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Flashcards in Renal - Pictures Deck (46)
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RPGN

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Rapidly Progressive Glomerulonephritis (Crescentic). Also known as Crescentic Glomerulonephritis.

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acute tubular necrosis

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The brush border in the proximal tubule is not nearly so distinct as it is in the intestine, but it’s nonetheless present, and in favorable sections it can be made out

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Light micrograph of focal segmental glomerulosclerosis, hilar variant. Kidney biopsy. PAS stain.

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Focal segmental glomerulosclerosis

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FSGS

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Membranous nephropathy

Thick GBM, no proliferative change

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[MEMBRANOUS NEPHROPATHY]. Membranous nephropathy is characterized by diffuse thickening of the glomerular capillary basement membrane by subepithelial immune complex deposition. This results in damage and increased permeability of the basement membrane to plasma proteins and hence nephrotic range proteinuria. The disease may be primary or secondary to a variety of causes including drug toxicity, certain carcinomas, certain infections, and SLE. A routine H&E stain usually shows identifiable thickening as seen in this case. (Contributed by Dr. William J. Hunter, Professor of Pathology, Creighton University Medical Center, USA).

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[MEMBRANOUS NEPHROPATHY]. A silver methenamine stain complements other routine stains in highlighting capillary basement membrane thickening (arrow). The variable thickening seen in some capillary loops is due to tangential sectioning affecting those capillary loops. (Contributed by Dr. William J. Hunter, Professor of Pathology, Creighton University Medical Center, USA).

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[MEMBRANOUS NEPHROPATHY]. IgG imunofluoresence shows diffuse granular deposits along the basement membrane in capillary loops. Complement components can also be demonstrated using this technique. (Contributed by Dr. William J. Hunter, Professor of Pathology, Creighton University Medical Center, USA)

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[MEMBRANOUS NEPHROPATHY]. The immune complex deposits are granular in contrast to smooth linear deposits seen in anti-GBM disease. The granularity results from the presence of subepithelial immune complex deposits in a discontinuous fashion along the basement membrane of capillary loops. (Contributed by Dr. William J. Hunter, Professor of Pathology, Creighton University Medical Center, USA)

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[MEMBRANOUS NEPHROPATHY]. Darker electron-dense deposits (arrows) can be seen at the subepithelial aspect of basement membrane (BM). Note also fused foot processes of podocytes at the top. The capillary lumen is lined by fenestrated endothelium seen underneath the capillary basement membrane. (Contributed by Dr. William J. Hunter, Professor of Pathology, Creighton University Medical Center, USA).

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Light micrograph of an essentially normal glomerulus in minimal change disease. There are only 1 or 2 cells per capillary tuft, the capillary lumens are open, the thickness of the glomerular capillary walls is normal, and there is neither expansion nor hypercellularity in the mesangial areas in the central or stalk regions of the tuft (arrows).

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Subendothelial deposits

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ICs are trapped between the endothelial cell and the GBM

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Subepithelial deposits

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ICs pass through the GBM but are trapped beneath the podocytes

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Intramembranous IC deposit

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ICS deposited within the GBM

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What are subendothelial deposits associted with?

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MPGN

DPGN (diffuse proliferative glomerulonephritis) which is also associated with nitramembranous

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What are subepithelial deposits associated with?

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Acute post-strep glomerulonephritis

Membranous nephropathy

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Renal cell carcinoma

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[MINIMAL CHANGE DISEASE]. A silver methenamine stain is used to highlight glomerular capillary and Bowman’s capsule basement membranes and any thickening thereof. This photomicrograph shows a glomerulus with normal thickness of capillary basement membranes (arrow). Although most cases of minimal change disease are seen in children a small number of patients are adults in whom the recovery is not as rapid as in children and some adults are also afflicted with Hodgkin lymphoma (Contributed by Dr. William J. Hunter, Professor of Pathology, Creighton University Medical Center, U.S.A).

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[MINIMAL CHANGE DISEASE]. The diagnostic finding in minimal change disease (MCD) can only be detected using transmission or scanning electron microscopy which shows effacement of the foot processes of visceral epithelial cells (podocytes). However, this finding is not unique to MCD as other renal glomerular disorders may also show effacement of the foot processes. The diagnosis of MCD rests upon typical clinical features with normal light microscopic appearance of glomeruli but effacement of the foot processes as seen by electron microscopy. The effacement is reversible after successful treatment (Contributed by Dr. William J. Hunter, Professor of Pathology, Creighton University Medical Center, U.S.A).

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Fig 2: membranoproliferative glomerulonephritis with huge intracapillary deposits (thrombi) totally filling the capillary lumina (PAS x 250)

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Subendothelial deposit

In this case associated with membranoproliferative glomerulonephritis - can also be associated with DPGN

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In membranoproliferative glomerulonephritis, mesangial interposition gives a “tram track” appearance to the glomerular basement membranes

This is Type I MPGN - Type II is associated with diffuse intramembranous deposits (dense deposit disease) and there are tram tracks

Type I - subendothelial Is with granular IF

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Fatty cast with maltese cross, associated with nephrotic syndrome

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Urine sediment with a fatty cast

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Acute post-streptococcal glomerulonephritis - note the starry sky appearance

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Uric acid crystals - note the rhomboid or rosette shapes

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Uric acid crystals in urine

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Cystine crystal urine

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Coffin lid ammonium magnesium phosphate struvite crystals

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calcium oxalate monohydrate crystal (dumbbell shaped) and a calcium oxalate dihydrate crystal (envelope shaped

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Uric acid crystals

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Renal oncocytoma - note large eosinophilic cells with abundant mitochondria - no perinuclear clearing versus chromophobe renal carcinoma

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Renal oncocytoma

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Thyroidization of the kidney as a result of chronic pyelonephritis

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Linear IgG and C3 associated with goodpastures

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Glomerular tuft with mild global mesangial hypercellularity; direct immunofluorescence demonstrated diffuse mesangial IgA deposits.

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Lupus nephritis, Class V, PAS stain. Click picture to enlarge. Close window to return. Pure membranous glomerulonephritis. The thick “wire-loop” capillaries

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Kimmelsteil-Wilson lesion

Glomeruli with Kimmelstiel-Wilson nodules. The smallest nodules can be more cellular and the greatest nodules tend to be acellular in the centre and surrounded by more cellular zones. Capillaries are seen around these nodules, sometimes adopting an aspect in garland (like in the three nodules indicated with arrows); in some cases we see microaneurisms around nodules. Notice the variability of size of the nodules (H&E, X.400).

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This is nodular glomerulosclerosis (the Kimmelstiel-Wilson lesion) of diabetes mellitus. Nodules of pink hyaline material form in regions of glomerular capillary loops in the glomerulus. This is due to a marked increase in mesangial matrix from damage as a result of non-enzymatic glycosylation of proteins. This is one form of chronic kidney disease (CKD) with loss of renal function over time.

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With Congo Red stain, amyloid deposits produce characteristic apple-green birefringence under polarized light.

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