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Renal Path Lab 1

Renal Path Lab 1

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?: Normal Kidney

Gross of normal kidney shows cortex and medulla; ureter in yellow, arteries-red, venous supply-blue.
?: Normal Kidney

Renal cortex with capsule and glomeruli as well as medullary rays. The cortex contains: glomeruli, proximal convoluted tubules, distal convoluted tubules.
?: Normal Kidney

Illustration of a portion of the glomerulus. Bowman's capsule is not represented here. The visceral epithelial cells and their foot processes are in blue. The endothelial cell bodies and their fenestrated cytoplasm are in red. The solid black is the glomerular basement membrane. The black, cross-hatched area is the mesangial matrix with a lone mesangial cell nucleus near the center of the matrix.
?: Normal Kidney

Light microscope view of glomerulus with a silver stain. The "spikes" of basement membrane are seen along the glomerular capillary walls. This is a feature of membranous glomerulopathy.
?: Normal Kidney

Higher power view of glomerulus showing detail of structure.
?: Normal Kidney

Electron microphotograph of normal glomerulus. E=endothelium, M=mesangial cells, EP=epithelial, and BM=glomerular basement membrane.
?: Normal Kidney

Transitional cell epithelium of renal calyx and collecting tubules of medulla.
?: Adult Polycystic Kidney: Autosomal Dominant Polycystic Kidney Disease (ADPKD)

A single polycystic kidney. ADPKD is the most common monogenic disorder that is potentially fatal. ADPKD-1, the most common form (80-90% cases) is caused by a mutation on the short arm of chromosome 16. End-stage renal failure develops in about 50% of patients. Exact pathogenic mechanism remains unknown.
?: Adult Polycystic Kidney: Autosomal Dominant Polycystic Kidney Disease (ADPKD)

A number of cysts of varying size are present; some contain luminal protein. Other features to note are compression of glomeruli, loss of glomeruli, periglomerular fibrosis, and interstitial fibrosis.
?: Adult Polycystic Kidney: Autosomal Dominant Polycystic Kidney Disease (ADPKD)

A number of cysts of varying size are present; some contain luminal protein. Other features to note are compression of glomeruli, loss of glomeruli, periglomerular fibrosis, and interstitial fibrosis.
?: Renal Dysplasia

Whole mount section in which the kidney is filled with small and large cysts randomly placed throughout the parenchyma.
?: Renal Dysplasia

Cysts either have no epithelium or are lined by flattened inconspicuous cells. Note the single nodule of hyaline cartilage (arrow), loose connective tissue, and lack of any polarity in the arrangement of the cysts.
?: Renal Dysplasia

Primitive ducts--a diagnostic feature of renal dysplasia--are defined as ducts with undifferentiated, columnar-to-cuboidal epithelium surrounded by thick collars of loose, fibromuscular mesenchyme.
?: Renal Dysplasia

Primitive nephrotic structures (immature glomeruli and tubules) exist in close proximity to metaplastic cartilage nodule (arrow).
?: Infantile Polycystic Kidney

Cut surface of IPKD shows radially arranged cylindrical cysts with no fibrosis of the parenchyma.
?: Infantile Polycystic Kidney

Irregular dilated tubules in cortical region with dispersed immature and infantile glomeruli with distended capsules. Note the polarity (radial arrangement) of these elongated cysts.
?: Infantile Polycystic Kidney

Immature glomeruli with prominent epithelial cells are normally present between cysts.
?: Acute Proliferative Glomerulonephritis (Post Streptococcal Glomerulonephritis)

The tissue comes from four biopsies so the amount of material and the number of glomeruli vary. All, however, show a proliferative lesion (mesangial in nature) with exudate of polymorphs, and in general, there is lobular accentuation of glomeruli. C3 and IgG were seen on immunofluorescence and all glomeruli had typical subepithelial electron-dense deposits on electron microscopy. These patients had clinical and other evidence indicating that the original disease was streptococcal in nature.
?: Acute Proliferative Glomerulonephritis (Post Streptococcal Glomerulonephritis)

The tissue comes from four biopsies so the amount of material and the number of glomeruli vary. All, however, show a proliferative lesion (mesangial in nature) with exudate of polymorphs, and in general, there is lobular accentuation of glomeruli. C3 and IgG were seen on immunofluorescence and all glomeruli had typical subepithelial electron-dense deposits on electron microscopy. These patients had clinical and other evidence indicating that the original disease was streptococcal in nature.
?: Crescentic Glomerulonephritis

A number of different conditions can produce a crescentic glomerulonephrities including post-streptococcal disease, lupus erythematosus, Wegener's granulomatosis, and antiglomerular basement membrane disease. Clinically patients present with rapidly progressive deterioration of renal function. Early diagnosis is critical.

High power view. PAS stain.
?: Crescentic Glomerulonephritis

A number of different conditions can produce a crescentic glomerulonephrities including post-streptococcal disease, lupus erythematosus, Wegener's granulomatosis, and antiglomerular basement membrane disease. Clinically patients present with rapidly progressive deterioration of renal function. Early diagnosis is critical.

A single glomerulus being overwhelmed by crescent formation. Note the cellularity of the interstitium. Crescents are more difficult to appreciate in H/E stained sections as in this image.
?: Chronic Glomerulosclerosis (End-Stage Kidney)

Completely hyalinized glomeruli with surrounding tubular atrophy, and tubular dilatation.
?: Chronic Glomerulosclerosis (End-Stage Kidney)

PAS stain: Globally sclerotic glomeruli.
?: Cholesterol Embolus

Some of the histological slides show infarcts associated with the arterial occlusions. The infarct, if present, is clearly visible as a wedge-shaped red area.

Low power view of kidney with thickening of arcuate arteries and clefts within the lumen of one artery which is surrounded by lymphocytic inflammatory infiltrate. The emptiness of the clefts is due to the dissolution of cholesterol by the lipid solvents during histological preparation.
?: Cholesterol Embolus

Some of the histological slides show infarcts associated with the arterial occlusions. The infarct, if present, is clearly visible as a wedge-shaped red area.

Higher power of occluded artery with numerous cholesterol clefts surrounded by multinucleate giant cells.
?: Amyloidosis

Note the continuation of the arteriolar amyloid deposit into the glomerulus. Tubules contain amyloid casts.
?: Amyloidosis

High power view of glomerulus. Congo red.
?: Amyloidosis

Polarization of Congo-red stained amyloid.
?: Amyloidosis

Electron micrograph showing non-branching 7-10 nm diameter fibrils of amyloid.
?: Diabetic Glomerulosclerosis

This material comes from a long standing diabetic who first became nephrotic and then went into renal failure with subsequent dialysis. Things to note are 1) the sclerotic condition of most glomeruli leading to renal failure 2) arterial and arteriolar thickening 3) chronic interstitial inflammation.

This glomerulus (from another case) is an example of diffuse diabetic glomerulosclerosis. The mesangium is markedly increased without an increase in cellularity. Because the lesion is not that far advanced, peripheral capillary loops still contain patent capillary lumina.
?: Diabetic Glomerulosclerosis

This material comes from a long standing diabetic who first became nephrotic and then went into renal failure with subsequent dialysis. Things to note are 1) the sclerotic condition of most glomeruli leading to renal failure 2) arterial and arteriolar thickening 3) chronic interstitial inflammation.

Acellular nodules of diabetic glomerulosclerosis (Kimmelstiel-Wilson lesion).
?: Diabetic Glomerulosclerosis

This material comes from a long standing diabetic who first became nephrotic and then went into renal failure with subsequent dialysis. Things to note are 1) the sclerotic condition of most glomeruli leading to renal failure 2) arterial and arteriolar thickening 3) chronic interstitial inflammation.

High power shows patent peripheral capillary loops. These nodules are PAS-positive and must be differentiated from amyloid, light chain disease, and lobular glomerulonephritis.
?: Diabetic Glomerulosclerosis

This material comes from a long standing diabetic who first became nephrotic and then went into renal failure with subsequent dialysis. Things to note are 1) the sclerotic condition of most glomeruli leading to renal failure 2) arterial and arteriolar thickening 3) chronic interstitial inflammation.

Hyaline sclerosis of afferent arteriole.
?: Congenital Malformations

Normal fetal lobulation of infant kidney.
?: Congenital Malformations

Abdomen opened at autopsy after removal of the bowel showing the huge size of the adult type of polycystic kidney.
?: Congenital Malformations

Close-up of adult polycystic kidney. The cause of this autosomal dominant inherited disease has recently been localized to an errant gene on chromosome 16 in most cases.
?: Congenital Malformations

Hypoplastic kidney with renal dysplasia. Pure hypoplasia is very uncommon, and is more commonly associated with vascular occlusion, long-standing urinary reflux, a chronic inflammatory process, or in conjunction with renal dysplasia. The latter is the case in this example which also had uretero-pelvic junction obstruction.
?: Congenital Malformations

Infantile polycystic kidney. These massively enlarged kidneys retain their reniform shape. Cysts are much smaller than adult polycystic kidney.
?: Congenital Malformations

Renal dysplasia. Some forms of dysplasia contain numerous cysts. These are usually termed multicystic kidney by clinicians. This should be easily differentiated from adult polycystic kidney.
?: Degenerative Changes Slides

Cortical necrosis. The specimen shows the subcortical yellow discoloration characteristic of ischemic infarction.
?: Degenerative Changes Slides

Recent infarct of kidney. The specimen shows yellow necrotic areas surrounded by a hemorrhagic edge. The surface in the region of the infarct is depressed indicating loss of substance. The infarct is probably 7 to 10 days old. The distribution of infarcted area follows the distribution of the renal arteries.
?: Degenerative Changes Slides

Chronic infarct scar. The healing of the infarct produces one very deep scar surrounded by normal renal tissue.

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