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Renal biopsy
/content/chapter/10.22233/9781910443354.chap13
Renal biopsy
- Authors: Shelly L. Vaden and Cathy Brown
- From: BSAVA Manual of Canine and Feline Nephrology and Urology
- Item: Chapter 13, pp 161 - 171
- DOI: 10.22233/9781910443354.13
- Copyright: © 2017 British Small Animal Veterinary Association
- Publication Date: January 2017
Abstract
Dogs and cats with renal diseases can often be described as having acute kidney injury, chronic kidney disease or a glomerulopathy on the basis of the patient history and the results of the physical examination and clinical laboratory tests. This chapter considers indications, contradictions, procurement of the specimen, care of the patient following renal biopsy, complications, and morphological classification of renal disease.
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Figures
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13.4
(a) Ultrasound-guided renal biopsy in a dog. Note that the probe is held in one hand while the needle is held in the other hand. (b) The ultrasonographic image of the dog in (a). This image is used to guide the needle to the kidney and through the cortex. (Reproduced from
Vaden (2004)
with permission from Elsevier) © 2017 British Small Animal Veterinary Association
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13.4
(a) Ultrasound-guided renal biopsy in a dog. Note that the probe is held in one hand while the needle is held in the other hand. (b) The ultrasonographic image of the dog in (a). This image is used to guide the needle to the kidney and through the cortex. (Reproduced from
Vaden (2004)
with permission from Elsevier)
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13.5
Schematic demonstrating correct and incorrect methods of directing the renal biopsy needle. Note that the needle should remain in the renal cortex, preferably in either the cranial or caudal pole. The needle should not cross the corticomedullary junction nor enter either the renal medulla or pelvis. (Reproduced from
Vaden (2004)
with permission from Elsevier) © 2017 British Small Animal Veterinary Association
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13.5
Schematic demonstrating correct and incorrect methods of directing the renal biopsy needle. Note that the needle should remain in the renal cortex, preferably in either the cranial or caudal pole. The needle should not cross the corticomedullary junction nor enter either the renal medulla or pelvis. (Reproduced from
Vaden (2004)
with permission from Elsevier)
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13.7
Normal renal cortex containing glomeruli, tubule cross-sections and scant interstitium. Most tubular profiles are proximal in origin, with fewer distal tubules (DT) present. (H&E stain; original magnification X100) © 2017 British Small Animal Veterinary Association
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13.7
Normal renal cortex containing glomeruli, tubule cross-sections and scant interstitium. Most tubular profiles are proximal in origin, with fewer distal tubules (DT) present. (H&E stain; original magnification X100)
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13.8
Acute tubular necrosis in a dog with acute leptospirosis. Proximal tubules are dilated with attenuation of the epithelium, brush border loss and occasional sloughing of necrotic epithelial cells into the lumen (arrowed). The tubules are no longer touching due to expansion of the interstitium with oedema and erythrocytes (*). (H&E stain; original magnification X200) © 2017 British Small Animal Veterinary Association
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13.8
Acute tubular necrosis in a dog with acute leptospirosis. Proximal tubules are dilated with attenuation of the epithelium, brush border loss and occasional sloughing of necrotic epithelial cells into the lumen (arrowed). The tubules are no longer touching due to expansion of the interstitium with oedema and erythrocytes (*). (H&E stain; original magnification X200)
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13.9
(a) Toxic acute tubular necrosis in a cat with Easter lily toxicosis. Segments of the proximal tubule are devoid of viable epithelium, and are lined or filled with necrotic cellular debris (*). (b) Toxic acute tubular necrosis in a cat with ethylene glycol toxicosis. Tubules are mildly dilated and the epithelium is attenuated, with individual cell necrosis and karyorrhexis (arrowed). Histological diagnosis is dependent on the finding of large numbers of oxalate crystals (*) within tubules. (H&E stain; original magnification X400) © 2017 British Small Animal Veterinary Association
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13.9
(a) Toxic acute tubular necrosis in a cat with Easter lily toxicosis. Segments of the proximal tubule are devoid of viable epithelium, and are lined or filled with necrotic cellular debris (*). (b) Toxic acute tubular necrosis in a cat with ethylene glycol toxicosis. Tubules are mildly dilated and the epithelium is attenuated, with individual cell necrosis and karyorrhexis (arrowed). Histological diagnosis is dependent on the finding of large numbers of oxalate crystals (*) within tubules. (H&E stain; original magnification X400)
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13.10
(a) Subacute puruloplasmacytic tubulointerstitial nephritis in a dog with leptospirosis. Tubules are separated (double arrows) by large numbers of neutrophils (PMNs) and plasma cells (PCs, arrowed), and fewer macrophages. Neutrophils are also present within tubules (*). (H&E stain; original magnification X200). (b) Typical positive leptospiral immunohistochemistry, showing clumps of positive staining material in interstitial macrophages, tubular epithelial cells and the tubular lumen. Intact spirochaetes (arrowed) are also present within the tubular lumen. (Avidin–biotin–peroxidase method, haematoxylin counterstain; original magnification X400) © 2017 British Small Animal Veterinary Association
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13.10
(a) Subacute puruloplasmacytic tubulointerstitial nephritis in a dog with leptospirosis. Tubules are separated (double arrows) by large numbers of neutrophils (PMNs) and plasma cells (PCs, arrowed), and fewer macrophages. Neutrophils are also present within tubules (*). (H&E stain; original magnification X200). (b) Typical positive leptospiral immunohistochemistry, showing clumps of positive staining material in interstitial macrophages, tubular epithelial cells and the tubular lumen. Intact spirochaetes (arrowed) are also present within the tubular lumen. (Avidin–biotin–peroxidase method, haematoxylin counterstain; original magnification X400)
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13.11
Normal canine glomerulus stained with periodic acid–Schiff haematoxylin (PASH). The basement membranes of Bowman’s capsule, tubules and the glomerular capillaries, and the mesangial matrix stain dark pink. (PASH stain; original magnification X400) © 2017 British Small Animal Veterinary Association
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13.11
Normal canine glomerulus stained with periodic acid–Schiff haematoxylin (PASH). The basement membranes of Bowman’s capsule, tubules and the glomerular capillaries, and the mesangial matrix stain dark pink. (PASH stain; original magnification X400)
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13.12
(a) Normal glomerular capillary. Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission. (b) Electron micrograph of the normal glomerular capillary wall. Note the fenestrated capillary endothelium that results in endothelial cell pores, the glomerular basement membrane (*) and the podocyte foot processes. (b Reproduced from
Vaden (2005)
with permission from Elsevier. Original image courtesy of JC Jennette, Chapel Hill, NC, School of Medicine, University of North Carolina) © 2017 British Small Animal Veterinary Association
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13.12
(a) Normal glomerular capillary. Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission. (b) Electron micrograph of the normal glomerular capillary wall. Note the fenestrated capillary endothelium that results in endothelial cell pores, the glomerular basement membrane (*) and the podocyte foot processes. (b Reproduced from
Vaden (2005)
with permission from Elsevier. Original image courtesy of JC Jennette, Chapel Hill, NC, School of Medicine, University of North Carolina)
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13.13
Glomerular amyloidosis in a dog. Large nodular accumulations of eosinophilic homogeneous material (amyloid, arrowed) displace nuclei to the periphery. Glassy eosinophilic casts (*), indicative of proteinuria, are present in distal tubules. (H&E stain; original magnification X400) © 2017 British Small Animal Veterinary Association
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13.13
Glomerular amyloidosis in a dog. Large nodular accumulations of eosinophilic homogeneous material (amyloid, arrowed) displace nuclei to the periphery. Glassy eosinophilic casts (*), indicative of proteinuria, are present in distal tubules. (H&E stain; original magnification X400)
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13.14
Membranous glomerulonephropathy (MGN). (a) MGN is characterized by normal glomerular cellularity or mild mesangial cell hyperplasia; endocapillary hypercellularity is absent. Global diffuse capillary wall thickening may be appreciated in more chronic cases (arrowed) due to remodelling; special stains are required to visualize these changes. Podocytes are hypertrophied (arrowhead), which is a non-specific indication of podocyte injury. Protein in a renal tubule (*) is also seen here.(H&E stain; original magnification X400) (b) Well developed spikes (yellow arrowheads) of remodelled glomerular basement membrane (GBM) extending from the abluminal aspect of the capillary wall. Occasional holes, representing immune complexes surrounded by GBM, are also present (light blue arrow). (PASH stain; original magnification X600) (c) Peripheral capillary loops in chronic MGN. Numerous large electron-dense deposits are present on the subepithelial aspect of the GBM (yellow arrows), with new GBM present as spikes on either side (yellow arrowheads) or encircling them (holes) (light blue arrow). Note diffuse podocyte foot process effacement and mild microvillus transformation. E = endothelium; P = podocyte; red arrowheads = native GBM. (Electron micrograph; original magnification X4000) © 2017 British Small Animal Veterinary Association
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13.14
Membranous glomerulonephropathy (MGN). (a) MGN is characterized by normal glomerular cellularity or mild mesangial cell hyperplasia; endocapillary hypercellularity is absent. Global diffuse capillary wall thickening may be appreciated in more chronic cases (arrowed) due to remodelling; special stains are required to visualize these changes. Podocytes are hypertrophied (arrowhead), which is a non-specific indication of podocyte injury. Protein in a renal tubule (*) is also seen here.(H&E stain; original magnification X400) (b) Well developed spikes (yellow arrowheads) of remodelled glomerular basement membrane (GBM) extending from the abluminal aspect of the capillary wall. Occasional holes, representing immune complexes surrounded by GBM, are also present (light blue arrow). (PASH stain; original magnification X600) (c) Peripheral capillary loops in chronic MGN. Numerous large electron-dense deposits are present on the subepithelial aspect of the GBM (yellow arrows), with new GBM present as spikes on either side (yellow arrowheads) or encircling them (holes) (light blue arrow). Note diffuse podocyte foot process effacement and mild microvillus transformation. E = endothelium; P = podocyte; red arrowheads = native GBM. (Electron micrograph; original magnification X4000)
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13.15
Membranoproliferative glomerulonephritis (MPGN). (a) MPGN is characterized by global diffuse glomerular endocapillary hypercellularity, extending to the peripheral capillary loops (arrowed), and variable thickening of the capillary walls. (H&E stain; original magnification X400) (b) Capillary wall thickening in MPGN is due to the formation of GBM double contours, demonstrated with special stains. In contrast to MGN, remodelling occurs on the vascular side of the GBM, associated with mesangial cell (*) interposition. Yellow arrowheads = new remodelled GBM; arrows = native GBM. (JMS stain; original magnification X400) (c) Electron micrograph of a peripheral capillary loop from a dog with MPGN. Large granular electron-dense deposits (immune complexes, black arrows) are present on the subendothelial aspect of the GBM (yellow arrows). Mesangial cell processes (*) are interposed between the native GBM and the overlying endothelial cells (E), with production of new GBM (arrowheads, double contours). There is multifocal podocyte foot process effacement. P = podocyte; rbc = intracapillary red blood cell. (Original magnification X4000) © 2017 British Small Animal Veterinary Association
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Membranoproliferative glomerulonephritis (MPGN). (a) MPGN is characterized by global diffuse glomerular endocapillary hypercellularity, extending to the peripheral capillary loops (arrowed), and variable thickening of the capillary walls. (H&E stain; original magnification X400) (b) Capillary wall thickening in MPGN is due to the formation of GBM double contours, demonstrated with special stains. In contrast to MGN, remodelling occurs on the vascular side of the GBM, associated with mesangial cell (*) interposition. Yellow arrowheads = new remodelled GBM; arrows = native GBM. (JMS stain; original magnification X400) (c) Electron micrograph of a peripheral capillary loop from a dog with MPGN. Large granular electron-dense deposits (immune complexes, black arrows) are present on the subendothelial aspect of the GBM (yellow arrows). Mesangial cell processes (*) are interposed between the native GBM and the overlying endothelial cells (E), with production of new GBM (arrowheads, double contours). There is multifocal podocyte foot process effacement. P = podocyte; rbc = intracapillary red blood cell. (Original magnification X4000)
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13.16
Focal segmental glomerulosclerosis in a dog, involving solidification of a portion of the capillary tuft by extracellular matrix and mesangial cells (black arrows). The sclerotic segment is adhered to Bowman’s capsule (synechiae, arrowheads) and there are areas of hyalinosis (white arrows). (PASH stain; original magnification X400) © 2017 British Small Animal Veterinary Association
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13.16
Focal segmental glomerulosclerosis in a dog, involving solidification of a portion of the capillary tuft by extracellular matrix and mesangial cells (black arrows). The sclerotic segment is adhered to Bowman’s capsule (synechiae, arrowheads) and there are areas of hyalinosis (white arrows). (PASH stain; original magnification X400)
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13.17
Glomerular basement membrane (GBM) defect in a young dog. Ultrastructurally, the GBM shows diffuse splitting with a multilayered appearance (arrowheads) and spreading (effacement) of the podocyte foot processes. © 2017 British Small Animal Veterinary Association
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13.17
Glomerular basement membrane (GBM) defect in a young dog. Ultrastructurally, the GBM shows diffuse splitting with a multilayered appearance (arrowheads) and spreading (effacement) of the podocyte foot processes.