Renal Path Images Flashcards
Renal Cell Carcinoma
The kidney is partially replaced by a circumscribed tumor measuring 10 x 6 cm. The cut surfaces reveal the characteristic variegated appearance of a clear cell RCC, being yellow in color, interspersed by hemorrhage and white fibrosis. Focal cystic changes are frequently seen. Despite the sharp demarcation from the adjacent normal kidney, RCC invariably shows infiltrative growth on microscopic examination.
Renal Cell Carcinoma
RCC has a propensity to invade the renal pelvis causing hematuria or to grow along the renal vein (as shown in cross section on the bottom left). In some cases tumor can propagate into the inferior vena cava and can give rise to lower extremity venous obstruction.
Renal Cell Carcinoma
. A. RCC has a predilection for hematogenous metastases to lung and bone (seen here are metastatic lesions in the rib and lung). Up to 30% of patients have metastases at presentation.
B. Metastases to unusual sites are also common as in this testicular specimen
Renal Cell Carcinoma
Histologically, the clear cell variant is the most common type. The tumor has an alveolar architecture created by prominent network of thin-walled vascular septae demarcating collections of tumor cells. Tumor cells have abundant clear cytoplasm. The nuclei are round and fairly uniform in appearance in low-grade tumor (as seen here) to highly pleomorphic, vesicular and prominent nucleoli in high-grade tumor.
Renal Cell Carcinoma
Renal cell carcinoma: papillary variant. The cuboidal neoplastic cells rest on elongated fibrovascular stalks. This tumor arises from distal convoluted tubular epithelium cells.
Renal Cell Carcinoma
Renal cell carcinoma: papillary variant. The cuboidal neoplastic cells rest on elongated fibrovascular stalks. This tumor arises from distal convoluted tubular epithelium cells.
Renal Cell Carcinoma
Renal cell carcinoma: chromophobe variant. Histologically it shows a mixture of granular cells and pale, transparent cells with distinct cell borders. It appe to arise from the intercalated cells of renal collecting ducts.
Renal Cell Carcinoma
Renal cell carcinoma: chromophobe variant. Histologically it shows a mixture of granular cells and pale, transparent cells with distinct cell borders and perinuclear halos.
Autosomal Dominant Polycystic Kidney Disease
. Cut surface of a kidney with adult polycystic disease. The specimen weighed 2,500 g and appears to be composed solely of multiple cysts of varying sizes. Normal renal parenchyma cannot be delineated grossly
Autosomal Dominant Polycystic Kidney Disease
The cysts are lined by a flattened epithelium. The residual intervening renal parenchyma appears relatively normal although interstitial fibrosis and tubular atrophy can often be seen.
Autosomal Dominant Polycystic Kidney Disease
Multiple hepatic cysts in a patient with ADPKD.
Autosomal Dominant Polycystic Kidney Disease
A well-documented association with adult polycystic disease is berry aneurysm of cerebral arteries (15% of cases). This ADPKD patient had a fatal subarachnoid hemorrhage as a result of rupture of one such aneurysm involving the internal carotid artery (arrow).
Autosomal recessive polycystic kidney disease (ARPKD)
This is an infant with Potter sequence secondary to oligohydramnios.
Autosomal recessive polycystic kidney disease (ARPKD)
Potter facies. Note the receding chin, flattened nose and large ears.
Autosomal recessive polycystic kidney disease (ARPKD)
. This is a gross photograph of an enlarged kidney from an infant with this disorder. Notice that the cysts are arranged in a radial fashion, like spokes of a wheel. The reason for this radial arrangement is that the cysts are formed from the collecting tubules of the kidney
Autosomal recessive polycystic kidney disease (ARPKD)
Note that the tubules, which are dilated, again run perpendicular to the renal capsule resulting in the same linear appearance seen during gross examination. We see that although the cysts involve both cortex and medulla, the glomeruli just beneath the capsule and their associated tubules are unaffected. Although these dilated tubules are connected to the normal glomeruli, apparently they do not drain in a normal fashion, thus producing a picture somewhat akin to what you might see in complete obstruction of the kidneys. As a result, since the obstruction is not reparable, these infants typically die at a very early age.
Autosomal recessive polycystic kidney disease (ARPKD)
This cut section of liver from an infant with ARPKD displays tan-white streaks expanding throughout the liver
Autosomal recessive polycystic kidney disease (ARPKD)
Image 6. The portal area in this case of ARPKD contains increased numbers of bile ducts in a circular configuration. Note the dense connective tissue (blue in this Masson Trichrome stain) within the portal area.
Autosomal recessive polycystic kidney disease (ARPKD)
Image 7. Urethral atresia and pulmonary hypoplasia. The opened thorax and abdomen in this infant show an enlarged urinary bladder and large dilated cystic kidneys due to an atresia of the urethra. As a result of the enlarged hydronephrotic kidneys and oligohydramnios, the thorax is compressed allowing little space for lung development. Note the horizontal position of the heart in the small thorax.
Autosomal recessive polycystic kidney disease (ARPKD)
Image 8. Urethral atresia and hydronephrosis. The congenital hydronephrosis of the kidneys secondary to the urethral atresia has resulted in these fluid filled sacs with little remaining renal parenchyma. Note the adrenals on the top of these sacs.
renal obstruction
Image 2. Enlarged prostate compressing the urethra.
renal obstruction
Image 3. A. Hydronephrosis. Note the markedly dilated pelvis and thinning of the cortex.
B. A staghorn calculus filling the pelvis. These stones are a mixture of magnesium ammonium phosphate and calcium phosphate. They arise in a setting of chronic urinary infection with urease-splitting bacteria.
acute tubular injury
Image 1. Kidney with acute tubular injury (loss of nuclei), dilation of tubules, interstitial edema, sloughing of epithelium, and glomerular congestion.
acute tubular injury
Image 3. In ATI (ATN) there is epithelial sloughing within renal tubules.
chronic obstructive pyelonephritis
Image 1. Here is a case of chronic obstructive pyelonephritis secondary to prostatic hyperplasia. Both kidneys were involved. Long standing obstruction results in dilation of renal pelvis and calyces (hydronephrosis). Deep cortical pits are present due to scarring and contraction over deformed calyces
chronic obstructive pyelonephritis
Image 2. A low-power view of atrophic renal parenchyma compressed by markedly dilated pelvis. The normal distinction between the cortex and medulla is no longer present. Fibrosis (homogeneous pink areas) and inflammation (patchy blue areas) are evident in this H&E slide.
chronic obstructive pyelonephritis
Image 3. High-power view showing patchy interstitial fibrosis and characteristic linear streaks of chronic inflammatory cell infiltrates.
chronic obstructive pyelonephritis
Image 4. Global glomerulosclerosis is present in some of the glomeruli
chronic obstructive pyelonephritis
Image 5. Hypertrophy and dilation of the tubules (called thyroidization due to its similar appearance to thyroid follicles) are common. The small arteries show evidence of mild arteriosclerosis (arrow).
chronic obstructive pyelonephritis
Image 6. Artery demonstrating intimal sclerosis.
nephritic syndrome: post-streptococcal glomerulonephritis
Image 1. This low-power view shows three enlarged, hypercellular glomeruli. Several tubules contain red cells and proteinaceous material. Mild interstitial edema is also evident.
nephritic syndrome: post-streptococcal glomerulonephritis
Image 2. A high-power view of a glomerulus clearly shows the hypercellularity caused by proliferation of mesangial cells, endothelial cells and global leukocytic infiltration in all lobules of the glomerulus. Bowman’s space contains red cells and white cells that have escaped into the urinary space.
nephritic syndrome: post-streptococcal glomerulonephritis
Image 3. Red cells and red cell casts (“active” urinary sediment) are characteristic of acute nephritic syndrome.
nephritic syndrome: post-streptococcal glomerulonephritis
Image 4. White cell cast and significant proteinuria are not uncommon in severe cases.
nephritic syndrome: post-streptococcal glomerulonephritis
Image 5. A. Schematic representation of normal glomerulus. B. Schematic representation of PSGN.
nephritic syndrome: post-streptococcal glomerulonephritis
Image 6. The characteristic EM findings are the discrete electron-dense deposits (“humps”) on the epithelial side of the basement membrane, which represent immune complexes (red arrows).
nephritic syndrome: post-streptococcal glomerulonephritis
Image 7. Immunofluorescence microscopy shows granular (lumpy-bumpy) deposits of IgG, IgM and C3 along the glomerular basement membrane and in the mesangium.
nephritic: rapidly progressive glomerulonephritis
Image 1. Both glomeruli in this field show varied amounts of cellular accumulation in Bowman’s space. Note the presence of RBCs and RBC casts in the tubules
nephritic: rapidly progressive glomerulonephritis
Image 2. A high-power view shows a characteristic crescent formed by proliferation of parietal cells. The crescent compresses and partially obliterates the glomerular tuft.
nephritic: rapidly progressive glomerulonephritis
Image 3. Note the migration of inflammatory cells into the crescent. Two mitotic figures are also present (arrow). Fibrin strands are seen between the crescent cells and are thought to be an inciting factor for crescent formation
nephritic: rapidly progressive glomerulonephritis
Image 4. Immunofluorescence micrograph in this case reveals a continuous linear staining for IgG (anti-GBM antibodies) along the glomerular capillary loops. This pattern is a classic example of Goodpasture syndrome.
nephrotic: minimal change disease
Image 1.This is an example of generalized edema in an infant with nephrotic syndrome. Note the presence of pitting edema on the dorsal body surface.
nephrotic: minimal change disease
Image 2. A low-power view shows four glomeruli without significant pathological changes. Several tubules contain proteinaceous precipitate. Note the fixation artifact of retraction seen in some of the tubules in the field.
nephrotic: minimal change disease
Image 3. A high-power view of a glomerulus reinforces the previous impression of normal morphology. Mild interstitial edema is present.
nephrotic: minimal change disease
Image 4. The only significant finding by light microscopy the foamy (or granular) appearance of the cells of the proxi tubules due to reabsorption of lipoproteins leaking through diseased glomeruli.
nephrotic: minimal change disease
Image 5. A. Schematic representation of a normal glomerulus.
B. Schematic representation of minimal change disease
nephrotic: minimal change disease
Image 6. EM shows the principal lesion of this disorder, i.e., the diffuse effacement (“fusion”) of the visceral epithelial foot processes (arrows). It should be emphasized here that foot process effacement is not unique for minimal change disease. It can also be seen in other proteinuric diseases. A diagnosis of minimal change disease can only be made when the nephrotic syndrome is associated with glomeruli showing diffuse foot process loss on EM. Note that no electron-dense deposits are present.
nephrotic: membranous nephropathy
Image 1. Three glomeruli in the field exhibit diffuse, regular thickening of the glomerular capillary wall. There is mild focal interstitial chronic inflammation
nephrotic: membranous nephropathy
Image 2. A high-power view shows a glomerulus with diffuse, uniform thickening of capillary wall without increase in number of cells (Masson trichrome stain).
nephrotic: membranous nephropathy
Image 3. A silver methenamine-stained section delineates the characteristic spike-like projections of the newly formed basement membrane (colored black by silver stain) between which are the immune deposits, which are not stained and appear as negative images.
nephrotic: membranous nephropathy
Image 4. A. Schematic representation of a normal glomerulus. B. Schematic representation of membranous nephropathy.
nephrotic: membranous nephropathy
Image 5. This electron micrograph reveals irregular subepithelial electron-dense deposits (red arrow). Between deposits are extensions of the basement membrane forming protruding spikes (yellow arrow). As the disease progresses the basement membrane is markedly thickened and eventually surrounds the deposits. Note the obliteration of foot processes by the epithelial cells overlying deposits.
nephrotic: membranous nephropathy
Image 6. Immunofluorescence shows granular IgG deposits outlining the glomerular capillary loops. Rubin and Farber, figure 16- 23, with permission.
2* glomerular disorder: IgA Nephropathy
Image 1. IgA nephropathy can have variable histological findin ranging from normal to overt crescentic GN. The glomerulus in this high-power view (PAS stain) shows mild changes consistin of segmental proliferation of mesangial cells and mesangial widening by matrix accentuated by the PAS stain.
2* glomerular disorder: IgA Nephropathy
Image 2. Here is a Masson’s trichrome stain of another glomeru with greater degree of involvement. Segmental fibrosis (blue color) and focal adhesions to Bowman’s capsule are evident in addition to proliferative mesangial processes.
2* glomerular disorder: IgA Nephropathy
Image 3. A higher-power view of a glomerular tuft reveals discrete red mesangial droplets that have been shown to correspond to IgA deposits on immunostaining.
2* glomerular disorder: IgA Nephropathy
Image 4. Immunofluorescense stain shows deposits of IgA primarily in mesangial regions.
2* glomerular disorder: Henoch-Schonlein
Image 5. Photograph of a child with purpura over both lower extremities who also presented with fever, joint pain, and hematuria. What is the most likely diagnosis? (Henoch-Schonlein)
IgA
diabetic glomerulosclerosis
Image 1. This image illustrates the morphologic change of diffuse glomerulosclerotic lesion of diabetic nephropathy. The glomerulus is enlarged with expanded mesangial areas and mild proliferation of mesangial cells. The basement membrane is diffusely thickened.
diabetic glomerulosclerosis
Image 2. This image shows a glomerulus with striking diffuse glomerulosclerosis. In addition, one finds the presence of ovoid hyaline nodules within the mesangium of the glomerular tufts. The changes seem to be continuous with the invariably hyaline thickening of the arterioles (arrow). It is felt that both the diffuse and the nodular lesions of glomerulosclerosis are essentially similar mesangial lesions. With rare exceptions, the nodular lesion is pathognomonic of diabetic glomerulosclerosis (Kimmelstiel-Wilson disease).
diabetic glomerulosclerosis
Image 3. As the disease progresses, the nodules enlarge and eventually obliterate the glomerular tufts forming large, sclerotic glomeruli, one of which is seen in this low-power view.
Alport: Hereditary Nephritis
EM of GBM with irregular thickening and lamination of lamina densa.
Immunofluorescense features: 1. Antibodies to α3, α4c and α5chains are negative in contrast to Goodpasture syndrome where antibodies are present to the α3 chain. Individuals with absent α3 chain do not demonstrate the linear pattern seen in Anti-GBM disease.
chronic pyelonephritis
(162)
diabetic glomerulosclerosis
167
rapid progressive glomerulosclerosis (goodpasture)
455
renal cell carcinoma
547
membraneous nephropathy
subepithelial IgG and C3
spike and dome
hair on end (membrane projection)
