Renal pathology 1

Adulthood polycystic kidney disease From: Stevens A. J Lowe J. Pathology. Mosby 1995

Adulthood polycystic kidney disease

Fig. 19.1. Enlarged and irregular kidneys (4 kg), composed of various sized cysts, (5-6 cm) containing a serous or bloody fluid, separated from normal renal parenchyma

Childhood polycystic kidney disease

Fig. 19.2. Kidney is enlarged with a preserved shape appearing spongious on the cut surface due to the presence of cystic fusiforme dilatation that extend radiary to the cortex and medulla.

RENAL GLOMERULAR STRUCTURE From: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig.19.3

Fig.19.3: Glomerulus: capillaries, mesangial, Bowman layers and space

Glomerular nephropathies From: Stevens A. J Lowe J. Pathology. Mosby 1995

After degree of glomerular damage 4 types of glomerular diseases: • (a) global: entire glomerulus is affected; • (b) segmental: glomerulus is partially affected (1-2 segments); • (c) diffuse: all glomeruli are affected; • (d) focal: only some glomeruli are affected.

a b c d Fig.19.4

Minimal change disease (lipoid nephrosis) From: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig.19.5. EM-fusion of extracapilary epithelial cell processes (podocyte processes).

From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi

Fig.19.6. MO- (a) glomeruli are normal in appearance; (b) tubular epithelial cells are loaded with lipids (tubular resorbtion of lipoproteins abnormal filtered through glomerulus)(Scharlach staining).

Membranous Glomerulonephritis From: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig.19.7. EM: (a) early, immune complex deposits on the external surface of GBM with GBM expansion between these deposits looking as radiary spikes (aspect of wheel); (b) late, the spikes fuse and include immune deposits resulting a lacy appearance.

Fig.19.8. MO (HE): (a) early-normal appearance of glomerular capillary walls; (b) late-diffuse thickening of GBM. MO (metenamin silver stain): deposition of new matrix of GBM around immune complexes

Diffuse proliferative glomerulonefritis From: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig.19.9.

Fig.19.9. Proliferation of endothelial cells and mesangial cells and influs of neutrophils

Fig.19.10. Nodular electron dense deposits of immune complexes, named “humps“, located on the external glomerular basement membrane.

Acute Postinfectious Diffuse Proliferative Glomerulonephritis

From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi

Fig.19.11.

Fig.19.11-12. MO - all glomeruli are affected by glomerular increasing and hypercellularity due to endothelial and mesangial cell proliferation and neutrophil influx in the lumen of glomerular capillaries; renal tubules are normal

Rapidly progressive glomerulonefritis (crescent glomerulonefritis)

From: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig.19.13.

Fig.19.13.Proliferation of parietal epithelial cells of Bowman capsule

Rapidly progressive glomerulonefritisFrom cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi

Fig.19.14. MO - proliferation of parietal epithelial cells of Bowman capsule with obstruction of Bowman space and compresses of the glomerular capillaries.

Diabetic glomerulosclerosis From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi

Fig.19.15

Fig.19.15-16.MO (PAS stain) - Diabetic microangiopaty in kidney: (a) Thickening of glomerular basement membrane (PAS + deposits on glomerular basement membrane); (b) diffuse deposits of PAS + material in glomerular mesangium (digitiforme extensions which radiate from glomerular vascular pole to periphery); (c) nodular deposits of PAS + material in glomerular mesangium.

Diabetic glomerulosclerosisFrom cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi

• manifestation of diabetic microangiopathy: retinopathy, ischemic heart disease and peripheral vascular insufficiency

• MO-3 types of glomerular lesions – GBM thickening is the most

early form of diabetic microangiopathy = PAS (+) deposits

– diffuse GS (Sdr. Bell) consists of diffuse deposits of PAS (+) material into glomerular mesangium

– nodular GS (Kimmelstiel-Wilson sdr) consists of nodular deposits of PAS (+) material into glomerular mesangiulm

• Evolution-deposits increase with obliteration of capillary lumen and development of CRF

Fig.19.17

Chronic glomerulonephritisFrom cases of the Pathology Department - U.M.F. Iasi

• end stage of glomerular nefropathies and is the main cause of chronic renal failure

Morphology MA • both kidneys are atrophied, pales with an

adherent capsule and fine granular external surface

• On the cut section, the cortex is atrophied with hilar adipose tisuue hyperplasia

MI • Glomeruli are hyalinized and

corresponding tubules are replaced by connective tissue

• A reduced number of glomeruli and tubules are normal, but hypertrophied (increased in volum) by taking the function of destroyed glomeruly (give the appearance of cortical microgranulararity)

• There is a marked interstitial fibrosis associated with chronic inflammation

hyalinized glomeruli, tubular atrophy, interstitial fibrosis

Small kidney with microgranular external surface

Fig.19.18

Chronic glomerulonephritis From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi

Fig.19.19

Fig.19.19-20 MO - advanced stage disease: (a) partial or complete glomerular hyalinosclerosis; (b) related tubules to affected glomeruli are atrophied; (c) unaffected tubules are compensatory distend with hyalin cylinder into their lumen (pseudothyroidization); (d) interstitium - chronic inflammatory infiltrate and diffuse fibrosis; (e) arteriolosclerosis (afferent hyalinoarteriolosclerosis).

Fig.19.20

Obstructive uropathy From: Stevens A. J Lowe J. Pathology. Mosby 1995

1. Renal lithiasis

Fig.19.21.Small and multiple calculi and large calculus (hornstag) fill calyces causing obstruction of the urinary drainage and urinary stasis (hidronephrosis and secondary infections).

2. Hydronephrosis

Fig.19.22.Hydronephrosis: (a) dilatation of the renal pelvis, with wall thinning; (b) renal parenchyma is attenuated and the cortex is thinned by irreversible atrophy and fibrosis of renal parenchyma.