Kidney Flashcards
average wt adult of kidney
150 g
lower urinary tract division
pelvicalcyceal system
ureters
bladder
urethra
cortical thickness of normal kidney
1-1.5 c,
elevation of BUN and creatinine levels
decreased GFR
azotemia
prerenal azotemia
hypoperfusion of kidneys that impairs renal fxn without parenchymal damage
postrenal azotemia
obstruction beyond the level of the kidney
failure of renal excretory function
metabolic and endocrine alterations resulting from renal damage
uremia
classic presentation of acute poststreptococcal GN
nephritic syndrome
nephritic syndrome signs
acute onset of grossly visible hematuria mild to mod proteinuria azotemia oliguria edema hytpertension
nephritic syndrome with rapid decline - hours to days
RPGN
nephrotic syndrome signs
heavy proteinuria >3.5 g/day hypoalbuminemia severe edema hyperlipidemia lipiduria
acute renal failure
oliguria or anuria
recent onset of azotemia- acute tubular necrosis
renal tubular defects
polyuria
nocturia
electrolyte dsorders
renal tubular defect cause
dse that directly affect tubular structure
or
cause defects in tubular functions
urinary tract infection
bacteriuria
pyuria
symptomatic or not
kidney uti
pyelonephritis
bladder uti
cystitis
nephrolothiasis
severe spasms of pain
hematuria
recurrent stone formation
end result of all renal parenchymal diseases
chronic renal failure
cause of chronic renal failure
azotemia -> uremia
chronic
stage 1
DIMINISHED RENAL RESERVE
GFR 50%
normal serum BUN and creatine
asymptomatic
susceptible to azotemia with additional renal insult
stage 2
RENAL INSUFFICIENCY
GFR 20-50% azotemia anemia hypertension polyuria nocturia uremia precepitated by stress
stage 3
CHRONIC RENAL FAILURE
<20-25% GFR edema metabolic acidosis hyperkalemia overt uremia dneuroooig GI CV complications
stage 4
END STAGE RENAL DISEASE
<5% GFR
terminal stage of uremia
systemic manifestations:
FLUID AND ELECTROLYTES
metabolic acidosis
edema
hyperkalemia
dehydration
systemic manifestations:
CALCIUM
PHOSPHATE
BONE
hyperphosphatemia
secondary hyperparathyroidism
hypocalcemia
renal osteodystrophy
systemic manifestations:
HEMATOLOGIC
anemia
bleeding diathesis
systemic manifestations:
CARDIOPULMONARY
cardiomyopathy congestive heart failure hypertension uremic pericarditis pulmonary edema
gastrointestinal manifestations
bleeding esophagitis gastritis colitis nausea vomiting
systemic manifestations
NEUROMUSCULAR
peripheral neuropathy
encephalopathy
myopathy
systemic manifestations
DERMATOLOGIC
pruritus
sallow color
dermatitis
cavity in which plasma filtrate collects first
urinary space
supporting network of the interconnecting capillary lumen
mesangium
glomerulus fxn
maintain the integrity of the glomerular filtration barrier
glomerular filtration barrier composition
fenestrated endothelial cells
basement membrane
epithelial podocytes layer or visceral layer
factors that determine filtration
size of the molecule
charge of the barrier
MW of molecules that can pass through the filter
<70 kilodalton
responsible for the slit like diaphragm
podocytes or visceral epithelium
charge of the barrier
anionic
charge of the substance
cationic
coats the membranes of endothelial and epithelial together with the basement membrane
responsible for the negative charge of the barrier
proteoglycans
sialoglycans
increase in number of cells in the glomerular tufts
hypercellularity
hypercellulariy characteristics
cellular proliferation of mesangial, endothelial, epithelial cells
leukocytic infiltration of neutrophils, monocytes, lymphocytes
crescents
composition of crescents
parietal epithelial cells
leukocytes
elicits crescenteric response
fibrin
basement membrane thickening is due to deposition of
immune complexes on the endothelial and epithelial side of the basement membrane or within GBM itself
hyalinosis denotes accumulation of
plasma proteins as a consequence of capijllary or endothelial wall injury
sclerosis is accumulations of
extracellular collagenous matrix in mesangial areas and or capillary loops
common feature of focal segmental glomerulosclerosis
hyalinosis
capillary lumen obliteration by sclerosis could lead to formation of
fibrous adhesions between the sclerotic portions of the glomeruli and the nearby parietal epithelium
hyalinosis and sclerosis are manifestations of
end stage irreversible injury
numerous discrete electron-dense deposits along the subepithelial aspect of the basement membrane
granular pattern
Heymann Nephritis
Heymann antigen with homology to LDL receptor
megalin
immune mechanism which includes cationic molecules that bind to anionic components of the glomerulus
DNA, nucleosomes, and other nuclear proteins, bacterial products, etc
granular pattern
antibodies against planted antigens
antibodies are directed against intrinsic fixed antigens that are normal components of the GBM
diffuse linear pattern
anti GBM antibody induced GN
anti GBM cross react to lung alveoli, a feature of
Goodpasture Syndrome
GBM antigen responsible for classic anti GBM GN and Goodpature syndrome is a component of
NC1 of the alpha 3 chain of collagen type 4
fxn of NC1 of the alpha 3 chain of collagen type 4
maintenance of GBM suprastructure
anti GBM GN are characterized by —- and the clinical syndrome of —–
severe cresenteric glomerular damage
RPGN
caused by trapping of circulating ag ab complex
granular
circulating immune complex GN
endogenous origin of antigens that trigger circulating immune complexes
SLE
exogenous origin of antigens that trigger circulating immune complexes
hepa b, c
treponema
plasmodium
tumor
continuous cycles of immune complex formation as seen in SLE and viral hepatitis may lead to
membranous or membranoproliferative type of GN
alternative complement pathway activation occurs in
dense deposit disease
MPGN type 2
-may occur in some proliferative GN
epithelial cell injury is seen in
minimal change disease
focal segmental glomerulosclerosis
Primary glomerular diseases under acute nephritis
acute diffuse GN
rapid progressive/crescentic GN
Primary glomerular diseases under nephrotic presentation
minimal change disease
focal segemental glomerulosclerosis
membranous GN
membranoproliferative GN
Primary glomerular diseases under primary hematuria
IgA nephropathy or Berger’s dse
prototype of acute diffuse glomerulonephritis
Poststrep GN
histologic alterations in acute diffuse GN
hypercellularity
features of acute diffuse GN
1-4 weeks after strep infection 6-10 years old hematuria, edema, HTN can be endogenous or exogenous GRANULAR
etiologic agent of acute diffuse GN
nephritogenic strains of group A- beta hemolytic strep types 12,14,1
pathogenesis of acute diffuse GN
circulating ab-ag complexes➡️entrapped in glomeruli➡️glomerular injury by activation of complement by immune complexes
deposited in the GBM and mesangium in acute diffuse GN
IgG
IgM
C3
electron microscopy feature of acute diffuse Gn
discrete amorphous electron dense deposit on the epithelial side of the membrane
HUMPS
clinical course of acute diffuse GN
good prognosis
young child develops malaise, fever, nausea, oliguria, hematuria
other postinfectious GN
staphylococcal endocarditis pneumococcal pneumonia meningococcemia hep b,c varicella hiv infectious mononucleosis malaria toxoplasmosis
severe proliferation that obliterates the glomerular tuft resulting to rapid and progressive decline
rapid progressive GN
manifestation of RPGN
severe olioguria
nephritis
crescent formation
3 groups based on immuno mechanism RPGN
1: anti GBM antibody induced ( renal limited)
2: immune complex mediates
3: pauci-immune type
syndrome associated with type 1 RPGN
Goodpasture syndrome
pattern of IgG and C3 deposition
linear
complication of post infectious GN, lupus nephritis, henoch-schonlein purpura
granular pattern
type 2 immune complex mediated
has circulating ANCAs which attacks visceral epithelial cells
type 3: pauci immune type
RPGN gross morphology
enlarged, pale, with cortical petechial hemorrhage
RPGN light microscopy features
crescent formation by proliferation of parietal epithelial cells
obliterated bowman’s space
WBC migration and some fibrin strands between crescent layers
electron microscopy RPGN features
subepithelial deposits and rupture of the GBM
cause fibrin to escape the glomerulus and settle in space
manifestations of nephrotic syndrome
massive proteinuria hypoalbuminemia generalized edema hyperlipidemia lipiduria
most important primary glomerular dse
primary: children: lipoid nephrosis
secondary: adults: membranous GN
all ages: focal segmental GS
may occur with lipiduria in patients susceptible to infection
globinuria
loss of anticoagulant glycoprotein factors in patients with nephrotic syndrome may lead to
thrombotic or thromboembolic complications
most common nephrotic syndrome in adults
membranous GN
membranous GN histological features
uniform diffuse thickening of capillary walls
irregular SPIKES of silver staining matrix
effaced foot processes
pathogenesis of membranous GN
direct action of c5-c9 which activates the glomerular mesangial and epithelial cells ➡️liberates proteases and oXidants➡️capillary wall injury➡️increased protein leakage
most common type of membranous GN 85%
idioipathic or primary
2ary membranous GN etiologies
hep b, c
penicillamine, captopril, gold therapy, NSAIDs
lung ca, colon, melanomas
SLE 15%
clinical course of membranous GN
40% of cases can proceed to renal failure adults nonselective proteinuria poor response to corticosteroid therapy sudden presentation, minimal hematuria
most frequent cause of nephrotic syndrome in children
minimal change disease or lipoid nephrosis
most characteristic feature of minimal change disease
good response to corticosteroid therapy
pathogenesis of minimal change disease
abscence of immune complexes
elaboration of cytokine (t cell derived)like circulating substance leads to proteinuria
proteinuria selective to albumin only
light microscopy feature of minimal change disease
normal
immunofluorescence feature of minimal change dse
normal, no deposits
electron microscopy feature of minimal change disease
uniform and diffuse foot processes replaced by a rim of cytoplasm often showing vacuolization, swelling, and hyperplasia of villi
MCD in adults is associated with
Hodgkin’s lymphoma
secondary MCD may follow
NSAID therapy
associated with acute interstitial nephritis
most common form of glomerulosclerosis in adults
focal segmental GS
hallmark of FSFGS
epithelial damage
pathogenesis of FSGS
epithelial damage
hyalinosis
sclerosis
on LM, FSGS initially involves only
juxtamedullary glomeruli
immunoflorEscence features of FSGS
deposition of IgM and c3 in sclerotic areas and or mesangium
FSGS may lead to
global glomerulosclerosis with pronouced tubular atrophy and interstitial fibrosis
morphologic variant of FSGs
collapsing glomerulopathy
cause of collapsing glomerulopathy
idiopathic but is the most characteristic lesion of HIV associated nephropathy
clinical course of FSGS
poor corticosteroid response