آزمايشگاه رز - Ackerman Atlas(chaptr23)

Kidney Non-neoplastic

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Figure 23.1 Plastic-embedded semi-thin section stained with toluidine blue showing numerous humps along the capillary walls (arrows) and obliteration of the glomerular capillary loops by endocapillary cell prolifera- tion in a case of poststreptococcal glomerulonephritis

Figure 23.2 Electron Micrograph of Normal Glomerulus Showing the Relationship of Different Cell Types. The epithelial aspect of the basement membrane is covered by foot processes (arrows) and the capillary lumen lined by attenuated endothelium. EN, Endothelial cell; EP, epithelial cell; ME, mesangium (x13,000)

Figure 23.3 Scanning electron micrograph showing the capillary loops covered by visceral epithelial cells and interdigitating foot processes (x8000)

Figure 23.4 Glomerulus From a Patient With Minimal Change Disease. The glomerulus is normocellular, the capillary loops are patent, and the basement membrane is normal in thickness

Figure 23.5 Portion of a glomerulus from a patient with minimal change disease showing obliteration of foot processes. The visceral epithelial cell cytoplasm shows microvillus and cyst formation (x8400)

Figure 23.6 Immunofluorescence preparation demonstrating numerous albumin-positive resorption droplets in the proximal tubular epithelial cells

Figure 23.7 Biopsy From a Patient With Focal and Segmental Glomerulosclerosis. One of the glomeruli shows segmental sclerosis, while the other appears unremarkable. Tubular atrophy is also seen (periodic acid-Schiff stain; PAS)

Figure 23.8 Tip variant of focal segmental glomerulosclerosis shows Bowman capsular adhesion and hyaline insudation at the tubular pole. The adjacent podocytes also show hypertrophy with cytoplasmic protein droplets (PAS)

Figure 23.9 Immunofluorescence microscopy demonstrating segmental deposition of IgM in a biopsy from a patient with focal and segmental glomerulosclerosis (anti-IgM)

Figure 23.10 Collapsing variant of focal segmental glomerulosclerosis lesion is characterized by the retracted glomerular basement membrane and hyperplastic overlying podocytes obliterating the Bowman space. The podocytes have prominent cytoplasm protein droplets (PAS)

Figure 23.11 Membranous Glomerulonephritis, Stage I. Basement membrane is normal thickness. Small subepithelial deposits (arrows) are separated from the basement membrane by a thin clear zone (inset). The epithelial foot processes are obliterated (x6000; inset x9100)

Figure 23.12 A, Membranous glomerulonephritis, stage II. Subepithelial deposits are separated by projections of the basement membrane (x18,000). B, Silver preparation showing spike formation along the thickened basement membrane (methenamine silver)

Figure 23.13 Membranous Glomerulonephritis, Stage III. The basement membrane is markedly thickened and the deposits appear surrounded by a newly formed basement membrane (arrows) (x6900)

Figure 23.14 Membranous Glomerulonephritis, Stage IV. The basement membrane is markedly irregular and most of the deposits have been reabsorbed, leaving large electron-lucent areas (x9360)

Figure 23.15 Immunofluorescence preparation of membranous glomeru- lonephritis showing peripheral granular deposits of IgG (anti-IgG)

Figure 23.16 Diffuse granular capillary wall staining with antibody to PLA2R supports a diagnosis of primary membranous nephropathy (anti-PLA2R)

Figure 23.17 Diabetic glomerulosclerosis with segmental mesangial Kimmelstiel-Wilson nodule and adjacent microaneurysm. Other mesangial areas have mild diffuse mesangial sclerosis. Arteriolar hyaline insudation is seen near the vascular pole (methenamine silver stain)

Figure 23.18 Nodular Diabetic Glomerulosclerosis. The massive enlargement of the mesangium is due to an increase in mesangial matrix. The basement membrane is markedly thickened and a capsular drop is present at the left upper corner of the figure (x4400)

Figure 23.19 Diabetic glomerulosclerosis with linear staining for IgG along the glomerular basement membrane (anti-IgG)

Figure 23.20 Acellular Amorphous Deposits of Amyloid in the Mesangium With Patchy Glomerular Capillary Wall Extension. A, These deposits are weakly PAS positive in comparison to the Bowman capsule. B, Amyloid deposits have a grayish blue appearance on trichrome stain

Figure 23.21 A, Deposits of amyloid exhibiting birefringence under polarized light (Congo red stain). B, Fluorescence of amyloid under ultraviolet light (thioflavin T stain)

Figure 23.22 Portion of a glomerulus with large amounts of mesangial deposits of amyloid. The typical fibrillary ultrastructural appearance of the amyloid fibrils is shown at high magnification (x5000; inset x54,000)

Figure 23.23 Fibrillary Glomerulonephritis. A, Mild mesangial hypercellularity and expansion by PAS positive material. The glomerular basement membranes are also mildly thickened (PAS). B, Randomly oriented fibrils in the mesangium and along the glomerular basement membrane (x25,000). C, Granular mesangial and segmental capillary wall deposits stain with IgG (anti-IgG)

Figure 23.24 Biopsy from a patient with light chain deposition disease showing nodular mesangial lesions resembling those of diabetes mellitus

Figure 23.25 Light Chain Deposition Disease. Immunofluorescence preparation demonstrating reactivity for kappa light chain along the glomerular basement membrane, mesangium, Bowman capsule, tubular basement membrane and vessel walls (anti-kappa)

Figure 23.26 Light Chain Deposition Disease. A, Subendothelial and mesangial deposition of granular electron dense material (x7000). B, Similar granular electron-dense deposits are seen along the outer aspect of tubular basement membrane (x8000)

Figure 23.27 Microcystic dilation of proximal tubules and interstitial scarring in a 1-year-old child with congenital nephrotic syndrome, Finnish type

Figure 23.28 Mesangial sclerosis and consolidation with prominent overlying podocytes are typical for diffuse mesangial sclerosis (methe- namine silver)

Figure 23.29 Diffuse Proliferative Glomerulonephritis. There is marked hypercellularity due to an increase in mesangial and endothelial cells and infiltration by inflammatory cells

Figure 23.30 Biopsy From a Patient With Acute Poststreptococcal Glomerulonephritis. There are numerous humps along the basement membrane. The capillary loops are obliterated by cell proliferation and inflammatory cells. Small amounts of fibrin are present in the subendothelial areas (arrows) (x9800)

Figure 23.31 Poststreptococcal Glomerulonephritis. The coarse granular immunostaining for C3 along the capillary loops corresponds to the humps seen by electron microscopy (anti-C3)

Figure 23.32 Membranoproliferative Pattern Glomerulonephritis. There is an increase in lobulation, diffuse mesangial hypercellularity, and thickening of the capillary walls

Figure 23.33 Silver preparation showing marked increase in mesangial matrix in the centrolobular areas with peripheral extension of the mesan- gium producing a double contour (membranoproliferative) pattern in the loops (methenamine silver)

Figure 23.34 Glomerular capillary loop from a patient with membrano- proliferative pattern glomerulonephritis showing peripheral extension of the mesangium into capillary loop, basement membrane duplication, and subendothelial deposits (x5400)

Figure 23.35 Dense deposit disease has variable histologic manifestations. Crescent formation with mild segmental mesangial expansion by inflam- matory cells in a young patient (PAS)

Figure 23.36 A, There is homogeneous, highly dense material within the lamina densa (short arrows) and nodular deposits (long arrows) of the same electron density in the mesangium. The capillary lumen (CL) in the left lower portion of the figure is narrowed due to peripheral extension of the mesangium. Numerous neutrophils are also present (x4000). B, Immunofluorescent staining for C3 showing weak linear staining along glomerular capillary and tubular basement membranes (right lower corner) and bright granular deposits in the mesangium, some of which have a ring-like pattern

Figure 23.37 C3 Glomerulonephritis. A, Segmental mesangial proliferation and glomerular basement membrane thickening (methenamine silver). B, Intramembranous and subepithelial electron-dense deposits with focal glomerular basement membrane duplication (x7000). C, Granular segmental mesangial and capillary wall deposits with C3. No immunoglobulin staining was observed by immunofluorescence (anti-C3)

Figure 23.38 Membranoproliferative Glomerulonephritis With Immune Complexes. Immunofluorescence preparation demonstrating immuno- reactivity for IgG (and C3) in the mesangium and along patchy capillary loops (anti-IgG)

Figure 23.39 Mesangial enlargement with increase in mesangial matrix and cellularity in IgA nephropathy (PAS)

Figure 23.40 Portion of a glomerulus from a patient with IgA nephropathy showing paramesangial electron-dense mesangial deposits (arrows) (×6000)

Figure 23.41 Immunofluorescence preparation of a glomerulus dem- onstrating mesangial deposits of IgA (anti-IgA)

Figure 23.42 Silver-stained histologic preparation of a glomerulus with epithelial crescent obliterating the Bowman space and extending into the proximal tubule. The glomerular tuft is entrapped in the crescent

Figure 23.43 Immunofluorescent preparation showing massive fibrin deposition within the crescent and glomerular capillary tuft (anti-fibrinogen)

Figure 23.44 Disruption of the glomerular basement membrane (arrows) in a case of crescentic glomerulonephritis (×9000)

Figure 23.45 Continuous linear IgG reactivity along the capillary walls in a case of anti-GBM glomerulonephritis (anti-IgG)

Figure 23.46 Coarse granular deposits of IgG are prominent in the mesangium and along the capillary walls in a patient with crescentic lupus nephritis (anti-IgG)

Figure 23.47 Destruction of the capillary tuft by a cellular crescent in a patient with pauci-immune glomerulonephritis. It is characterized by the absence of deposits on immunofluorescence, and note the lack of mesangial or endocapillary proliferation in preserved portions of the capillary tuft

Figure 23.48 Lupus Nephritis, ISN/RPS Class II. There is mild diffuse mesangial hypercellularity and an increase in matrix. Mesangial deposits can be identified by immunofluorescence and electron microscopy

Figure 23.49 Lupus Nephritis, International Society of Nephrology/ Renal Pathology Society Class III. A, There is focal and segmental glomerulonephritis characterized by segmental necrosis, adhesions to the Bowman capsule, and leukocytic infiltration. B, A glomerulus with a well-circumscribed area of necrosis containing numerous small hematoxylin bodies. C, Glomerulus with necrosis, fibrin extravasation, and a cellular crescent

Figure 23.50 Lupus Nephritis, ISN/RPS Class IV. Glomerulus from a patient showing several wire loops (subendothelial deposits) and intraluminal hyaline thrombi (deposits) (PAS)

Figure 23.51 Immunofluorescence showing large amounts of granular immune complex deposits not only in the mesangium and glomerular capillary loops, but also along tubular basement membranes, interstitium, blood vessels, and Bowman capsule (anti-IgG)

Figure 23.52 A, Capillary loop showing marked accumulation of deposits in the mesangium and subendothelial regions. The deposits in the latter location represent the wire loop seen by light microscopy. CL, Capillary lumen; EN, endothelial cell; ME, mesangium (x7000). B, Subendothelial deposits displaying a fingerprint-like pattern (x77,000). C, Tubuloreticular inclusions in an endothelial cell (x30,000)

Figure 23.53 Lupus Nephritis, ISN/RPS Class V. The capillary walls are thickened and the mesangial matrix is segmentally increased

Figure 23.54 Transmural vasculitis and fibrinoid necrosis involving a medium-sized artery, likely an interlobar artery, in polyarteritis nodosa. The glomeruli sampled in the kidney biopsy lacked crescents

Figure 23.55 Renal biopsy from a patient with microscopic polyangiitis showing a small vessel with necrosis and inflammatory infiltrate. The glomerulus has a segmental area of necrosis, and an early crescent (methenamine silver). (Image courtesy Megan Troxell, MD, PhD.)

Figure 23.56 Cryoglobulinemic glomerulonephritis with diffuse proliferation, lobular accentuation and intraluminal hyaline thrombi (deposits) (PAS)

Figure 23.57 Subepithelial deposits demonstrating fibrillary configuration in a case of cryoglobulinemic glomerulonephritis (x21,500)

Figure 23.58 Glomerulus with capillary fibrin thrombi, karyorrhexis and entrapped fragmented red blood cells in acute thrombotic microangiopathy

Figure 23.59 Glomerulus From a Patient With Antiphospholipid Antibody Syndrome. Diffuse glomerular basement membrane multilayering is seen along with mesangiolysis and endothelial swelling (PAS)

Figure 23.60 Portion of a glomerulus showing a prominent subendothelial electron-lucent zone (arrows) and mesangiolysis in a case of acute thrombotic microangiopathy (x9000)

Figure 23.61 Interlobular artery showing stenosing intimal mucoid edema in a patient with systemic sclerosis and acute renal failure (trichrome)

Figure 23.62 Preeclamptic Renal Disease. The glomerular capillary lumina are obliterated by swollen endothelial cells

Figure 23.63 Interstitial foam cells and focal segmental glomerulosclerosis in a patient with microscopic hematuria and ultrastructural features of Alport syndrome (PAS)

Figure 23.64 Glomerular capillary loop showing diffuse, irregular, thickening of the glomerular basement membrane. The lamina densa is split into multiple interwoven lamellae (x11,400)

Figure 23.65 Capillary loop showing marked uniform thinning of the glomerular basement membrane (x4200). (Reproduced from Spargo BH, Seymour AE, Ordóñez NG. Renal Biopsy Pathology with Diagnostic and Therapeutic Implications. New York, NY: John Wiley and Sons; 1980:398. By permission of John Wiley and Sons, Inc.)

Figure 23.66 Plastic-embedded semi-thin section of a portion of a glomerulus stained with toluidine blue showing numerous deeply stained visceral epithelial cell inclusions in a case of Fabry disease

Figure 23.67 Portion of a glomerulus from a patient with Fabry disease demonstrating numerous laminated inclusions in the epithelial cell cytoplasm (x7750)

Figure 23.68 Collagen-like fibers in the glomerular basement membrane in nail-patella syndrome (x35,000). (Reproduced from Spargo BH, Seymour AE, Ordóñez NG. Renal Biopsy Pathology with Diagnostic and Therapeutic Implications. New York, NY: John Wiley and Sons; 1980:400. By permis- sion of John Wiley and Sons, Inc.)

Figure 23.69 Hyperacute Rejection. There is endothelial denudation of the glomerular basement membrane and capillary occlusion by degranulated platelets (x7980)

Figure 23.70 Peritubular Capillaritis With Dilated Capillaries and Intraluminal Mononuclear Cells. Prominent interstitial edema is also seen (PAS)

Figure 23.71 Endothelial Injury in Antibody-Mediated Rejection. Portion of a glomerulus showing prominent widening of the subendothelial region by electron lucent material (arrows) (x3500)

Figure 23.72 Immunofluorescence microscopy testing with antibody to C4d shows diffuse peritubular capillary wall staining (anti-C4d)

Figure 23.73 Tubulointerstitial T cell-mediated acute rejection with interstitial edema and inflammation. Intraepithelial lymphocytes are seen in the tubules and many demonstrate acute injury with dilated lumens and brush border loss (PAS)

Figure 23.74 Acute Vascular Rejection (Banff IIA). An interlobular artery with intimal arteritis (PAS)

Figure 23.75 Transplant Glomerulitis and Glomerulopathy. The glomerulus shows increased intraluminal mononuclear inflammatory cells, consistent with transplant glomerulitis. The glomerular basement membrane double contours are a feature of chronic rejection (PAS)

Figure 23.76 Prominent Interstitial Lymphoplasmacytic Inflammation in Polyomavirus Nephropathy. A few tubular nuclei are enlarged with fine chromatin. The presence of viral inclusions is confirmed on immu- nohistochemical stain (anti-SV40) as seen in the inset

Figure 23.77 Acute Tubular Necrosis. A, There is focal necrosis and desquamation of the cells into the tubular lumen. B, The tubules are dilated and lined by flattened epithelium

Figure 23.78 Acute Pyelonephritis in a Patient Presenting With Fever and Elevated Serum Creatinine. There is acute inflammatory infiltrate in the interstitium and tubular lumina

Figure 23.79 Nephrectomy Specimen From a Patient With Obstructive Hydronephrosis. There is interstitial scarring with intense mononuclear inflammatory cell infiltration. The tubules are atrophic, and the glomeruli are relatively spared with periglomerular fibrosis

Figure 23.80 Foamy Histiocytes in Xanthogranulomatous Pyelone- phritis. Lymphocytes and plasma cells were also present at the edges of this mass-like lesion

Figure 23.81 Nephrectomy Specimen From a Patient With Malako- plakia. The interstitium is infiltrated by numerous macrophages with granular cytoplasm. Inset: Several Michaelis-Gutmann bodies are seen in the cytoplasm

Figure 23.82 Electron micrograph of a histiocyte showing numerous phagolysosomes and a Michaelis-Gutmann body with calcified central core (x11,400)

Figure 23.83 Antibiotic therapy-related acute allergic tubulointerstitial nephritis with interstitial edema and inflammation composed of lympho- cytes, monocytes, plasma cells, and eosinophils

Figure 23.84 IgG4-related tubulointerstitial nephritis with dense storiform fibrosis, tubular destruction, and intense lymphoplasmacytic infiltrate. In the appropriate clinical setting, the presence of greater than 10 IgG4+ cells/HPF supports the diagnosis

Figure 23.85 Intranuclear lead inclusions showing dense central cores surrounded by fibrillar material (x15,600)

Figure 23.86 Severely distorted kidney with dilated pelvicalyceal system containing numerous stones in a case of primary oxalosis

Figure 23.87 Oxalate Crystal Under Polarized Light

Figure 23.88 Light Chain Cast Nephropathy. Large, dense PAS-negative tubular casts associated with tubular injury and intratubular neutrophils (PAS)

Figure 23.89 Afferent Arteriole With Subintimal Homogeneous Hyaline Material. Inset: Immunofluorescence preparation showing reaction for C3. (Reproduced from Spargo BH, Seymour AE, Ordóñez NG. Renal Biopsy Pathology with Diagnostic and Therapeutic Implications. New York, NY: John Wiley and Sons; 1980:297. By permission of John Wiley and Sons, Inc.)

Figure 23.90 Malignant Hypertension. Interlobular artery with thinning of the media and marked intimal edema and early fibrosis. The cortex shows glomerular ischemic changes and extensive tubular atrophy (PAS)

Figure 23.91 Malignant Hypertension. Fibrinoid necrosis and intimal edema of the afferent arteriole with ischemic shrinkage of the glomerular capillary tuft (trichrome)

Figure 23.92 Eccentric arteriosclerotic plaque in renal artery causing almost complete obstruction and hypertension. This was resected and arterial continuity reestablished

Figure 23.93 Fibromuscular Dysplasia in a Young Woman With Hypertension. Note aneurysmal formations in this longitudinally sectioned artery demonstrating medial fibrodysplasia with mural aneurysms

Figure 23.94 Fibromuscular Dysplasia in a 23-Year-Old Woman With Hypertension. Segmental resection revealed an artery with the perimedial variety of fibrodysplasia

Figure 23.95 Dysplastic Kidney of an Infant. Opposite kidney appeared normal by pyelogram

Figure 23.96 Dysplastic kidney showing embryonic-like connective tissue and primitive tubules. Immature cartilage is also seen focally (inset)

Figure 23.97 External and cut surface of a nephrectomy specimen from a patient with autosomal dominant polycystic kidney disease