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216 Cards in this Set
- Front
- Back
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people with mild kidney disease are at greater risk for
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cardiovascular disease
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4 divisions of kidney disease
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glomeruli, tubules, interstitium, or blood vessels
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glomerular diseases are most likely to be caused by
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immunologic reactions
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tubular and interstitial disorders are frequently caused by
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toxic or infections agents
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azotemia
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elevation of blood uria nitrogen (BUN) and creatinine levels
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prerenal azotemia
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hypoperfusion of kidneys; impairs fxn in absence of perenchymal damage
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postrenal azotemia
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urine flow obstructed beyond kidney
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uremia
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azotemia associated with a constellation of clinical signs and symptoms and biochemical abnormalities
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frequent secondary manifestations of uremia
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GI, peripheral nerve, heart involvement
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nephritic syndrome
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due to glomerular disease and dominated by acute hematuria, mild-moderate proteinuria, and hypertension
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example of classic nephritic syndrome
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acute poststreptococcal glomerulonephritis
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rapidly progressive glomerulonephritis
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nephritic syndrome with rapid decline (hours/days) in GFR
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Nephrotic syndrome
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due to glomerular disease characterized by heavy proteinuria, hypoalbuminemia, severe edema, hyperlipidemia, and lipiduria
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asymptomatic hematuria or proteinuria
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manifestation of subtle or mild glomerular abnormalities
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acute renal failure
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dominated by oliguria or anuria, recent onset of azotemia
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what can cause acute renal failure
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can results from glomerular, interstitial, or vascular/acute tubular injury
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chronic renal failure
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prolonged symptoms and signs of uremia
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renal tubular defects
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polyuria, nocturia, electrolyte disorders
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what can cause renal tubular disease
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directly affect tubular structure (medullary cycstic disease) or cause defects in specific tubular fxns (familial nephogenic diabetes, cystinuria, renal tubular acidosis, lead nephropathy)
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urinary tract infection
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bacteriuria and pyuria
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pyuria
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bacteria and leukocytes in urine
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nephrolithiasis (renal stones)
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severe spasms of pain and hematuria
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4 broad stages of chronic renal failure
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1) diminished renal reserve (50% normal) 2)renal insuficiency (GFR 20-50% normal) 3) chronic renal failure (GFR 20-25% normal) 4) end-stage renal disease (GFR less than 5% normal)
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what appears in stage 2 of chronic renal failure
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azotemia, generally with anemia and hypertension
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what appears in stage 3 of chronic renal failure
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cannot reguate volume and solute composition, dvlp edema, metabolic acidosis, hyperkalemia
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glomerulopathy
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does not have inflammatory component
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familial disease that often affects glomerulus
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Fabry disease
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what other things can cause glomerular diseases
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systemic immunological diseases (Lupus), hypertension, metabolic diseases, other hereditary conditions
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lamina densa
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thick electron-dense central layer of glomerular basement membrane
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what component are in the glomerular basement membrane
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collagen (mostly IV), laminin, polyanionic proteoglycans (heparan sulfate), fibronectin, entactin, others
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what is the fxn of collagen IV in the basement membrane
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network suprasturcture to which other glycoproteins attach
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what domain is important for helix formation and for assembly of collagen monomers into the basement membrane suprastructure
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NC1 (globular noncollagenous domain at the C terminus)
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building block of collagen network
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triple helical molecule with 3 alpha chains; each molecule contains 7S domain at N terminus, triple helical domain in middle, and NC1
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what are interdigitating podocyte processes embedded in
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lamina rara externa of BM
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where are mesangial cells located
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btwn capillaries in glomerulus
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properties of mesangial cells
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contractile, phagocytic, able to proliferate, lay down matrix and collagen
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what cell type is mostly responsible for synthesis of glomerular BM
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podocytes
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slit disphram proteins responsible for permeability
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nephrin, CD2-associated protein, Podocin
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nephrin
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transmembrane protein migh large extracellular portion making up Ig-like domains; dimerize across slit diaphragm
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mutations in slit diaphram proteins results in
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nephrotic syndrome
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hypercellularity is characterized by
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1) proliferation of mesangial or endothelial cells 2) leukocyte infiltration 3) formation of crescents
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what do crescents consist of
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accumulations of proliferating parietal epithelial cells and infiltrating leukocytes
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when does cresent formation generally occur
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following an immune/inflammatory injury
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what molecule is thought to elicite crescent formation
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fibrin-leaks into urinary space from ruptured BM
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BM thickening 2 forms
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1) deposition of amorphous electron dense material 2) increased systhesis of protein components
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when does deposition of amorphous electron dense material generally occur
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immune complex deposition
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when does increased synthesis of protein components causing thickening occur
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diabetic glomerulosclerosis
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hyalinosis of glomerulus
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acumulation of material homogeneous and eosinophilic by light microscopy
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what is the hyalin material as seen in electron microscopy
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extracellular and amorphous made up of plasma proteins insudated from circulation into glomerular structures
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what is hyalinosis a consequence of
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endothelial or capillary wall injury; end result of various forms of glomerular injury
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sclerosis
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accumulations of extracellular collagenous matrix
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sclerosis location in diabetic glomerulosclerosis
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confined to mesangial areas
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what can sclerosis process result in
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obliteration of some or all of the capillary lumens in affected glomeruli--formation of fibrous adhesions btwn scerotic portions of glomeruli and parietal epithelium and Bowman capsules
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histological classifications of glomerulopathies
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diffuse, global, focal, segmental; capillary loop or mesangial
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what is found in the majority of patients with glomerulonephritis
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glomerular deposits of immunoglobulins often with components of complement
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two forms of antibody-associated injury
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1) antibodies reacting in situ with glomerulus 2) deposition of circulating antigen-antibody complexes
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Heymann nephritis
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antigen in proximal tubular brush border and antibodies are dvlped against it; membranous nephropathy dvlps
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what occurs once antibodies bind antigen
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complement activation and shedding of immune aggregates from cell surface to form subepithelial deposits
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what are anti-GBM antibody-induced disease and membraneous nephropathy considered
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autoimmune diseases
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what are examples of 'planted' antigens
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cationic molecules like DNA, nucleosomes, other nuclear proteins with an affinity for GBM, bacterial products, free antigen, complement
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anti GBM antibody induced glomerulonephritis
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antibodies directed against fixed intrinsic antigens that are normal components of the GBM
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pattern of involvement for anti GBM antibody induced glomerulonephritis
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diffuse linear patterns (unlike Heymann with granular lumpy pattern)
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Goodpasture syndrome
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antibodies cross react with BM in lung and kidney
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what GBM antigen is responsible for classic anti-GBM induced and goodpasture syndrome
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component of the noncollagenous domain NC1 of alpha 3 chain of collagen IV
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clinical picture of anti GBM antibody induced glomerulonephritis
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severe crescentic glomerular damage and rapidly progressive glomerulonephritis
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deposits in the mesangium btwn endothelial cells and GBM
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subendothelial deposits
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deposits bltwn the outer surface of GBM and podocytes
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subepithelial deposits
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what occurs when continuous shower of antigen dvlps with repeated cycles of immune complex formation
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more chronic membraneous or membranoproliferative type of glomerulonephritis
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What factors affect glomerular localization of antigen, antibody, or complexes of both (in circulating complex glomerunephritis)
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molecular charge, size, glomerular hemodynamics, mesangial fxn, integrity of charge-selective barrier
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where do highly cationic immunogens generally deposit
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tend to cross GBM and reside in subepithelial location
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where do highly anionic immunogens generally dposit
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excluded from GBM and trapped subendothialially or not nephrogenic at all
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where neutral charge immunogens generally deposit
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in mesangium
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alternative complement pathway activation occurs in
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dense-deposit disease aka membranoproliferative flomerulonephritis (MPGN type II)
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changes in epithelium when injured
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effaement of foot processes, vacuolization, retraction, detachement from GBM, proteinuria
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neutrophils and monocytes in glomerular injury
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infiltrate as result of complement activation; realease proteases damaging GBM, free radicals cause cell damage, arachildonic acid reduces GFR
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Macrophages, T lymphocytes, and NK cells in glomerular damage
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infiltrate in antibody and cell mediated immunity; release large number of biologically active molecules
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Platelets in glomerular damage
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aggregate and release eicosanoids and GFs
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Resident glomerular cells in glomerular injury
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stimulated to produce inflammatory mediators
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chemotactic complement components
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induce leukocyte influx and leads to C5b-C9 formation (membrane attack complex)
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eicosanoids, NO, angiotensin, endothelin
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involved in hemodynamic changes
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cytokines IL-1 and TNF
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induce leukocyte adhesion and other effects
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chemokines like monocyte chemoattractant protein 1 and CCL5
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promote monocyte and lymphocyte influx
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coagulation system
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fibrin present in glomerulonephritis and may serve as stimulant for crescent formation
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At what GFR does end-stage renal failure proceed at a relatively constant rate independent of original stimulus
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30-50%
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two major histological characteristics of progressive renal damage
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focal segmental glomerulosclerosis and tubulointerstitial fibrosis
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focal segmental glomerulosclerosis effects
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proteinuria; result of adaptation of functioning nephrons
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how can focal segmental glomerulosclerosis be slowed down
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inhibitors of renin-angiotensin system
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what contributes to progressive injury of focal and segmental glomeruloslerosis
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inability of mature visceral epithelial cells (podocytes) to proliferate after injury
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tubulointerstitial fibrosis causes
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ischemia, aute and chronic inflammation, damage/loss of peritubular capillary blood supply
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nephritic syndrome characterized by
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inflammation to glomeruli
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symptoms of nephritis syndrome
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hematuria, red cell casts in urine. Azotemia, oliguria, mild/moderate hypertension; proteinuria and edema common, but not as severe
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acute nephrotic syndrome occurs in
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multisystemic diseases as SLE and microscopic polyangiitis; acute proliferative glomerulonephritis
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most common underlying infection in acute proliferative glomerulonephritis
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streptococcal
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strains of streptococcal that cause acute proliferative glomerulonephritis
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B-hemolytic streptococci group A; more than 90% trace to types 12, 4, and 1
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morphology of streptococcal acute proliferative glomerulonephritis
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enlarged, hypercellular glomeruli (diffuse); granular deposits of IgG, IgM, and C3 in mesangium and along GBM
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clinical outcome of streptococcal acute proliferative glomerulonephritis
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95% children recover totally; 60% adults recover sporatically
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Rapidly progressive (crescentic) glomerulonephritis (RPGN)
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associated with severe glomerular injury and does not denote a specific etiologic form of glomerulonephritis; generally immunologic
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3 types of RPGN
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1) anti-GBM antibody-induced 2) immune complex deposition 3) lack of anti-GBM antibodies or immune complexes (pauci-immune type)
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characteristics of anti-GBM antibody induced RPGN
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linear deposits of IgG and many times C3 in GBM
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treatment of anti-GBM antibody induced RPGN
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plasmapheresis to remove circulating antibodies as well as therapy to suppress underlying immune response
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goodpasture antigen
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peptide within noncollagenous portion of alpa 3 chain of collagen IV
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what is present in the 3rd type of RPGN
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circulating antineutrophil cytoplasmic antibodies (ANCAs); 90% of idiopathic cases contain
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what is the target antigen of most p-ANCAs
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myeloperoxidase
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morphology of RPGN
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kidneys enlarged and pale, petechial hemorrhages, distinctive crescents, fibrin strands frequently prominent; ruptures in GBM
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clinical course of RPGN
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hematuria, red blood cell casts in urine, moderate proteinuria, variable hypertension and edema
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nephrotic syndrome maifestations
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massive proteinuria (3.5 g daily), hypoalbuminemia, generalized edema, hyperlipidemia and lipiduria
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initial event in nephrotic syndrome
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derrangement in glomerular capillaries resulting in increased permeability to plasma proteins
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highly selective proteinuria
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mostly low MW proteins like albumin 70 kD and transferrin 76 kD
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why does hyperlipidemia result in neprotic syndrome
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increase synthesis of lipoproteins in liver, abnormal transport of circulating lipid particles, and decreased catabolism
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oval fat bodies
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lipoprotein resorbed by tubular cells and then shed along with degenerated cells
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what infections are nephrotic patients vulnerable to and why
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staph and pneumococcal; loss of immunoglobulins in urine
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why are thrombotic and thromboembolitic complications present in neprotic syndrome
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loss of endogenous anticoagulants and antiplasmins in urine (antithrombin III)
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usual cause of nephrotic syndrome if under 17 in north america
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lesion primary to kidney
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most frequent systemic causes of nephrotic syndrome
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diabetes, amyloidosis, SLE
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membranous nephropathy
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common cause of nephrotic syndrome in adults; diffuse thickening of glomerular capillary wall due to accumulation of electron-dense Ig-containing deposits along subepithelial side of BM
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secondary membranous nephropathy causes
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drugs, underlying malignant tumors, SLE, infections, other autoimmune diseases (thyroiditis)
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what percentafe of membranous nephropathy is idiopathic
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~85%
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how does glomerular capillary wall become leaky in membranous glomerulopathy
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direct action of C5b-C9 (formation of membrane attack complex)
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morphology of membranous nephropathy
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normal in early stages or uniform diffuse thickening or glomerular capillary wall; IgG and complement present; sclerosis as progresses
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what is difference in proteinuria of membranous nephropathy and minimal-change disease
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it is non-selective and doesn't respond well to corticosteroid therapy
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minimal-cahnge disease
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relatively benign disorder that is most frequent cause of nephrotic syndrome in children
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minimal-change disease characteristics
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diffuse effacement of foot processes if visceral epithelial cells in glomeruli that applear virtually normal by light microscope; no Ig or complement deposits
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most characterisitc feature of minimal-change disease
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dramatic response to corticosteroid therapy
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what contributes to proteinuria in minimal-change diease
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defects in charge barrier
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possible protein defects in minimal change disease (either genetic or immune related)
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nephrin, podocin
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what other proteinuric states cuase foot process effacement besides minimal change disease
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membranous glomerulopathy, diabteic nephropathy
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when can minimal change disease be diagnosed
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only when effacement is associated with normal glomeruli by light microscope
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what are proximal tubules often laiden with in minimal-change disease
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lipid and protein (lippoid nephrosis is old name for this disease)
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what can minimal change disease be associated with in adults
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Hodgkin lymphoa and sometimes other lymphomas and leukemias
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What does focal segmental glomerulosclerosis frequently manifest with clinically
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nephrotic syndrome or heavy proteinuria
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When does focal segmental glomerulosclerosis occur
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1) primary disease (idiopathic) 2) association with other diseases 3) secondary event (scarring of previously active necrotizing lesions) 4) cocmponent of adaptive response 5) uncommon inherited forms
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example of focal segmental glomerulosclerosis in association with other known conditions
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HIV infection, sickle-cell disease, massive obesity
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example of focal segmental glomerulosclerosis as a secondary event
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focal glomerulonephritis (IgA nephropathy)
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What genetic mutation can cause focal segmental glomerulosclerosis
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proteins localized to slit diaphram like podocin, alpha-actinin, and TRPC6
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how does FSGS differ from minimal change disease
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1) higher incidence of hematuria, reduced GFR, and hypertension 2) proteinuria often more selective 3) poor response to corticosteroid therapy 4) progression to chronic kidney disease; at least 50% dvlp end stage within 10 years
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Is FSGS a disinct disease?
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may be a phase of a subset of minimal-change disease patients
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What is the hallmark of FSGS
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epithelial damage (caused by multiple mechanisms)
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what makes circulating cytokines suspect of epithelial damage in FSGS
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recurrence of proteinuria, sometimes within 24 hours after transplantation
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what do the lesions in FSGS tend to initially involve
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Juxtamedullary glomeruli, then become generalized
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what occurs in sclerotic segments in FSGS
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collapse of capillary loops, increase in matrix, and segmental deposition of plasma proteins along capillary wall (hyalinosis)
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morphologic variant of FSGS
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collapsing glomerulopathy
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collapsing glomerulopathy
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retraction of the entire glomerular tuft with or without FSGS lesions; HIV associated; poor prognosis
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what gene encodes nephrin
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NPHS1 on chromosome 19q13
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what is nephrin
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key component of slit diaphragm; zipper-like structure btwn podocyte foot processes that may control permeability
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what does a mutation in nephrin cause
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congenital nephrotic syndrome; a minimal-change disease
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What is the gene for podocin
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NPHS2 on chromosome 1q25-q31
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What are the effects of a podocin mutation
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syndrome of steroid-resistant nephrotic syndrome of childhood onset
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What may TRPC6 cause in adult onset FSGS be caused from
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perturb podocyte fxn by increasing calcium influx
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when does renal ablation FSGS occur
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complication of glomerular and nonglomerular diseases casuding reduction in fxning renal tissue
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clinical course of FSGS
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little spontaneous remission in idiopathic form, corticosteroid response variable; reoccurs in 25-50% patients receiving allografts
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Morphologic features of HIV associated renal complications
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high frequency of collapsing variant FSGS, striking focal cystic dilation of tubule segments, presence of large numbers of tubuloreticular inclusions within endothelial cells
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what is present with the striking focal cystic dilation of tubule segments
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filled with proteinaceous material, and inflammation and fibrosis
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what are the tubuloreticular inclusions within endothelial cells modifications of
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ER induced by circulating interferon-alpha; not present in idiopatic FSGS
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What HIV gene products may cause renal complications
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vpr and nef expression by podocytes; may also be caused by systemic release of cytokines
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membranoproliferative glomerulonephritis (MPGN) histology
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alterations in alomerular BM, proliferation of glomerular cells, and leukocyte infiltration
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where is proliferation dominant in MPGN
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mesangium, but may involve capillary loops; MPGN also called mesangiocapillary glomerulonephritis
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what percent of nephrotic cases in children and young adults are MPGN
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10-20%
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Two major types of primary MPGN
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type I and II
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type I MPGN
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evidence of immune complexes in glomerulus and activation of both classic and alternative complement pathways; unknown antigens
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what are antigens in many cases of MPGN believed to come from
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proteins from hep C and B
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type II MPGN (dense-deposit disease)
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activation of alternative complement pathway; decreased serum C3, normal C1 and C4; diminished fator B and properdin
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what circulating antibody is found in 70% of MPGN type II
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C3 nephritic factor (C3NeF); autoantibody that binds to the alternative pathway C3 convertase stabilizing it
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what genetically determined disease can cause MPGN type II
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partial lipodystrophy
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MPGN type I and II morphology
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large and hypercellular; sometimes crescents; glomeruli lobular due to proliferation; GBM thickened; glomeruar capillaty wall has tram-track appearance
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type I MPGN morphology different from type II
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discrete subendothelial electron-dense deposits; mesangial and occasional subepithelial deposits may be present; C3 deposited in granular pattern; IgG and early complement proteins often present
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type II MPGN morphology different from type I
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lamina densa of GBM transformmed into an irregular, ribbon-like, extremely electron-dense structure due to deposition of unknown dense material in GBM proper; C3 present in irregular granular or linear foci in BMs; C3 also in mesangial rings; IgG ususally absent as are early complement components
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how does MPGN present clinically
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adolescent/young adult with nephrotic syndrome with nephritic component manifested by hematuria or mild proteinuria
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MPGN progression
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few spontaneous remissions, slowlyprogressive and unrelenting course; 50% chronic renal failure in 10 years
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what occurs to MPGN patients with allograft
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up to 90% reoccurance, although renal failure less common
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When does secondary MPGN arise in adults
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1) chronic immune complex disorders 2) alpha1-antitrypsin deficiency 3) malignant diseases 4) hereditary deficiencies of complement regulatory proteins
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IgA nephropathy (Berger disease) is characterized by
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presence of prominent IgA deposits in mesangial regions
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What is the most common glomerulonephritis worldwide
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IgA nephropathy; frequent cause of recurrent gross or microscopic hematuria
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what can patients with IgA nephropathy present with
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mild proteinuria, nephrotic syndrome occasionally, rarely with cresentic RPGN
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Henoch-Schonlein purpura
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systemic disorder in children similar to IgA nephropathy
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when can secondary IgA nephropathy dvlp
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liver and intestinal diseases
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what is IgA the main Ig secretion of
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mucosal secretions
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What subclass of IgA molecules in humans causes neprogenic deposits of IgA
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IgA1
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what complement acivation occurs in IgA nephropathy
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presence of C3 without C1q and C4, indicating alternative activation
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When does IgA nephropathy have an increased frequency of occurance
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gluten enteropathy (celiac disease); liver disease where there is decreased clearance of IgA complexes
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What may cause autoimmunity against IgA
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defect in galactosylation
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clinical outcome for IgA nephropathy
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highly variable; hematuria for several days that subsides, then returns every few months; slow progression to chronic renal failure over 20 years in 15-40%
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what is outcome of allograft in IgA nephropathy
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reoccurance frequent and in 15% follows same progressive course
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Alport syndrome maifestations
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hematuria with progression to chonic renal failure accompanied by nerve deafness and varius eye disorders
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how is alport inherited
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X-linked; are some autosomal recessive and dominant pedigrees
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what causes alport
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abnormal COL4A3, COL4A4, or COL4A5 of type 4 collagen
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which mutation causes the classic X-linked form
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COL4A5 (alpha 5)
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what does the alpha 3 chain contain (COL4A3)
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Goodpasture antigen
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Morphology of alport
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glomeruli always involved; difuse GBM thinning; interstitial foam cells; focal segmental and global glomerulosclerosis as progresses
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Thin BM lesion (benign familial hematuria)
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diffuse thining og GBM to 150-250 nm (normally 300-400 nm);
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Outcome of thin BM lesion
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mild-moderate proteinuria; renal fxn is normal and prognosis is excellent
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what causes thin M lesion (benign familial hematuria)
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defect in collagen type 4; may be more progressive is homozygous or cmpd herterozygous
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chronic glomerulonephritis
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pool of end-stage glomerular disease fed by several streams of specific types of glomerulonephritis
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morphology of chronic glomerulonephritis
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kidneys symmetrically contracted, diffuse granular coritcal surfaces; cortex is thinned with increase in peripelvic fat; oblitertation of glomeruli; hypertension
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what are common dialysis changes seen in kidneys that are unrelated to the primary disease
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arterial intimal thickening, extensive deposition of calcium oxalate crystals, aquired cystic disease
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what do the obliterated glomeruli contain
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acellular eosinophilic masses with trapped plasma proteins, increased mesangial matrix, BM-like material, and collagen
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common uremic complications in chronic renal failure
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pericarditis, uremic gastroenteritis, secondary hyperparathyroidism, L ventricular hypertrophy, pulmonary changes
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what are pulmunary changes generally caused by
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uremia that causes diffuse alveolar damage (uremic pneumonitis)
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lupus nephritis clinical maifestations
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recurrent micoscopic or gross hematuria, nephritic syndrome, nephrotic syndrome, chronic renal failure, hypertension
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henoch-schonlein purpura consists of
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purpuric skin lesions involving exstensor surfaces, abdomen, nonmigratory arthralgia, renal abnormalities
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henoch-schonlein purpura renal abnormalities
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1/3 occurance; gross or microscopic hematuria, nephritis syndrome, nephrotic syndrome, or combination
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what disease may be the same as henoch-schonlein purpura
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IgA nephropathy
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bacterial endocarditis associated glomerulonephritis
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immune complex nephritis initiated by complexes of bacterial antigen and antibody
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diabetic nephropathy occurance
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advanced/end-stage in up to 40%; most commonly involve glomeruli
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3 glomerular syndromes in diabetic nephropathy
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non-nephrotic proteinuria, nephrotic syndrome, and chronic renal failure
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what else does diabetes affect in kidneys
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arterioles--increase susceptability to pyelonephritis, papillary necrosis, and a variety of tubular lesions
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morphologic glomeruli changes in diabetes
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1) capillary BM thickening 2) diffuse mesangial sclerosis 3) nodular glomerulosclerosis
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metabolic defect in diabetes that cause renal issues
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metabolic defect: insulin deficiency, hyperglycemia, some other glucose intolerance aspect
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other issues in diabetes that contribute to renal diseases
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nonenzymatic glycosylation of proteins, hemodynamic changes
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amyloidosis
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deposits of amyloid within slomeruli; generally of light-chain (AL) or AA type
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what do patients with amyloidosis present with
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nephrotic syndrome and may later die of uremia
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fibrillary glomerulonephritis
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morphologic variant of glomerulonephritis associated with characteristic fibrillar deposirs in mesangium and glomerular capillary walls that resemble amyloid fibrils superficially but don't stain with Congo red
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deposition of what Ig in fibrillary glomerulonephritis
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polycolonal IgG, often IgG4 subclass, complement C3, Igk and Igdelta light chains
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size of fibrous material in fibrillary glomerulonephritis vs amyloidosis
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18-24 nm vs 10-12 nm
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what is clinical picture of fibrillary glomerulonephritis
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nephrotic syndrome, hematuria, progressive renal insufficiency; reoccurs in allograft
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immunotacoid glomerulopathy
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deposits are microtubular in structure 30-50 nm width; circulating paraproteins and/or monoclonal Ig deposition in glomeruli
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essential mixed cryglobulinemia
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systemic condition in which deposits of cryoglobins composed of IgG-IgM complexes induce cutaneous vasculitis, synovitis, and proliferative glomerulonephritis (typically MPGN); associated with hep C
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