Renal Flashcards
Glomerular BM collagen
TIV
Immunofluorescence pattern glomerular disease
granular - immune complexes
linear - auto antibodies against GBM
Post strep glomerulonephritis
acute proliferative glomerulonephritis
1-4 weeks post infection (nephritic)
TIII hypersensitivity
pyogenic exotoxin B
inc anti strep AB, dec C3
malaise, fever, haematuria, periorbital oedema
95% kids recover
Post staph glomerulonephritis AB
IgA (rather than IgM)
Rapidly progressive GN
severe oliguria and signs nephritic
T1 anti GBM ABs e.g. goodpastures
T2 immune complex e.g. post infective
T3 pauci immune, anca
Tx steroids and cytotoxic
can be fatal
Morphology rapidly progressive GN
crescents - proliferative parietal epitelium bowmans capsule with monocytes an macrophages
fibrin strands between layers in crescents
ruptures in GBM
Diagnostic criteria nephrotic
massive proteinurea (3.5g/d)
Hypoalbuminaemia
Oedema
Hyperlipidaemia and lipiduria
Membranous nephropathy
nephrotic
accumulation Ig causing thickening glomerular capillary wall
75% primary
secondary - gold, penicillamine, captopril
doesn’t respond steroids
Minimal change disease
most frequent nephrotic in children
age 2-6
benign
responsive to steroids
massive proteinuria, no HTN
Focal segmental glomerulosclerosis
most frequent nephrotic in adults
primary or secondary
minimally responsive to steroids
20% develop renal failure in 2y
Membranoproliferative glomerulonehritis
nephrotic and nephritic
GBM thickened tram track like
T1 IgG and complement
T2 alternate complement (dense deposit disease)
poor prognosis 50% ERF
IgA nephropathy (bergers)
most common glomerulonephritis
IgA deposits in mesangial cells and recurrent haematuria
renal failure over 20y
Allport syndrome
hereditory nephritis
genes encoding TIV collagen
haematuria and slowly progressive proteinuria
ATN
causes 50% ARF hospitalised pateints
ischaemic or toxic injury
Ischaemia - PCT and LOH
cast deposition - DCT
toxic 95% recovery, shock related - 50% mort
ATN clinical course
initiation phase - 36h, initial insult, slight dec UO
maintenance phase - inc K, metabolic acidosis, oliguria, Na and H2O overload
recovery phase - dec K and Na, massive diuresis
Morphology tubointerstitial nephritis
acute - interstitial oedema, leukocytes
chronic - interstitial fbrosis, mononuclear leukocytes, tubular atrophy
Signs tubointerstitial nephritis
no nephritic or nephrotic
defects tubular function with salt wasting and metabolic acidosis
% UTI gram -ve
85%
Cause viral pyelonephritis
polyomavirus (mainly post kidney transplant)
Complications pyelonephritis
papillary necrosis (DM, sickle, obstructive)
pyonephrosis (with almost complete obstruction)
perinephric abscess
Causes chronnic pyelonephritis
reflux - most common
obstruction
Drug induced nephritis
15d post exposure
fever, eosinophilia, rash
TIV reaction
50% inc creatinine, oliguria
Malignant nephrosclerosis
assoc HTN malig
fibrinoid necrosis arterioles and hyperplastic arteriolitis (onion skinning)
5y survival 75%, normal renal function 50%
Renal artery stenosis
70% due to atheroma origin renal art
other fibromuscular dysplasia age 30-40
Calcium oxalate and phosphate stones
70%
55% have normal blood calcium
radioopaque
furosemide, aetazolamide, antacids, glucocorticoids, crohns
Magnesium ammonium phosphate stones
15-20%
struvite, staghorn
urea splitting bacteria (proteus)
inc pH urine
Uric acid stones
5-10%
50% idiopathic
acidic urine
radiolucent
Cysteine stones
1-2%
form in acidic urine
genetic defect reabsorption AAs
Urine in hepatorenalsyndrome
Hyperosmolar
Low in sodium
No proteins
Type of hypersensitivity post strep
Rheumatic fever - II
Glomerulonephritis - III
Triad tubulointerstitial nephritis
15d post exposure
Rash, fever, eosinophilia
Renal problem associated HIV
FSGS
Buffer urine chronic acidosis
Ammonia
(Normally phosphate predominant)
