Nephrology Pathology Slides

K-2

Normal glomerulus (PAS periodic acid Schiff stain). Note PAS positive capillary basement membranes, Bowman's capsule, and tubular basement membranes.

K-3

Normal glomerulus (silver stain).  Note staining of basement membranes.  What discriminatory value has the silver staining method compared to the PAS method in diagnosis of glomerular disease?

K-4

Normal glomerulus (EM electron microscopy).  Note uniform thickness of capillary basement membrane, central lamina densa area, endothelial cell cytoplasm on the luminal aspect, and discrete epithelial cell foot processes opposed to the outer aspect of  the capillary, with epithelial cell cytoplasm.

K-5

Diffuse proliferative glomerulonephritis (GN), H & E.  Note enlarged, hypercellular glomeruli.  What cells proliferate?

K-6

Diffuse proliferative GN, H & E, very high power.  Note swelling of capillary endothelial cells which has led to marked reduction in the capillary lumina.  What effect would this have on glomerular filtration?

K-9

Rapidly progressive (crescentic) GN, H & E.  Note the hypercellular glomerulus with an epithelial crescent.  What does the presence of crescents denote?  What is the fate of these crescents?

K-10

Focal segmental proliferation GN, H & E.  Cellular proliferation is limited to a segment of the glomerular tuft.  This is from a case of Berger's disease.

K-11

Berger's disease, immunofluorescence IgA.  Note granular pattern of IgA predominantly in mesangial areas.  This disease is also called IgA nephropathy.  (Compare to K-27).

K-13

Membranous nephropathy, H & E.  Note enlarged but normocellular glomeruli.

K-15

Membranous nephropathy, silver stain.  This stain reveals a spiked pattern to the thickened basement membrane, with silver resistant areas between the spikes, representing the sites of immune-complex deposition.

K-16

Membranous nephropathy, immunofluorescence IgG.  Note finely granular IgG along capillary walls.

K-17

Membranous nephropathy, EM.  Electron-dense deposits are present, largely in a subepithelial location.

K-19

Focal segmental glomerulosclerosis, Masson trichrome stain for collagen.  A segment of the glomerulus is sclerosed as shown by the presence of blue-staining collagen.  What is the clinical significance of such a finding in childhood nephrotic syndrome?

K-26

Goodpasture's syndrome.  Renal biopsy, H & E.  There is a proliferative GN with epithelial crescent formation.

K-27

Kidney (normal) used to demonstrate anti-GBM antibody from patient with Goodpasture's syndrome.  Immunofluorescence, IgG.  There is continuous linear deposition of IgG along the capillary basement membrane.  What is the pathogenesis of the renal and pulmonary lesions of Goodpasture's syndrome?  (Compare to K-27)).

K-28

Systemic lupus erythematosus (SLE), renal biopsy.  The peripheral capillary loops are eccentrically thickened due to deposition of large immune complexes, to form the so-called "wire loop" lesions.

K-30

SLE nephropathy, EM.  A characteristic large subendothelial electron-dense deposit is present.

K-31

Polyarteritis nodosa, renal biopsy, H & E.  There is necrotising inflammation in a segment of the wall of a medium-sized intrarenal artery.  A proliferative endarteritis is also present.

K-36

Diabetes mellitus:  Diffuse glomerulosclerosis, H & E.  There is a diffuse increase in mesangial matrix and glomerular capillary basement membrane thickening.

K-37

Diabetes mellitus:  Focal nodular glomerulosclerosis, (Kimmelstiel-Wilson lesion), H & E.  There is a nodular hyaline expansion at the centre of glomerular lobules.  What is the mechanism of formation of the renal lesions in diabetes mellitus?  What are the clinical manifestations of diabetic renal disease?

K-38

Renal amyloidosis, H & E. Glomeruli and vessel walls contain amorphous, hyaline, eosinophilic material encroaching upon vascular lumina.

K-39

Renal amyloidosis, Congo red stain. Note that the amyloid has an affinity for the dye Congo red.

K-40

Renal amyloidosis, Congo red staining viewed in polarized light. Note yellow-green birefringence of the Congo red stained amyloid in polarized light.

K-41

Renal amyloidosis, EM of glomerular capillary. Note fibrillar material (amyloid) expanding the mesangium and encroaching upon the capillary lumen, resulting in narrowing.

K-43

Myeloma kidney, H & E. The renal tubules are dilated and filled with dense casts surrounded by necrotic tubular epithelial cells and giant cells. There is interstitial fibrosis and a scanty round cell infiltrate. What is the derivation of the tubular casts?

K-44

Chronic glomerulonephritis, gross specimen of kidneys. The kidneys are markedly contracted and reduced in weight with reduction in the cortical parenchyma.

K-45

Chronic glomerulonephritis, renal biopsy, H & E. All the glomeruli are hyalinized and obsolete with accompanying renal tubular atrophy. What may be etiology of chronic GN? What are the clinical effects? Name some secondary effects in other organs due to chronic GN, end stage.

K-46

Acute tubular necrosis, gross specimen of kidney. The kidney is swollen and shows a pallor of the cortex on the cut surface.

K-48

Acute renal tubular necrosis, H & E (ischemic type). Necrotic tubular epithelial cells have detached from the tubular basement. How does acute tubular necrosis present clinically? What is the importance of its recognition? What happens in favourable circumstances?

K-50

Ethylene glycol nephrosis, H & E, polarized light. There is ballooned vacuolar degeneration of tubular epithelial cells with birefringent oxalate crystals in the tubular lumina. How may ethylene glycol nephrosis occur?

K-51

Acute pyelonephritis, gross specimen of kidney. The outer surface of the kidney is studded with small pale abscesses.

K-52

Renal papillary necrosis, gross specimen of kidney. The bisected kidney shows necrosis of the tips of the renal papillae. A zone of hyperemia marks the junction between necrotic and viable papillary tissue. Under what circumstances does renal papillary necrosis occur? What are the clinical manifestations?

K-54

Acute pyelonephritis, microscopy, H & E. Neutrophils pack the tubules and are present in the interstitium. What are predisposing causes in acute pyelonephritis? What are the clinical features? What are the urinary findings? What is the usual outcome in treated cases? What are the complications?

K-56

Chronic pyelonephritis, gross specimen of kidney. The kidney shows irregular, coarse scarring on its outer aspect.

K-57

Chronic pyelonephritis, gross specimen of kidney. The bisected aspect of the kidney reveals calyceal scarring and papillary blunting while the outer aspect is coarsely granular. What accounts for the gross appearance of the kidney is chronic pyelonephritis?

K-58

Renal calculus, gross specimen of kidney. A large staghorn calculus fills the pelvi-calyceal system with marked atrophy of cortical parenchyma.

K-59

Chronic pyelonephritis, microscopy, H & E. There is tubular atrophy and dilatation with eosinophilic casts in dilated tubules to give a thyroidization appearance, interstitial chronic inflammatory infiltrate and fibrosis, periglomerular fibrosis and hyaline arteriosclerosis. What etiological mechanisms play a role in chronic pyelonephritis? How do patients present clinically?

K-60

Renal tuberculosis, gross specimen of kidney. There is pelvi-calyceal dilatation and distortion with irregular, blunted renal papillae and cortical thinning, and the characteristic caseous necrotic material is present in markedly dilated calyces. How does renal tuberculosis arise? What are the clinical manifestations? What are the complications?

K-61

Chronic analgesic nephropathy, gross specimen of kidney.  The renal papillae show distortion and blunting with cortical atrophy, scarring ad depression in areas overlying distorted papillae.  What is the etiology and pathogenesis of this disorder?  How does it present clinically?

K-68

Renal artery dysplasia, gross specimen of renal artery and hilar area of kidney. Note a segment of narrowing in the mid-portion of the renal artery. What may be the mechanisms of hypertension in these patients?

K-69

Hemolytic uremic syndrome, renal biopsy, H & E. Glomerular capillaries are occluded by fibrillar eosinophilic material.

K-74

Horseshoe kidney, gross of kidneys. The upper poles of the kidneys are fused.

K-75

Hypoplastic kidney, gross of kidney. The kidney is tiny (15 gm). Note the double ureter in its upper portion.

K-76

Infantile polycystic kidneys, gross of kidneys. The cut surfaces of each kidney reveal a sponge-like cystic structure in both cortex and medulla with no normal renal parenchyma.

K-78

Adult polycystic disease, gross of kidney. This kidney weighed 1000 gms (normal weight is 150 gm) and consisted of a mass of cysts, some with hemorrhage within them, to give an appearance likened to a mass of grapes. What may be the clinical presentation? Do you know of associated lesions these patients may have?

K-80

Simple renal cyst, gross. A large cortical cyst is present, lined by a glistening smooth membrane

K-82

Infantile hydroureters and hydronephrosis, gross of kidneys, ureters and bladder. There is marked bilateral hydroureter, with dilatation of the renal pelvis. The etiology here was congenital posterior urethral valves in a male infant with urethral obstruction and dilatation in the proximal urinary tract. What is the outcome of this disorder uncorrected? How would you recognize it clinically?