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Pathology Chapter 20 Images Kidney

Pathology Chapter 20 Images Kidney

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What do these pictures demonstrate: Renal dysplasia. A, Gross appearance. B, Histologic section showing disorganized architecture, dilated tubules with cuffs of primitive stroma, and an island of cartilage (H&E stain).
What do these pictures demonstrate: A and B, Autosomal-dominant adult polycystic kidney disease (ADPKD) viewed from the external surface and bisected. The kidney is markedly enlarged with numerous dilated cysts. C, Autosomal-recessive childhood polycystic kidney disease, showing smaller cysts and dilated channels at right angles to the cortical surface. D, Liver with cysts in adult PKD.
What does this picture demonstrate: Uremic medullary cystic disease. Cut section of kidney showing cysts at the corticomedullary junction and in the medulla
What do these pictures demonstrate: D and E, Two patterns of deposition of immune complexes as seen by immunofluorescence microscopy: granular, characteristic of circulating and in situ immune complex nephritis (D) and linear, characteristic of classic anti-GBM disease (E).
What do these pictures demonstrate: Membranous glomerulonephritis. A, PAS stain. Note the marked diffuse thickening of the capillary wall without an increase in the number of cells. B, Electron micrograph showing electron-dense deposits (arrow) along the epithelial side of the basement membrane (B). Note the obliteration of foot process overlying deposits. CL, capillary lumen; End, endothelium; Ep, epithelium. C, Characteristic granular immunofluorescent deposits of IgG along GBM. D, Diagrammatic representation of membranous glomerulonephritis.
What do these pictures represent: Acute proliferative glomerulonephritis. A, Normal glomerulus. B, Glomerular hypercellularity is due to intracapillary leukocytes and proliferation of intrinsic glomerular cells. C, Typical electron-dense subepithelial "hump" and a neutrophil in the lumen.
What does this picture demonstrate: Crescentic glomerulonephritis (PAS stain). Note the collapsed glomerular tufts and the crescent-shaped mass of proliferating cells and leukocytes internal to Bowman capsule.
What do these pictures represent: Acute proliferative glomerulonephritis. A, Normal glomerulus. B, Glomerular hypercellularity is due to intracapillary leukocytes and proliferation of intrinsic glomerular cells. C, Typical electron-dense subepithelial "hump" and a neutrophil in the lumen.
What does this picture demonstrate: Rapidly progressive glomerulonephritis. Electron micrograph showing characteristic wrinkling of GBM with focal disruptions in its continuity (arrows).
What does this picture demonstrate: Minimal change disease. Glomerulus stained with PAS. Note normal basement membrane and absence of proliferation. Compare with membranous glomerulopathy
What do these pictures demonstrate: A, Ultrastructural characteristics of minimal change disease: effacement of foot processes (double arrows), absence of deposits, vacuoles (V), and microvilli in visceral epithelial cells (single arrow). B, Schematic representation of minimal change disease, showing diffuse effacement of foot processes.
What do these pictures represent: Focal segmental glomerulosclerosis, PAS stain. A, Low-power view showing segmental sclerosis in one of three glomeruli (at 3 o'clock). B, High-power view showing hyaline insudation and lipid (small vacuoles) in sclerotic area.
What does this picture demonstrate: Membranoproliferative glomerulonephritis, showing mesangial cell proliferation, increased mesangial matrix (staining black with silver stain), basement membrane thickening and focal splitting, accentuation of lobular architecture, swelling of cells lining peripheral capillaries, and influx of leukocytes.
What do these pictures demonstrate: A, Membranoproliferative glomerulonephritis, type I. Note the large subendothelial deposit (arrow) incorporated into mesangial matrix (M). E, endothelium; EP, epithelium; CL, capillary lumen. B, Type II membranoproliferative glomerulonephritis, dense-deposit disease. There are markedly dense homogeneous deposits within the basement membrane proper. CL, capillary lumen. C, Schematic representation of patterns in the two types of membranoproliferative GN. In type I there are subendothelial deposits; type II is characterized by intramembranous dense deposits (dense-deposit disease). In both, mesangial interposition gives the appearance of split basement membranes when viewed in the light microscope.
What do these pictures demonstrate: IgA nephropathy. A, Light microscopy showing mesangial proliferation and matrix increase. B, Characteristic deposition of IgA, principally in mesangial regions, detected by immunofluorescence
What does this picture demonstrate: Hereditary nephritis. Electron micrograph of glomerulus with irregular thickening of the basement membrane, lamination of the lamina densa, and foci of rarefaction. Such changes may be present in other diseases but are most pronounced and widespread in hereditary nephritis. CL, capillary lumen; Ep, epithelium
What does this picture demonstrate: Hereditary nephritis. Electron micrograph of glomerulus with irregular thickening of the basement membrane, lamination of the lamina densa, and foci of rarefaction. Such changes may be present in other diseases but are most pronounced and widespread in hereditary nephritis. CL, capillary lumen; Ep, epithelium
What does this diagram show: Primary glomerular diseases leading to chronic glomerulonephritis (GN). The thickness of the arrows reflects the approximate proportion of patients in each group who progress to chronic glomerulonephritis: poststreptococcal (1% to 2%); rapidly progressive (crescentic) (90%), membranous (30% to 50%), focal glomerulosclerosis (50% to 80%), membranoproliferative glomerulonephritis (50%), IgA nephropathy (30% to 50%).
What does this picture demonstrate: Chronic glomerulonephritis. A Masson trichrome preparation shows complete replacement of virtually all glomeruli by blue-staining collagen
What does this picture demonstrate: Electron micrograph of advanced diabetic glomerulosclerosis. Note the massive increase in mesangial matrix (Mes) encroaching on the glomerular capillary lumina (CL). The GBM and Bowman capsule (C) are markedly thickened. Ep, epithelium; E, endothelium.
What does this picture demonstrate: Diffuse and nodular diabetic glomerulosclerosis (PAS stain). Note the diffuse increase in mesangial matrix and characteristic acellular PAS-positive nodules
What does this diagram demonstrate: Patterns of tubular damage in ischemic and toxic acute tubular necrosis. In the ischemic type, tubular necrosis is patchy, relatively short lengths of tubules are affected, and straight segments of proximal tubules (PST) and ascending limbs of Henle's loop (HL) are most vulnerable. In toxic acute tubular necrosis, extensive necrosis is present along the proximal tubule segments (PCT) with many toxins (e.g., mercury), but necrosis of the distal tubule, particularly ascending Henle's loop, also occurs. In both types, lumens of the distal convoluted tubules (DCT) and collecting ducts (CD) contain casts
What does this picture demonstrate: Acute tubular necrosis. Some of the tubular epithelial cells in the tubules are necrotic, and many have become detached (from their basement membranes) and been sloughed into the tubular lumina, whereas others are swollen, vacuolated, and regenerating
What are the different pathways of renal infection: Schematic representation of pathways of renal infection. Hematogenous infection results from bacteremic spread. More common is ascending infection, which results from a combination of urinary bladder infection, vesicoureteral reflux, and intrarenal reflux.
What does this picture demonstrate: Vesicoureteral reflux demonstrated by a voiding cystourethrogram. Dye injected into the bladder refluxes into both dilated ureters, filling the pelvis and calyces
What does this picture demonstrate: The vesicoureteral junction. In normal individuals (A), the intravesical portion of the ureter is oblique, such that the ureter is closed by muscle contraction during micturition. The most common cause of reflux is congenital complete or partial absence of the intravesical ureter (B).
What does this picture demonstrate: Acute pyelonephritis. Cortical surface exhibits grayish white areas of inflammation and abscess formation
What does this picture demonstrate: Acute pyelonephritis marked by an acute neutrophilic exudate within tubules and the renal substance.
What does this picture demonstrate: Papillary necrosis. Areas of pale gray necrosis are limited to the papillae
What do these pictures demonstrate: Polyoma virus nephropathy. A, The kidney shows enlarged tubular epithelial cells with nuclear inclusions (arrow) and interstitial inflammation (arrowheads). B, Intranuclear viral inclusions visualized by electron microscopy
What do these pictures demonstrate: A, Chronic pyelonephritis. The surface (left) is irregularly scarred. The cut section (right) reveals characteristic dilation and blunting of calyces. The ureter is dilated and thickened, a finding that is consistent with chronic vesicoureteral reflux. B, Low-power view showing a corticomedullary renal scar with an underlying dilated deformed calyx. Note the thyroidization of tubules in the cortex.
What does this picture demonstrate: Drug-induced interstitial nephritis, with prominent eosinophilic and mononuclear cell infiltrate.
What do these pictures demonstrate: Analgesic nephropathy. A, The brownish necrotic papilla, transformed to a necrotic, structureless mass, fills the pelvis. B, Microscopic view. Note the fibrosis in the medulla
What does this picture demonstrate: Urate crystals in the renal medulla. Note the giant cells and fibrosis around the crystals
What does this picture demonstrate: Myeloma kidney. Note the angulated and tubular casts with macrophages, including multinucleate cells, engulfing them
What does this picture demonstrate: Close-up of the gross appearance of the cortical surface in benign nephrosclerosis illustrating the fine, leathery granularity of the surface
What does this pictured demonstrate: Hyaline arteriolosclerosis. High-power view of two arterioles with hyaline deposition, marked thickening of the walls, and a narrowed lumen
What does this picture demonstrate: Malignant hypertension. A, Fibrinoid necrosis of afferent arteriole (PAS stain). B, Hyperplastic arteriolitis (onion-skin lesion).
What does this picture demonstrate: Fibromuscular dysplasia of the renal artery, medial type (elastic tissue stain). The medium shows marked fibrous thickening, and the lumen is stenotic.
What does this picture demonstrate: Fibrin stain showing platelet-fibrin thrombi (red) in the glomerular capillaries, characteristic of microangiopathic disorders
What does this picture demonstrate: Atheroemboli with typical cholesterol clefts in an interlobar artery
What does this picture demonstrate: Diffuse cortical necrosis. The pale ischemic necrotic areas are confined to the cortex and columns of Bertin
Where are the common obstructive lesions of the urinary tract: Obstructive lesions of the urinary tract.
What does this picture demonstrate: Hydronephrosis of the kidney, with marked dilation of the pelvis and calyces and thinning of the renal parenchyma
What does this picture demonstrate: Nephrolithiasis. A large stone impacted in the renal pelvis.
Compare clear cell and papillary renal cell carcinoma: Cytogenetics (blue) and genetics (red) of clear cell versus papillary renal cell carcinoma
What does this picture demonstrate: Renal cell carcinoma. Typical cross-section of yellowish, spherical neoplasm in one pole of the kidney. Note the tumor in the dilated thrombosed renal vein.
What do this pictures demonstrate: Renal cell carcinoma. A, Clear cell type, B, Papillary type. Note the papillae and foamy macrophages in the stalk. C, Chromophobe type
What does this picture demonstrate: Urothelial carcinoma of the renal pelvis. The pelvis has been opened to expose the nodular irregular neoplasm, just proximal to the ureter.

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