Renal Flashcards
Crescentic GN depositions
- RPGN crescents:
- glomerular parietal cells
- monocytes and macrophages
- FIBRIN on deckkk
type 1 RPGN (Goodpasture syndrome) deposits
C3 and IgG-linear depositis seen on IF microscopy
Acute PSGN depositions
- IF:
- IgG, IgM, C3: lumpy bumpy
- (will have DEC serum C3 levels)
- EM: subepithelial IC
DPGN deposits
- EM: (subendothelial, sometimes intramembranous)
- IgG based IC + C3
MPGN deposits
- Type 1: subendothelial IC +granular IF
- Type 2: intramembranous IC (dense deposits)
FSGS deposits
- IF: focal IgM, C1, C3
ACE inhibitors and bradykinin
- ACE metabolizes brady=LESS brady
- ACE inhibitors=less brady metab=MORE brady
TWO main causes of overflow incontinence
- impaired detrusor contractility
- bladder outlet obstruction (BOO)
- tumor obstructing the urethra
CP: involuntary+continuous urinary leakage when bladder is full
-incomplete emptying
what is the differential diagnosis for urinary incontinence
- stress
- loss of urethral support and abdo pressure>urethral sphincter pressure
- s/s: leaking with cough, sneeze,laugh, lift
- urge
- detrusor overactivity (PT with MS)
- s/s: sudden overwhelming or freq need to empty bladder
- overflow
- impaired detrusor contractility, BOO
- s/s: involuntry dribbling of urine, incomplete emptying
classifications for RP(crescentic)GN
- anti-GBM RPGN
- linear GBM of IgG and C3
- some: antiGBM in lungs (Goodpasture)
- immune-complex RPGN
- lumpy bumpy d/t IgA + IgG + complement
- d/t:
- PSGN
- SLE (serum anti-PHOSPHOLIPID Ab)
- IgA nepropathy
- HSP
- pauci-immune RPGN
- nada on BM
- ANCA in serum=
- granulomatosis with polyangiitis
- microscopic polyangiitis
- idiopathic
nephrotic syndrome and aldosterone
- plasma oncotic pressure is DEC
- net plasma filtration into interstitium
- DEC effective circulating intravascular volume
- compensatory INC in RAAS
- elevated circulating aldosterone
CP MCD
- 5yo boy w/ generalized edema after mild URI
- UA: proteinuria, albumin + trace IgG
- PP: loss of GBM anions=can no longer repell albumin=SELECTIVE albuminuria
- d/t immune dysregulation, systemic T cell dysfunction= overproduce glomerular permeability factor (GPF)
- GPF:
- causes podocyte foot process fusion
- DEC anionic properties of the glomerular basement membrane
**INC SELECTIVE FILTRATION OF PROTEINS**
Thrombotic microangiopathy
- PENTAD for TTP (thrombocytopenic thrombotic purpura-HUS is a thrombotic microangiopathy-TMA)…all in the setting of a GI illness
- fever
- neuro symptoms (progressive lethargy)
- renal failure
- anemia
- thrombocytopenia
what are the shared common clinical and pathologic features of TMA syndromes (thrombotic microangiopathy)
- platelet activation in arterioles and capillaries
- diffuse micro-vascular thrombosis (most commonly affect: brain, kidneys, heart)
- microangiopathic hemolytic anemia with schistocytes
- thrombocytopenia
FSGS CP
- (has a collapsing variant)
- CP: heavy proteinuria
- “collapse and sclerosis of glomerular tufts”
RP(crescentic)GN CP
- macroscopic hematuria
- HTN
- progresive renal failure
- three major classifications:
- anti-GBM (w/ hemoptysis in Goodpasture syndrome)
- immune-complex mediated (SLE)
- pauci-immune (w/ pulm, upper respiratory, and kidney involvement in granulomatosis with polyangiitis)
PSGN CP
- childhood dz
- can follow strep pharyngitis and lead to coke-colored urine + periorbital edema
- renal biopsy: diffuse proliferation and subepithelial Ig deposits
HSP vs. IgA nepropathy CP/renal bx
- HSP: childhood dz; NON-thrombocytopenic palpable purpura + arthritis
- IgA nephropathy presents w/ recurrent hematuria and low-grade proteinuria after URTI
- BOTH: IgA deposition in mesangium
ATN renal biopsy
patchy necrosis of tubular epithelium and loss of basement membrane
TMA renal bx
platelet-rich thrombi in glomeruli and arterioles
What does BPH do to the kidneys
- intermittent BOO + overflow incontinence
- urinary retention=INC pressure in the urinary tract and resultant reflux nephropathy
- ultimately: hydronephrosis and renal intersitial atrophy (“parenchymal pressure atrophy) and scarring
diabetic nephrosclerosis termed
glomerular sclerosis and hyalinosis
long-standing systemic HTN termed
hyperplastic arteriolar changes (intimal fibroelastosis)
-diagnostic of hypertensive nephropathy seen in pts with poorly controlled HTN
terms for the causes of ITN
- low-flow states: MI
- systemic vasodilation: sepsis
- s/s–INC sBUN & Cr: azotemia
dysplasia termed precursor of malignancy
- epithelial dysplasia=alteration in cell architecture
- cells change shape, size (pleomorphic) and staining (hyperchromatic); nuclei enlarge
urate nephropathy termed
- d/t tubular obstruction f/m urate crystal deposition
- seen in indivs wih ACUTE HYPER-uricemia (tumor lysis syndrome)
- CP: acute renal failure d/r chemo for a malignancy
