renal disease classification 2 Flashcards
hypertensive nephrosclerosis
may be benign or malignant
benign hypertensive nephrosclerosis
due to chronic hyper tension
most due to primary essential hypertension eg. usually elderly, multifactorial hypertension
malignant hypertensive nephrosclerosis
due to accelerated hypertension
causes acute end organ damage
medical emergency
pathogenesis of benign hypertensive nephrosclerosis
thickening (sclerosis) of small arteries and arterioles
ischaemic damage to glomeruli and tubules
glomeruloslcerosis - scarring
clinical presentation of benign hypertensive nephrosclerosis
asymptomatic urinary abnormalities - proteinuria
chronic renal failure
pathogenesis malignant hypertensive nephrosclerosis
- requires urgent but controlled reduction in blood pressure
- severe damage to small arteries and arterioles
- ischaemic injury to glomeruli and tubules
presentation of malignant hypertensive nephrosclerosis
acute renal failure
renal artery stenosis
uncommon cause of secondary hypertension
pathogenesis of renal artery stenosis
usually unilateral critical narrowing of main renal artery
due to atheromatous disease in elderly
rarely, due to fibromuscular dysplasia in young women
ischaemic damage to glomeruli and tubules
narrowing to main renal artery reduces blood perfusing the kidney
kidney recognises reduced oxygen and secretes renin which is an enzyme catalysing conversion of angiotensin to angiotensin 1
cells in the lungs secrete Ace which converts angiotensin 1 to angiotensin 2 which is a vasoconstrictor
systemic vasoconstriction occurs increasing blood pressure
ACE inhibitor drugs required
kidney response to narrowing of main renal artery
responds to decreased perfusion by secreting renin, an enzyme catalysing conversion of angiotensin to angiotensin 1
angiotensin 1
is converted to angiotensin 2 by ACE, which is secreted by cells in the lungs
angiotensin 2
a vasoconstrictor, causes systemic vasoconstriction and rise in blood pressure
fibromuiscular displasia
patients develop thinking of all layers of the blood vessel in the renal artery
angiogram shows alnernating patterns of narrowing and dilatation like beads on a string
cause of renal artery stenosis
acute tubular necrosis
one of the most common causes of acute renal failure
tubular injury/necorisi due too either
- iachaemia
- toxins
acute tubuler necrosis due to ischaemia
reduced renal perfusion
- shock, hypevolaemia, vascular compromise (vasculitis, malignant hypertension, thrombotic microangiopathy)
acute tubular necrosis due to toxins
endogenous - myoglobin, haemoglobin, light chains
exogenous - drugs, radio contrast dyes, heavy metals
clinical course of acute tubularr necrosis
initiation phase - mild oliguria with mild increase in serum creatinine
maintenance phase - sustained oliguria, rising serum creatinine with uraemia
recovery phase - massive diuresis with electrolyte disturbances
histology of acute tubular necrosis
injury to the tubular epithelial cells
tubulointerstitial nephritis
tubulointerstitial inflammation due to various causes
- acute - interstitial oedema with neutrophilic/eosinophiliss infiltrate
- chronic - lymphocytic infiltrate with tubular atrophy and interstitial fibrosis (chronic and irreversible)
aetiology of tubulointerstitial nephritis
- usually drugs - NSAIDs, PPIs, antibiotics
- others
pathogenesis drug related tubulointerstitial nephritis
drug-related TIN usually idiosyncratic and not dose related
drugs act as a happen, combining with components of tubular epithelial cells to elicit immune reaction
clinical presentation of tubulointerstitial nephritis
fever, peripheral eosinophilia, rash, mild proteinuria, eosinophils in urine and acute renal failure
histology of acute TIN
mixed inflammation with tubulitiss and tubular injury
histology of chronic TIN
chronic inflammation with tubular atrophy/interstitial fibrosis
acute TIN vs acute pyelonephritis
pyelonephritis usually cause by ascending UTI not drugs
inflammation of pyelonephritis usually centred around renal calyces, pelvis and tubulointerstitial compartment instead of just tubulointerstitial compartment
pyelonephritis has tubular micro abscesses not just tubulitis
pyelonephritis treated with antibiotics, whereas TIN treated with removal of offending agent and steroids
chronic pylonephritis
chronic inflammation and scarring centered on renal calyces, pelvis and tubulointerstitium
two main clinical settings
- reflux nephropathy due to congenital vesocoureteric reflux
- obstructive nephropathy due to chronic ureteric obstruction
myeloma kidney
- plasma cell myeloma - malignant clonal proliferation of plasma cells
- bone lesions, serum paraprotein, kidney injury
renal complications of plasma cell myeloma
- cast nephropathy
- amyloidosis
- acute tubular necrosis (calcium, light chains, uric acid)
- light chain deposition disease
- renal vein thrombosis
myeloma cast nephropathy
medical emergency
widespread tubular abstructiin by intraluminal light chain chants causing acute renal failure
immunoflourescence shoes kappa or lambda light chains (not both)
amyloidosis
accumulation of amyloid protein - which is abnormally folded causing it to be hard to degrade
resistant to enzymatic degradation
have unusual physiochemical properties - form beta pleased sheets
can be identified on the microscope using Congo red stain, where the proteins stain salmon pink colour
deposits in glomeruli, vessels and interstitial presenting as severe proteinuria
histology of myeloma kidney
large pink amorphous deposits - amyloidosis
- salmon pink under Congo red stain
- apple green on polarising LM stain
