suggest antibody-mediated mechanisms of acute rejection
 Good luck!!!
Vikul Patel, MD
Nephrology Fellow
Barry Wall, MD
Program Director
Univ of Tennessee, Memphis