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Renal pathology : 

Renal pathology Dr. Prabesh K Choudhary 2 nd Yr Resident, Path. NAMS

The kidneys contribute to the body's biochemical homeostasis by: : 

The kidneys contribute to the body's biochemical homeostasis by: eliminating metabolic waste products regulating fluid and electrolyte balance influencing acid-base balance. These vital functions are effected by the filtration of blood plasma in the glomeruli and subsequent processing of the filtrate by the tubules to eventually produce urine.

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The kidneys also produce the following hormones: ● prostaglandins, which are thought to affect salt and water regulation and influence vascular tone ● erythropoietin, which stimulates red cell production ●renin, which acts on the angiotensin pathway to increase vascular tone and aldosterone production.

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normal adult kidney with lobulations

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In cross section, this normal adult kidney demonstrates the lighter outer cortex and darker medulla with central pelvis.

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Normal structure Cortex: a—outer cortex d---renal columns Medulla: c--renal pyramids e—papillae f---renal calyx

Renal corpuscle: 

Renal corpuscle Renal corpuscle glomerulus Bowman’s capsule It has 2 poles: vascular pole and urinary pole.

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Nephron glomerulus from which a proximal convoluted tubule leads to a thin loop of Henle and then to a distal convoluted tubule. There are about 2 million nephrons per  kidney

Renal tubule: 

Renal tubule Proximal convoluted tubule Distal convoluted tubule Loop of Henle Descending L. Loop Ascending L. In cortex In cortex In medulla Renal tubule

Proximal convoluted tubule: 

Proximal convoluted tubule LM: the lumen is irregular. cell: large,cuboidal or pyramidal; cell boundaries are not clear; have brush border on luminal surface; show vertical striations on basal surface . EM: show lateral interdigitations between adjacent cells; have numerous microvilli on the luminal surfaces; have infoldings of cytoplasm on basal surface .

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Function of proximal convoluted tubule Main site of reabsorption: almost all glucose, amino acid and protein; most of H20,ion etc. Secretion : Na+,NH3,etc.

Loop of Henle : 

Loop of Henle Ascending limb: simple squamous epithelium Descending limb: low cuboidal Epithelium Permeability to ions and water

Distal convoluted tubule: 

Distal convoluted tubule The lumen is larger and more regular LM: cells are stained lightly; have distinct cell boundaries; no brush border on free surface; basal striations are obvious. EM: microvilli are much shorter; no lateral interdigitations developed infoldings of cytoplasm .

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Function of distal convoluted tubule Main site for ion exchanging. reabsorption of Na+,H20 and secretion of K+,H+ and NH3.

Collecting tubules: 

Collecting tubules Epithelium: simple cuboidal Function: concentration of urine. Location: in medulla

Formation of urine: 

Formation of urine Filtrate from the blood in glomerulus Renal space Absorption and excretion by renal tubules Further concentrated by collecting tubules Flow into the calyces and pelvis ,then leave the kidney Terminal Urine Primary Urine 180L/d

Juxtaglomerular complex: 

Juxtaglomerular complex Juxtaglomerular cells Modified smooth muscle fibers in tunica media of afferent arteriole at its entry to glomerulus. Function: Producing renin and erythropoietin Macula densa modified epi. of distal convoluted tubule densely packed together at the site of contact with arteriole. Function: Sensing the change of [Na+] Extraglomerular mesangial cells (lacis cells) Between macula densa and afferent and efferent arterioles. Function: Probably related to transferring information.

Juxtaglomerular complex: 

Juxtaglomerular complex

Glomerulus: 

Glomerulus

Mesangium: 

Mesangium Mesangial cells & mesangial matrix Mesenchymal origin Contractility Phagocytosis Matrix & collagen lay down Biologically akin to vascular smooth muscle & pericyte

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glomerulus proximal convoluted tubules

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Endothelial cells ; Basement membrane; Epthelial cells Glomerular filtration membrane (filter) consisting

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Foot processes Lamina rara ext. Lamina densa Lamina rara int. endothelium Glomerular fiter endothelial cells are fenestrated; they have small 'windows', allowing the plasma direct contact with the underlying basement membrane

glomerular filtration barrier: 

glomerular filtration barrier

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Foot processes of epithelium cell podocyte

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visceral epithelium

Basement membrane: 

Basement membrane Type IV collagen Laminin Polyanionic glycoproteins e.g. heparan sulfate Fibronectin Entactin Triple helix of collagen: alfa 1, alfa 2 & alfa 1

Basement membrane suprastructure: 

Basement membrane suprastructure

Glomerular barrier function: 

Glomerular barrier function Size & charge dependent barrier Factors responsible for this function: - Complex structure of the capillary wall - Collagenous suprastructure - Charged structures of the GBM - Anionic moieties in GBM e.g. acidic proteoglycan - Podocyte: Slit diaphragm; synthesis of GBM components

Glomerular slit diaphragm: 

Glomerular slit diaphragm

Glomerulonephritis--GN: 

G lomerulonephritis--GN Secondary GN—caused by a variety of factors and in the course of a number of systemic diseases . SLE , HTN, PAN, DM, Fabry’s disease… Primary GN --- kidney is the only or the predominant organ involved

Primary glomerulonephritis: 

Primary glomerulonephritis

Secondary glomerulonephritis: 

Secondary glomerulonephritis

Histological alterations: 

Histological alterations Hypercellularity Basement Membrane Thickening Hyalinization & Sclerosis Diffuse > involve all glomeruli; * Focal* Global > involve entire glomerulus; *Segmental* Mesangial

Hypercellularity: 

Hypercellularity Inflammatory disease: 3 ways: Cellular proliferation of mesangial or endothelial cells Leukocytic infiltration consisting og neutrophils, monocytes and lypmhocytes Crescents: consists of proliferating parietal epithelial cells and leukocytes; due to fibrin , tissue factor, IL-1, TNF, INF-gamma

Basement membrane thickening: 

Basement membrane thickening LM : thickening of the capillary wall, best seen in PAS stain EM : 2 types: 1> Deposition of amorphous electron dense material (immune complex) on the endothelial or epithelial side of BM or within the GBM itself. 2>Thickening of BM proper e.g. diabetic glomerulosclerosis

Hyalinization & Sclerosis: 

Hyalinization & Sclerosis LM: hyalinization defined as accumulation of homogenous & eosinophilic material EM: hyalinization seen as extracellular & consist of plasma proteins Hyalinization>> obliteration of capillary lumina of glomerullary tuft>> sclerosis Hyalinization & sclerosis: end result of various forms of glumerular damage

Pathogenesis of Glomerular Injury: 

Pathogenesis of Glomerular Injury

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1 、 In situ immune complex deposition : Anti-GBM Nephritis; Masugi mod. Heymann Nephritis; Heymann mod

Localization of immune complexes in the glomeruli: 

Localization of immune complexes in the glomeruli Subepithelial humps: acute GN Epimembranous deposits: membrane=ous & Heymann GN Subendothelial deposits: SLE & membranoproliferative GN Mesangial deposit: Ig A nephropathy Basement membrane

Epithelial cell injury due to antibodies, toxins, cytokines, minimum change disease & focal segmental glomerulosclerosis: 

Epithelial cell injury due to antibodies, toxins, cytokines, minimum change disease & focal segmental glomerulosclerosis

Mediators of glomerular damage : 

Mediators of glomerular damage Complement triggers attracts IC------complement cascade --------neutrophil Polymorphonuclear leukocytes : Attracted by c5a and release proteases>GBM degradation; O2derived free radicals>cell damage; Arachnoid acid metabolites> reduced GFR Macrophages, T-Lymphocytes & NK cell> biologically active molecules Platelets: eicosanoids & GFs Mesangial cells >> several inflammatory mediators

Mediators of glomerular injury: 

Mediators of glomerular injury

Mechanisms of progression in glomerular disease: 

Mechanisms of progression in glomerular disease 2 major histologic characteristics: 1. FSGS 2. Tubulointerstitial fibrosis Several factors involved: - initial severity of renal damage - Nature & persistence of antigens - Immune status, age & genetic predisposition of the host

Focal segmental glomerulosclerosis: 

Focal segmental glomerulosclerosis

Tubulointerstitial fibrosis: 

Tubulointerstitial fibrosis Tubular damage & interstitial inflammation Correlation of tubulointerstitial fibrosis with disease severity Cased by: - Ischemia of tubule segments downstream from sclerotic glomeruli - Acute & chronic inflammation in adjascent interstitium - Damage or loss of peritubular capillary blood supply

Chronic tubulo-interstitial injury: 

Chronic tubulo-interstitial injury

Renal Pathology; Contd.: 

Renal Pathology; Contd. Dr. Prabesh Kumar choudhary Resident pathology, 2 nd Year NAMS, Bir Hopspital

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Pathological types of primary glomerulonephritis Acute diffuse proliferative glomerulonephritis** Poststreptococcal Non-poststreptococcal Rapidly progressive (crescentic~) glomerulonephritis** Membranous glomerulopathy Lipoid nephrosis (minimal change disease) Focal segmental glomerulosclerosis Membranoproliferative glomerulonephritis IgA nephropathy Focal proliferative glomerulonephritis Chronic glomerulonephritis**

Acute diffuse proliferative glomerulonephritis***: 

Acute diffuse proliferative glomerulonephritis*** ( post-infectious GN) It is seen most frequently in children of primary school, 1-4 weeks after group A β-hemolytic streptococcal infection of pharynx or skin (Impetigo). This disease is characterized histologically by diffuse proliferation of glomerular cells, associated with influx of leukocytes.

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Pathogenesis: - Immune complex mediated exogenous antigens : infectious agents , Group A β-hemolytic streptococci 12, 4, & 1 , other causative organisms and conditions including : staphylococci, meningococci, pneumococci, viruses, toxoplasmosis, schitosomiasis, drugs….. Streptococcal antigens: cytoplasmic Ag>endostreptosin & cataionic Ag e.g. proteinase (nephritic strain-associated protein, NSAP) endogenous antigens : DNA, immunoglobulins,, IgA …

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2. Morphology kidney are swollen and enlarged,with petechial hemorrhages on the cortical surfaces

Light microscopy: 

Light microscopy Enlarged hypercellular glomeruli: Leukocytic infiltration, diffuse proliferation of endothelial & mesangial cells & crescent formation (severe cases) Endothelial swelling Capillary obliteration Edema, interstitial inflammation Red cell cast in tubules

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The hypercellularity of post-streptococcal glomerulonephritis is due to increased numbers of epithelial, endothelial, and mesangial cells as well as neutrophils in and around the capillary loops.

Immunofluorescence :granular deposits of IgG, IgM,and C3 The bright deposits scattered along capillary walls and in the mesangium

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Electron microscopy— “humps”like electron-dense deposits on the epithelial side. camel

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electron dense subepithelial "humps" above the basement membrane and below the epithelial cell.

3. Clinico-pathological correlations:: 

3. Clinico-pathological correlations : Acute nephritic syndrome : Hematuria, azotemia, red blood cell casts, variable proteinuria (<1g/day), oliguria, periorbital edema, and hypertension Raised ASO Decreased C3

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outcome : more than 95% of children recovered , 1-2% progress to chronic GN , and a small minority of children develop a rapidly progressive GN(<1%). In adults, the prognosis is poor, 15-50% develop chronic GN & some develop RPGN.

Rapidly progressive (Crescentic)GN: 

Rapidly progressive (Crescentic)GN ~ is a clinicopathologic syndrome in which there is a rapid progression to renal failure. The histologic picture is characterized by the presence of crescents in a majority of the glomeruli.

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Pathogenesis & classification 1. TypeⅠRPGN (anti-GBM Antibody) - Idiopathic - Goodpasture’s syndrome>NC1 of α 3 collagen; triggered by viruses, hydrocarbon, drug & cancer; HLA-DRB1 - IF: linear (IgG, C3) 2. TypeⅡ RPGN (Immune complex GN) - Idiopathic, postinfectious, SLE, HSP, IgA nephropathy IF: granular 3. TypeⅢ RPGN (Pauci-immune)> most common - ANCA;c/p in serum: Wegener-granulaomatosis, Microscopic PAN/ microscopic polyangitis; Isolated> idiopathic (90% show ANCA)>>localized vasculitis - IF: No deposits

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Morphology. Gross: the kidneys are pale and enlarged, often with petechial hemorrhages on the cortical surfaces. LM: crescents (proliferating parietal epithelial cells, monocyte-macrophages, and fibrin between the cellular layers). Obliteration of Bowman space and compression of the glomerular tuft.

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GMB with focal disruptions. Crescents are formed by-----F.fibrin, E. epithelial cell , P. Monocytes and macrophages,

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This immunofluorescence micrograph of a glomerulus demonstrates positivity with antibody to fibrinogen

EM: 

EM Subepithelial humps Small subendothelial and mesangial deposits Ruptures in the GBM Wrinkling of GBM with focal disruption in its continuity

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TypeⅡ RPGN reveals the granular pattern of staining

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Clinical course: R apidly progressive nephritic syndrome The onset of RPGN is much like that of the acute nephritic syndrome except that the oliguria and azotemia are more pronounced.

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Prognosis: poor (progression to end stage renal disease) Death from renal failure within weeks to months. patients with crescents in fewer than 80% of the glomeruli have a slightly better prognosis than those with higher percentages of crescents. The post infectious form of RPGN has a better prognosis than the other forms.

Causes of Nephrotic syndrome: 

Causes of Nephrotic syndrome

Membranous GN---MGN: 

Membranous GN---MGN MGN : is the most common cause of the nephrotic syndrome in adults. Aetiology - 85% of cases-idiopathic; MHC associated>autoimmune - Identifiable causes in some cases (secondary MGN) : -infective ---syphilis, malaria, hepatitis B/C -drugs--penicillamine, gold, mercury, heroin, NSAIDs -tumours --- carcinoma of the lung & Colon & melanoma; 5-10% of cases -SLE; 15% of GN in SLE>> MGN -other autoimmune disorders e.g. thyroiditis - C5b-C9> membrane attack complex>activation of epithelial & mesangial cells>>protease & oxidants>capillary wall injury & protein leakage

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Membranous glomerulonephritis shows deposits of mainly IgG and complement collect in the GBM and appear in a diffuse granular pattern by immunofluorescence.

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Granular deposits

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Histological features : 1. Capillary wall thickening without proliferation or inflammation is present in all glomeruli 2. Uniform, diffuse thickening of the glomerular capillary wall. 3. Eventually sclerosis of mesangium may occur and glomeruli become totally hyalinized.

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membranous glomerulonephritis in which the capillary loops are thickened and prominent, but the cellularity is not increased

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Electron microscopy 1. reveals the immune complexes deposited on the outer aspect of the basement membrane beneath the epithelial cells (epimembranous); effaced foot process 2. BM material between deposits>irregular spikes protruding from the GBM

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"spikes" A silver stain of the glomerulus highlights the proteinaceous basement membranes in black. Basement membrane material appears as projections around the capillary loops.

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Membranous glomerulonephritis IC deposited on the outer aspect of the GBM beneath the epithelial cells. Irregular spikes protruding from the GBM IC be embeded IC be dissolved

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Under the electron microscopy, the "spikes" seen with the silver stain represent the intervening matrix of BM between the deposits.

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By EM in membranous glomerulonephritis, the electron dense deposits are seen scattered within the thickened BM.

Clinical course.: 

Clinical course. nephrotic syndrome : massive proteiuria ( >3.5 gm/day, nonselective) Hypoalbuminemia---protein lost from urine. plasma albumin levels less than 3gm/dl hyperlipidemia---because hypoalbuminemia, synthesis of lipoprotein in liver increased Severe edema--- the losing of protein causes osmotic pressure in blood plasma to decrease

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Prognosis 10% die or progress to renal failure within 10 years <40% develop renal insufficiency A relative benign outcome occur in women and children

Minimal change GN (lipoid nephrosis): 

Minimal change GN (lipoid nephrosis) ~ is the most frequent cause of nephrotic syndrome in children and is much more common in children between 2 and 6 years of age.

Immunological basis of MCD: 

Immunological basis of MCD Association with respiratory infection & prophylactic immunization Response to corticosteroid & immunosuppressive therapy Association with atopic diseases e.g. eczema, rhinitis HLA predisposition Association with HL- defects in T-cell mediated immunity

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Etiology and Pathogenesis. 1. T cell dysfunction >>cytokine>>damages visceral epithelial cells>> Proteinuria 2. loss of polyanion from the GBM >> Proteinuria **Routes of protein through epithelial cells>>transcellular passage through the epithelial cell; Passage through residual spaces between damaged foot processes; Leakage through foci of epithelial cell detachment** **Mutation of nephrin protein**

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Morphology Light microscopy: the glomeruli are normal. Proximal tubular cells> laden with lipid & protein>>lipoid nephrosis (absorption of lipoprotein) Electron microscopy: normal BM; No deposits; visceral epithelial cells>>uniform and diffuse flatening, retraction, and swelling of foot processes>>incorrectly termed fusion of foot processes Foot processes replaced by a rim of cytoplasm showing vacuolization, swelling, & hyperplasia of villi

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This is minimal change disease (MCD) which is characterized by effacement of the epithelial cell foot processes and loss of the normal charge barrier such that albumin selectively leaks out and proteinuria ensues.

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Clinical course nephrotic syndrome : >3.5 gm/day proteinuria, hypoalbuminemia, hyperlipidemia, lipiduria The proteinuria usually is highly selective, most of the protein consisting of albumin Despite massive proteinuria, renal function remains good, and there is commonly no hypertension or hematuria.

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The prognosis in children is good with no permanent renal damage. The disease respond rapidly to corticosteroid therapy (90% in children), but in adults are slower to respond .

Focal segmental glomerulosclerosis (FSGS): 

Focal segmental glomerulosclerosis (FSGS) As the name implies, this lesion is characterized by sclerosis of some glomeruli (thus, it is focal); and in the affected glomeruli, only a portion of the capillary tuft is involved (thus, it is segmental). The disease is accompanied clinically by the nephrotic syndrorne or heavy proteinuria. About 50% patients progress to CRF(chronic renal failure)

Classification and types: 

Classification and types Associated with known conditions: HIV nephropathy; Heroin nephropathy; Sickle cell disease & Massive obesity Adaptive response to renal ablation e.g. reflux nephropathy, hypertensive nephropathy, unilateral renal agenesis Inherited forms: mutation in nephrin, podocin or α -Actin 4 As a primary disease: idiopathic FSGS

Classification and types;contd.: 

Classification and types;contd. Idiopathic FSGS>10% & 35% of nephrotic syndrome in children & adults respectively Rising incidence in & most common cause of nephrotic syndrome in US C/F differing from MCD>>higher incidence of hematuria, reduced GFR & HTN; Non selective proteinuria; Poor response to steroids; Progression to chronic GS; IF>trapping of IgM & C3 in the sclerotic segment

Light microscopy: 

Light microscopy FSGS Juxtaglomerullary glomeruli>later become generalised Sclerotic segment: collapse of BM, increase in matrix & segmental insudation of plasma protein along the capillary wall (Hyalinois)>>aggregate>>obliteration of lumen Lipid droplets & foam cells Glomeruli not showing segmental lesion>>normal LM or may show increased mesangial matrix or mesangial proliferation

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focal segmental glomerulosclerosis (FSGS). An area of collagenous sclerosis runs across the middle of this glomerulus

Electron microscopy: 

Electron microscopy Both sclerotic & non-sclerotic areas>>diffuse effacement of foot processes & focal detachment of epithelial cells with denudation of GBM

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Focal segmental glomerulosclerosis: By IF, IgM and C3 are present within the hyaline masses in the sclerotic areas .

Collapsing glomerulopathy in HIV: 

Collapsing glomerulopathy in HIV Collapse & sclerosis of the entire glomerular tuft in addition to usual features Proliferation & hypertrophy of glomerular visceral epithelial cells Also seen in idiopathic cases Associated prominent tubular injury with formation of microcyst EM: tubular reticular inclusion in endothelial cells Poor prognosis

Pathogenesis: 

Pathogenesis Accentuation of diffuse epithelial cell change typical of MCD>>hall mark Hyalinosis & sclerosis>entrapment of plasma proteins in extremely hyper-permeable foci with increased ECM deposition NPHS1 mutations: mutant nephrin NPHS2 mutations: mutant podocin>>steroid resistant childhood nephrotic syndrome Mutation in α -actinin 4 Mutation in CD2AP

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Start questioning...

Membranoproliferative GN: 

Membranoproliferative GN MPGN is a disease which affects children and young adults. LM : glomeruli are large and hypercellular because the proliferation of mesangial cells, and increased mesangial matrix. GBM is thickened. The glomerular capillary wall shows a “double-contour” appearance.(especially evident in siver or PAS stains.

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Mesangial cell proliferation and BM thickening exaggerates the lobular architecture of the glomerulus.

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EM : typeⅠ— sub-endothelial diposits (C3)

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typeⅡ : there are markedly dense homogeneous deposits within the BM and mesangium.

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PAS stain

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Clinical course Nephrotic syndrome but some have haematuria. The disease follows a slowly progressive but unremitting course. Some patients develop numerous crescents and a clinical picture of RPGN. About 50% develop chronic renal failure within 10 years.

IgA nephropathy (Berger disease): 

IgA nephropathy (Berger disease) IgA nephropathy is one of the most common causes of recurrent microscopic or gross hematuria and is the most common glomerular disease worldwide . The Asia-Pacific area has the highest incidence.

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The clinic features : Affects children and young adults Episodic haematuria occurs within 1 or 2 days of an upper respiratory tract infection Mild proteinuria Raised serum IgA levels 25-50% cases progress to CRF in 20 years.

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Mesangial deposition of IgA

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Glomerulus Shows mesangial widening and proliferation

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Mesangial deposition ( IgA)

★Chronic GN: 

★Chronic GN ~ is the end stage of glomerular disease which have been discribed earlier. Many cases arise mysteriously with no history of GN.

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Morphology: grossly— the kidneys are symmetrically contracted , and their surface is red-brown and diffusely granular. The kidneys weigh about 80 to 90 gm. each. on section, the cortex is thinned to 0.5 cm. Or less histology--- evidence of the primary disease hyaline glomeruli(acellular eosinophilic masses)and atrophy of associated tubles, irregular interstitial fibrosis arterial and arteriolar sclerosis

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There is one relatively normal-sized kidney with a granular surface and a few scattered, shallow cortical scars. The other kidney shows atrophy

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atrophic kidneys with a thin cortex

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Atrophy of associated tubules , irrigular interstitial fibrosis.

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The glomeruli are replaced by hyaline collagen

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Clinic course About a third to half of patients with CRF slowly reach end stage without significant signs or symptoms along the way, and at the end stage there are no diagnostic features. chronic nephritic syndrome: polyuria and nocturia ---water reabsorbed ↓ hypertension—renin ↑ ; arterial and arteriolar sclerosis anaemia— results from failure to produce erythropoietin Azotemia(BUN ↑), uremia—gradual loss of nephrons, and waste products accumulats. Prognosis -- poor

Pyelonephritis: 

Pyelonephritis ~ is a renal disorder affecting tubles, interstitium, and renal pelvis. A common and important cause of renal disease Etiology: > 80% of cases of urinary tract infection,are the gram-negative bacilli.

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Acute pyelonephritis is characterised by pus in the tubules and by abscess formation. Chronic pyelonephritis is characterised by coarse scarring and contraction of the kidneys. Causative bacteria may reach the kidneys either through the blood (as in septicaemia) or by reflux of contaminated urine from the bladder

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There are two routes by which bacteria can reach the kidneys: (1) through the bloodstream (hematogenous infection) (2)from the lower urinary tract(ascending infection) organism can gain access to the kidney only if there is vesico-ureteric reflux.

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Septicemia ,endocarditis

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Acute pyelonephritis ~ is duto infection of the kidney by pyogenic organisms. It presentes with malaise and fever, and pain and tenderness in the loins is common. Morphology abscesses are grossly apparent on the renal surface. (They may be widely scattered when the infection is blood-borne, or limited to one region of the kidney when associated with urinary reflex.)

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The surfaces of both kidneys demonstrate multiple microabscesses from hematogenous spread of a bacterial infection. The microabscesses have yellow centers and prominent hyperemic borders

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The cut surface of the kidney reveals many small yellowish microabscessesThis type of pyelonephritis is most typical for hematogenous dissemination of infection to the kidney.

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LM: early ,-the suppurative infiltrate is limited to the interstitial tissue, later,-abscesses rupture into tubules . --- white cell casts found in the urine finally- fibrosis occurs in the interstitium. atrophy of tubles deformation of the calyx and pelvis.

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Complications: Papillary necnosis--- coagulative infarct necrosis Pyonephrosis--- in the renal pelvis, calyces and ureter perinephric abscess-- -suppurative inflammation extends into the perirenal tissues.

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Clinic course: The disease tends to be benign and self-limited.the symptomatic phase of the disease lasts no longer than a week. In the presence of urinary obstruction, diabetes mellitus, andimmunocompromise, the disease may become recurrent or chronic, leading to serious chronic pyolonephritis.

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Chronic Pyelonephritis ---CPN CPN --- chronic tubulointerstitial inflammation scarring of renal parenchyma assocoated with deformity of the pelvis and calyces CPN is an important cause of chronic renal failure, next only to CGN in importance.

Etiology and Pathogenesis: 

Etiology and Pathogenesis 1.Urinary tract obstruction --- calculi, prostatic enlargement, congenital urethral valves 2. Reflux Nephropathy ----vesico-ureteric refux VUR

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Morphology Gross examination--- Irregularly contracted small,granular kidney (may weigh < 50gm,each.) uneven scarring (if bilateral, the involvement kidneys are asymmetrically scarred.). scarring involving the pelvis or calyces. blunted, dilated calyces.

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Granular kidneys with deep irregular scarrs Involvement is characteristically asymmetrical

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There was a large renal calculus (stone) that obstructed the calyces of the lower pole of this kidney, leading to a focal hydronephrosis (dilation of the collecting system).

Microscopy: 

Microscopy (1)uneven interstitial fibrosis and an inflammatory infiltrate. (also chronic inflammatory infiltration and fibrosis involving the calyceal mucosa and wall) (2) Dilatation or contraction of tubules . Many of the dilated tubules contain pink to blue glassy-appearing casts known as "colloid casts," which suggest The appearance of thyroid tissue, hence the descriptive term "thyroidization" of the kidney.

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(3) Concentric fibrosis about the parietal layer of Bowman's capsule, termed peri-glomerular fibrosis. (4) Vascular changes similar to those of hyaline or proliferative arteriolosclerosis due to the invariable association with hypertension.

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interstitial fibrosis peri-glomerular fibrosis.

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"colloid casts,"

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"thyroidization"

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Clinical Course Chronic obstructive pyelonephritis --- may be insidious in onset or may present the clinical manifestations of acute recurrent pyelonephritis with back pain, fever, frequent pyuria, and bacteriuria.

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CPN associated with VUR (vesico-ureteric reflux) ----the patients come to medical attention relative late in the course of their disease because of the gradual onset of renal insufficiency or because signs of kidney disease are noticed on routine laboratory tests. Hypertension and mild proteinuria are typical manifestation.

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Pyelograms show the affected kidney to be asymmetrically contracted, with some degree of blunting and deformity of the calyceal system (Pyelograms are characteristic and therefore are important in confirming the diagnosis.)

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prognosis If the disease is bilateral and progressive, tubular dysfunction (loss of concentrating ability) manifested by polyuria and nocturia occurs early, followed ultimately by glomerular damage, with consequent azotemia. Death usually results from uremia.

Tumors of the kidney: 

Tumors of the kidney Benign tumors(e.g. fiberoma, hamartoma, angiomyolipoma, adenoma) Malignant tumors : Renal cell carcinoma Wilms’ tumor Transitional cell carcinoma of renal pelvis

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Renal cell carcinoma (hypernephroma, adenocarcinoma of kidney) ~ is the commonest primary kidney tumor in adults .( account for 85% of renal cancers ) It arise from epithelial cells of the tuble. RCC is most common in age of 50~70 years. Etiology. tobacco VHL (Von Hippel- lindau )disease.

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Morphology. spherical masses 3~15cm lies in the upper pole. Cut surface: a solid yellowish-grey tumor with areas of haemorrhage and necrosis. Margin: usually well demarcated Microscopy: RCC are composed of clear(vacuolated) or granular cells

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A renal cell carcinoma: the neoplastic cells have clear cytoplasm and are arranged in nests with intervening blood vessels. This appearance is often called "clear cell carcinomas".

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Clinical course Most frequent presenting manifestation is haematuria, in other patients, the tumors cause loin pain and palpable mass. Prognosis usually poor, no metastasis (70% 5-year survival) local invasion (15~20% 5-year survival) distant place ( lungs, bones)

Nephroblastoma(Wilms’ tumor): 

Nephroblastoma(Wilms’ tumor) ~ is the third most common organ cancer in children under the age of 10 years. clinical features A palpable abdominal mass, haematuria, abdominal pain, hypertention morphology tumors are usually huge spherical masses. the cut surface is variegated. Haemorrhage, necrosis, mucoid degeneration…..

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Histologically the tumor derived from the mesonephric mesoderm. both epithelial and mesenchymal tissues are seen. ① primitive glomeruli ② Abortive tubles ③ spindle cell stroma prognosis The tumor is aggressive and rapidly growing; Nowadays, the outlook for patients with ~ has changed drasticlly. In America, treatment gives a better than 90% 5 year survival.

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This is a Wilm's tumor that is composed microscopically of nests and sheets of dark blue cells at the left with compressed normal renal parenchyma at the right.

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Wilm's tumor resembles the fetal nephrogenic zone of the kidney. The tumor shows attempts to form primitive glomerular and tubular structures.

Transitional cell carcinoma of the bladder: 

Transitional cell carcinoma of the bladder Clinical manifestation. Bladder cancer produces painless hematuria and has a tendency to recur. Pathogenesis. Cigarette smoking----50~80% of all bladder cancers are associated with the use of cigrettes. Exposure to arylamines---the cancer appear 15 to 40 years after the first exposure. Schistosomiasis--egypt and sudan are the endemic areas The ova are deposited in the bladder wall and, in some instances induce neoplasia . Chronic cystitis---

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Morphology Gross patters . Papillary to nodular or flat (may muticentric origin ) Most arise from the lateral or posterior wall.

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transitional cell carcinoma. A presenting sign can often be hematuria.

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TCC is often multifocal and has a tendency to recur.

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Histological grading . GradeⅠ-- gross appearance is similar to that of papilloma. Tumor cells display some atypia but are well differentiated. GradeⅡ--- papillary or have contiguous flat region. The number of layers of cells is increased, tumor cells show obviously cytologic atypia. May have invasion Grade Ⅲ--- palillary, flat, or both. they tend to be larger, more extensive, and to invade more deeply. Tumor cells show anaplastic changes.

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papillary projections of the tumor above the surface to the left No invasion to the right is seen at this point.

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At high power, the thickness of the transitional cell carcinoma is much greater than normal and the cells show more pleomorphism.

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Grade II

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Prognosis. Depends on the histologic grade of the tumor and on the clinical stage when it is first diagnosed. GradeⅠ----low malignant potential. Yield a 98% 10-year survival rate GradeⅡ ---- The 10-year survival rate is between GradeⅠand Grade Ⅲ Grade Ⅲ----40% 10-year survival rate