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WorkshoP nr L9 - Renal PathologY ITopic

MICROSCOPY-MIl. Acute postinfectious diffuse GN (MO' ME)2. Progressive raPid GN (MO)3. Minimallesion GN (ME)4. Idiopathic membranous GP (ME)5. Diabetic GS (PAS, MO)6. Chronic GN (MO)MACROSCOPY-MA

Renal diseases

Glomerular nePhroPaties1. Lipoid nephrosis2. Chronic GNObstructive uroPathYl. Urolithiasis2. HydronephrosisMalformationsl. Horse Shoe kidney2. Polycystic kidneY3. Kidney with double pelvis and double ureter

. Glomerular nephropathies - GN. Tubulo-interstitial nephropathies Q'ITI). Vascular NPs-vascular kidney damages in HTAMICROSCOPY-MIGlomerular nephropathies - GN1. Acute postinfectious diffuse proliferative glomerulonefritis. immune complication with diffuse involvement of glomeruli that occurs at2-4weeks after an infection with B haemolytic streptococcus group A. ME - large electron-dense nodular deposits of immune complexes disposed on the

external surface of GBM.MO . diffuse glomerular lesion: all glomeruli are affected simultaneously,bilaterallY'g1'meril*i':i:il3lffr:f1";h+l jllifffi i].u,i,.,u.u,i.n.rcapillary lumen. tenal tubules are normal

II.

III.

2. Rapid progressive glomerulonefritis (RPG). ^ .upid atrd ptogtessive loss of renal function in several months and death. Mb - profiferation of parietal epithelial cells of Bowman capsule ) withobstruction of Bowman space and compressing of the glomerular capillariesMO-optic microscoPYME-electronic microscoPY

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3. Minimal change GN (lipoid nephrosis)EM. primary lesion is on glomerular ) fusion of extracapilary epithelial cell processes. epithelial cells come into direct contact with the GBM, which becomes permeablewith loss of lipoproteins, which are reabsorbed at the level of renal tubulesMO. glomenrli are normal. proximal tubular epithelial cells are loaded with lipids ) old term of lipoidnephrosis reflects the presence of numerous fat drops into renal tubules

4. Idiopathic membranous GP (ME)EM. early, immune complex deposits on the external surface of GBM with GBMexpansion between these deposits looking as radiary spikes (aspect of wheel). late, the spikes fuse and include immune deposits resulting alacy appearance

MO - thickening of basement membrane of golmerular cappilaries5. Diabetic GS (PAS--MO)MO-3 types of glomerular lesionsa. GBM thickening is the(+) deposits most early form of diabetic microangiopathy : PASb. diffuse GS (Sdr. Bell) consists of diffuse deposits of PAS (+') material intoglomerular mesangiumc. nodular GS (Kimmelstiel-Wilson sdr) consists of nodular deposits of PAS (+)material into glomerular mesangiumEvolution-deposits increase with obliteration of capillary lumen and development of CRF6. Chronic GN (MO). end stage of glomerular nefropathies; the main cause of chronic renal failureMI . Glomeruli are hyalinized and corresponding tubules are replaced by connective

tissueo I reduced number of glomeruli and tubules are hypertrophied, (increased involum but with a normal function) giving the appearance of corticalmicrogranulararitY. There is a marked interstitial fibrosis associated with chronic inflammationMACROSCOPY-MII. Glomerular nephropaties1. Minimal change disease (lipoid nephrosis). kidneys u.i itt.t"uted of volume, the renal cortex being pale-yellow (byaccumulation of lipids in the tubular epithelium) and with smooth external surface2. Chronic GN. both kidneys are atrophied, pales with an adherent capsule and fine granularexternal surface. On the cut section, the cortex is atrophied with hilar adipose tissue hyperplasia

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II. Obstructive uroPathY^. Urolithiasis- renal disease characterized by abnormal precipitation of urinary salts withformation of solitary or multiple, uni or bilateral calculi (calcium oxalate, calciumphosphate, etc )

- Locations (2)- pielo - caliceal systemo small and multiple calculi through mobilization produce lumbar paino large calculi cause obstruction and urinary stasis (hidronephrosis andsecondary infections)- bladdero calculi coming from uretero local calculi secondary formed by urethral obstruction

^. HydronePhrosis. renal pelvis dilation caused by chronic obstruction of the urinary tract of differentcauses

. Causes: nodular prostate hyperplasia, calculi, malignant tumors. Macroscopy (2 evolutive forms):"' j"'n*#:g,l*ru;ff i;lfl ffJli:#1tri?$war*hinningseclndlrulJlJ:?r'"I,li"",itr,n. renal pelvis, with verv thin wau' irreversible atrophy and fibrosis of renal parenchymaIll.Malformations. Horse Shoe kidneY. the fusion by connective tissue of the 2 kidneys at the inferior or superior poles

. the ureters are located on the front aspect of the kidneys. the renal function is not affected. Polycystic kidneY- the presence of cysts in the kidney- 2 types: adult and infantil tYPesAdult type. -enlarged and irregular kidneys (4 kg), composed of various sized cysts, (5-6 cm)containing a serous or bloody fluid, separated from normal renal parenchymaInfantil type. -kidneys are enlarged and have a preserved shape; they are spongious on the cutsurface due to the presence of cystic fusiforme dilatation that extend radiary to thecortex and medulla.. Kidney with double pelvis and double ureterthe 2 ureters can fuse to a point above the bladder junction or they may haveentire separate courses with different bladder entrances