Glomerular Diseases

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5 major glomerular syndromes

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acute nephritic syndrome, rapidly progressive glomerulonephritis, nephrotic syndrome, chronic renal failure, asymptomatic hematuria or proteinuria

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hematuria, azotemia, variable proteinuria, oliguria, edema, hypertension

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acute nephritic syndrome

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acute nephritis, proteinuria, and acute renal failure

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rapidly progressive glomerulonephritis

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>3.5 gm proteinuria, hypoalbuminemia, hyperlipidemia, lipiduria

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nephrotic syndrome

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azotemia-> uremia progressing for years

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chronic renal failure

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glomerular hematuria, subnephrotic proteinuria

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asymptomatic hematuria or proteinuria

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antibodies react directly with intrinsic tissue antigen (planted)

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In Situ Immune Complex Deposition

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antibodies directed against intrinsic fixed antigens that are normal components of GBM proper

diffuse linear pattern of staining on immunofluorescent

initial heterologous phase and more injurious anaologous phase

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Anti- GBM Antibody induced nephritis

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immunizing animal with antigen from preps of proximal tubular brush border

develop antibodies to antigen adn membranous glomerulopathy

numerous electron-dense deposits (largely of immune reactants) along subepithelial aspect of the basement membrane

granular pattern on immunofluorescence

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Heymann Nephritis

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glomerular injury caused by trapping of circulating antigen-antibody complexes within glomeruli

endogenous (SLE) or exogenous (infx)

electron dense deposits that lie in the mesangium (granular deposits)

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circulating immune complex nephritis

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electron dense deposits between the endothelial cells and GBM

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subendothelial deposits

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electron dense deposits between outer surface of GBM and podocytes

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sub epithelial deposits

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tubular damage and interstitial inflammation

history of ischemia of tubule segments downstream from sclerotic gomeruli, acute and chronic inflammation in adjacent interstitium, and damage or loss of peritubular capillary blood supply

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tubulointerstitial fibrosis

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inflammatory alterations in glomeruli

hematuria, red cell casts in urine, azotemia, oliguria, mild to moderate hypertension

proteinuria and edema

may happen with SLE or microscopic polyarteritis

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acute glomerulonephritis

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Enlarged hypercellular glomeruli

infiltration of leukocytes, proliferation of endothelial and mesangial cells, crescent formation (severe cases)

swelling of endothelial cells obliterates capillary lumen

granular deposits IgG, IgM, C3 in mesangium and along basement membrane

discrete, amorphous, electron dense deposits on epithelial side of membrane having appearence of humps

swelling of endothelial/mesangial cells
Children 6-10, following skin/pharynx infection

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post streptococcal glomerulonephritis

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abrupt malaise, fever, nausea, oliguria

smoky/coco colored urine

periorbital edema; elevations of ASO and decline in serum C3; presence of cryoglobins in the serum

therapy aimed at maintaining sodium sodium and water balance

prolonged and persistent heavy proteinuria and abnormal GFR= not good

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poststreptococcal glomerulonephritis

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kidneys are enlarged and pale often with petichial hemorrhages on the cortical surfaces

formation of distinctive crescents; proliferation of parietal cells adn by migration of monocytes and macrophages into the urinary space

Bowman space obliterated; tuft compression

fibrin strands prominent between cellular layers and crescents

distinct ruptures in GBM; granular deposits

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rapidly progressive glomerulonephrits

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massive proteinuria, hypoalbuminemia, generalized edema, hyperlipidemia and lipiduria

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nephrotic syndrome

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most common cause of nephrotic syndrome in adults

glomeruli either appear normal or exhibit uniform, diffuse thickening of the glomerular capillary wall

irregular dense deposits between the basement membrane and epithelial cells

effaced foot processes

irregular spikes from GBM-> thicken to produce dome like protrusions and eventually close ovre immune deposits

sclerosis of mesangium may occur

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membranous glomerulopathy

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peak incidence between 2 and 6
basement membrane appears normal, and no electron dense material is deposited

principal lesion= visceral epithelial cells

uniform and diffuse effacement of foot processes

vacuolization, swelling, hyperplasia of villi

diagnosis only made when effacement associated with normal glomeruli by light microscopy

reversible with corticosteroids

proximal tubules often laden with lipid protein

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minimal change glomerulopathy

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segmental lesions seen on light microscopy; may involve only a minority of the glomeruil

in sclerotic segments loss of BM, increase in matrix, segemental insudation of plasma proteins along the cap wall (hylinosis)

lipid droplets and foam cells often present

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focal segmental glomerulosclerosis

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Segmental lesions of the glomeruli; glomeruli that do not exhibit segmental lesions eiher appear normal on light microscopy or may show increased mesangial matrix and proliferation

effacement of foot processes characteristic of minimal change disease but additionally may be focal detachment of the epithelial cells with denudation of GBM

IgM and C3 in sclerotic areas, pronounced hyalinosis and thickening of afferent arterioles

eventual total scerosis of glomeruli with pronounced tubular atrophy adn interstitial fibrosis

responds to corticosteroid therapy

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focal segmental glomerulosclerosis

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collapse adn sclerosis of the entire glomerular tuft in addition to focal segmental glomerulosclerosis

proliferation adn hypertrophy of glomeruler epithelial cells

most characteristic lesion of HIV associated nephropathy

prominent tubular injury with formation of microcysts

poor prognosis

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collapsing glomerulopathy

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glomeruli are large and hypercellular; hypercellularity produced by proliferation of cells in the mesangium and endocapillary cell proliferation and infliltrating leukocytes

crescents

lobular appearance to glomeruli

glomerular capillary wall has tram track appearance

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membranoproliferative glomerulonephritis

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GBM has inclusion of interposistion of celluar elements which can be mesangial, endothelial, or leukocytic in origin

split basement membrane

C3, IgG, or early complement proteins present

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membranoproliferative glomerulonephritis

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membranoproliferative glomerulonephritis characterized by the presence of subendothelial electron dense deposits

C3 deposited in granular pattern; IgG and early complement proteins commonly present

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Type I MPGN

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membranoproliferative disease in which the lamina densa of the GBM is transformed into an irregular, ribbon-like, extremely electron dense structure

C3 present in mesangium in circular aggregates; IgG and early complement usually absent

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Type II MPGN

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glomeruli my be normal or may show mesangial widening and proliferation, segmental proliferation confined to some glomeruli, or overt crescentic glomerulonephritis

mesangial deposition of IgA often with C3 and properdin adn lesser amounts of IgG or IgM

Onset in old age, heavy proteinuria, hypertension are clues to increased risk progression

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Berger disease (IgA nephropathy)

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Early lesion is diffuse glomerular basement membrane thinning

foamy appearance to accumulation of neutral fats and mucopolysaccharides

vascular sclerosis, tubular atrophy, interstitial fibrosis

GBM shows irregular foci of thickening alterating with foci of attenuating

basket weave appearence

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Alport syndrome

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kidneys are symmetrically contracted and have diffusely granular cortical surfaces

cortex is thinned; increased peripelvic fat

eventual hyaline obliteration of glomeruli transforming glomeruli to acellular eosinophilic masses

arterial and arteriolar sclerosis may be conspicuous, marked atrophy of associated tubules, irregular interstitial fibrosis, mononuclear leukocytic infiltration

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chronic glomerulonephritis

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glomerulosclerosis with arteial intimal thickening caused by accumulation of smooth muscle-like cells and a loose proteoglycan rich stroma

focal calcification usually within residual tubular segments

extensive deposition of calcium oxalate crstals in tubules and interstitium

acquired cystic disease

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chronic glomerulonephritis associated with dialysis

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chronic glomerulonephritis exhibiting pathological changes outside the kidney

pericarditis, uremic gastroenteritis, secondary hyperparathyroidism with nephrocalcinosis and renal osteodystrophy, left ventricular hypertrophy, pulmonary changes of diffuse alveolar damage

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uremic changes of chronic glomerulonephritis

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purpuric skin lesions on the arms and legs

mild focal mesangial proliferation to diffuse mesangial proliferation to crescentic nephritis

deposition IgA, sometimes with IgG adn C3 in the mesangial region

subepidermal hemorrhages and a necrotizing vasculitis involving small vessels of the dermis

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Henoch-Schonlein Purpura

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Widespread thickening of the GBM; thickening of the tubular BM

diffuse increase in mesangial matrix with overall thickening of the GBM

intercapillary glomerulosclerosis (Kimmelstiel Wilson); ovoid or spherical , often laminated, nodules of matrix in periphery of glomerulus

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diabetic glomerulosclerosis

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features of mesangiolysis with fraying of the mesangial/capillary lumen interface, disruption of sites at which the capillaries are anchored into the mesangial stalks, and resultant capillary microaneurysm

even uninvolved lobules adn glomeruli show striking diffuse mesangial sclerosis

nodular lesions frequently accompanied by prominent accumulations of hyaline material in capillary loops or adherent to Bowman's capsule

kidney suffers ischemia, develops tubular atrophy adn interstitial fibrosis; overall contraction in size

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diabetic glomerulosclerosis

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fibrillar deposits in mesangium and glomerular capillary walls that resemble amyloid fibrils in appearance bu differ when measured ultrastructurally and do not stainwith Congo red

selective deposition of IgG with complement and Ig kappa nd delta light chains

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fibrillary glomerulonephritis

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rare condition in which deposits are microtubular in structure

circulating paraproteins adn /or monoclonal immunoglobulin deposition

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immunotactoid glomerulonephritis

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cryoglobulins composed principally of IgG-IgM complexes induce cutaneous vasculitis, synovitis, and a proliferative glomerulonephritis (membranoproliferative)

Hep C infx

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essential mixed cryoglobulinemia

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amyloidosis (monoclonal lambda light chains), deposition of monoclonal immunoglobulins in GBM, distinctive nodular glomerular lesions resulting from the deposition of nonfibrillar light chains

Ig kappa in glomeruli, proteinuria or nephrotic syndrome, hypertension, and progressive azotemia

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light chain or monoclonal immunoglobulin deposition disease

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mediators of glomerular injury

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neutrophils and monocytes, macrophages, t lymphocytes, natural killer cells, platelets, resident glomerular cells

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soluble mediators

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chemotactic complement components, eicosanoids, NO, angiotensin, endothelin, cytokines, chemokines, coagulation system