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Renal Flashcards

1
Q

what vessel blocks a horseshoe kidney

A

IMA

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2
Q

unilateral agenesis

A

hypertrophy of other one

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3
Q

bilateral renal agenesis

A
  • oligohydramnios
  • leads to lung hyperplasia (no stretch
  • low set ears and limb defects (Potter sequence)
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4
Q

dysplastic kidney

A
  • congenital malformation, non inherited
  • cartilage and cyst
  • usually unilateral
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5
Q

adult polycystic kidney

A
  • bilateral
  • autosomal dominant
  • enlarged kidney
  • APKD1/2
  • associated with berry aneurysm, hepatic cysts and mitral valve prolapse
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6
Q

newborn polycystic kidney disease

A
  • recessive

- congenital hepatic fibrosis and hepatic cysts (portal hypertension)

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7
Q

medullary cystic kidney disease

A
  • cysts are in medullary collecting ducts
  • shrunken kidneys
  • autosomal dominant
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8
Q

hallmark of renal failure

A
  • azotemia and oliguria
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9
Q

prerenal failure (labs)

A
  • lower GFR, azotemia and oliguria
  • high BUN:Cr (reabsorption still works)
  • tubular function is intact - low FeNa
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10
Q

postrenal (labs)

A
  • decrease GFR and azotemia
  • early = high BUN:Cr and normal FENa
  • late = decrease BUN:Cr ratio, high FENa, unconcentrated urine
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11
Q

ATN

A
  • injury of tubules (detachment of cells from BM)
  • azotemia with low BUN:Cr, high FENa
  • muddy brown casts in urine
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12
Q

etiology of ATN

A

ischemia and nephrotoxicity

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13
Q

areas susceptible to ischemia

A

proximal tubule and medullary segment or thick ascending limb

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14
Q

causes of ATN

A

antibiotics, lead, crush, ethylene glycol, radiocontrast dye, urate (tumor lysis)

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15
Q

crystals in ethylene glycol poisoning

A

oxalate crystals

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16
Q

features of ATN

A
  • oliguria with muddy brown casts
  • high BUN and creatinine
  • hyperkalemia and metabolic acidosis
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17
Q

what happens post ATN

A

cells are stable, takes time to regenerate

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18
Q

acute interstitial nephritis

A
  • drugs including NSAIDs, PCN and diuretics
  • inflammation in interstitium
  • eosinophils in urine
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19
Q

renal papillary necrosis

A
  • gross hematuria and flank pain

- caused by aspirin, sickle cell

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20
Q

labs in nephrotic syndrome

A
  • hypoalbuminemia (albumin >3.5)
  • hypergammaglobulinemia
  • hypercoagulable state (lose ATIII)
  • hyperlipidemia and hypercholesterolemia (blood is thin so fat goes in blood)
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21
Q

minimal change disease

A
  • children
  • associated with Hodgkins lymphoma
  • loss of foot processes from cytokines
  • normal glomeruli with no immune complexes
  • no loss of immunobloblulin
  • good response to steroids
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22
Q

focal segmental glomerulosclerosis

A
  • can be associated with HIV, heroin or sickle cell
  • effacement of foot processes on EM
  • no immune complexes
  • progression of MCD
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23
Q

membranous nephropathy

A
  • associated with hepatitis B/C, SLE or drugs
  • thick glomerular basement membrane
  • immune complex deposition (granular)
  • spike and dome - subepithelial
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24
Q

membranoproliferative glomerulonephritis

A
  • thick capillary membranes with tram-track appearance
  • immune complex deposition (granular)
  • mesangial cell is proliferating
  • deposits can be anywhere
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25
two types of membranoproliferative glomerulonephritis
type 1 - subendothelial (Hep B/C and tram tracks) type 2 - within BM (antibody C3 nephritic factor - too much C3 convertase)
26
locations of immune complexes
- subepithelial - membranous nephropathy - in BM - type 2 MPGN - subendothelial - type 1 MPGN
27
grouping of nephropathies
1. MCD and FSGN - effacement of foot process by cytokines 2. membranous and MPGN - membranes with immune complexes 3. diabetes and amyloidosis (systemic disease)
28
diabetes nephropathy
- high glucose leads to NEG of BM resulting in hyaline arteriolosclerosis - high GFR (hyperfiltration) leading to sclerosis - give ACE inhibitors to help
29
amyloidosis
- amyloid in mesangium | - apple green biregringence
30
hallmark of diabetic nephropathy
- sclerosis of mesangium and formation of Kimmelstiel-Wilson nodules
31
labs in nephritis syndrome
- limited proteinuria - oliguria and azotemia - salt retention and periorbital edema and hypertension - RBC casts
32
pathophys of nephritis
immune complexes activating complement, C5a attracts neutrophils causing damage
33
PSGN
- after group A strep - either skin or pharynx - M protein - subepithelial humps (complexes pile up)
34
findings in PSGN
- cola urine - oliguria - edema
35
RPGN (rapidly progressive glomerular nephritis)
- nephritic syndrome that progresses to renal failure | - crescent
36
crescent are made of...
macrophages and fibrin (inflammatory debris
37
types of immunofluorescence
1. linear (goodpasture) 2. granular (PSGN) 3. negative (vasculitis)
38
goodpasture
- antibodies to collagen 4 in BM
39
renal disease in lupus
diffuse proliferative glomerulonephritis (nephritic) and membranous nephropathy (nephrotic)
40
IgA nephropathy
- in mesangium - RBC casts - after mucosal infections - complex deposition - can progress to renal failure
41
Alport syndrome
- defect in type 4 collagen - thinning and splitting of GBM - isolated hematuria, sensory hearing loss and ocular disturbances
42
positive leukocyte esterase
- pus in urine
43
nitrites
bacteria in urine
44
sterile pyuria
chlamydia and neisseria
45
WBC casts
in pyelonephritis
46
chronic pyelonephritis
- malformation of valve from bladder to kidney - cortical scarring with blunted calyces - scarring at upper and lower poles
47
histology in chronic pyelonephritis
- thyroidization of tubules - atrophic tubules contain eosinophilic proteinaceous material - waxy casts
48
calcium stone
- have to exclude calcium causes - in Chrons disease (less absorption of oxalate) - treat with HCTZ
49
ammonium magnesium phosphate
- infection with urease positive organisms | - staghorn calculi that acts as a nidus
50
Uric acid stone
- radiolucent - in dry heat and acidic pH - in gout or myeloproliferative disorders - treat with alkalinization of urine
51
cysteine stone
- defect in tubules that decrease cysteine reabsorption | - staghorn calculi
52
most common causes of renal failure
diabetes, HTN and glomerular disease
53
EPO is produced by....
renal peritubular interstitial cells
54
clinical findings in renal failure
- hyperkalemia - acidemia - hypocalcemia (less vitamin D and can't excrete phosphate) - renal osteodystrophy
55
renal osteodystrophy
- low calcium causes PTH to rise and hit bone - osteitis fibrosa cystica - osteomalacia (can't mineralize new bone) - osteoporosis (metabolic acidosis)
56
dialysis kidneys
shrunken with cysts | - risk for RCC
57
angiomyolipoma
- hamartoma of vessels, muscle and fat | - increase frequency in tuberous sclerosis
58
renal cell carcinoma
- epithelial tumor - hematuria, palpable mass and flank pain - fever, weight loss and paraneoplastic - presents with left sided varicocele - yellow mass
59
pathogenesis of RCC
- loss of VHL - increases IGF-1 - increased HIF (VEGF and PDGF)
60
two pathways of RCC
sporadic - smoking RCC - yonger and bilateral - both with VHL
61
Von Hippel-Lindau disease
- loss of VHL gene | - risk for hemangioblastoma and RCC
62
Wilms tumor
- in children - blastema, primitive glomeruli and tubules - large flank mass and hypertension
63
syndromes with Wilms tumor
``` WAGR (aniridia, genital problems and retardation) Beckwith Wiedemann (hypoglycemia, hemihypertrophy and organomegaly) ```
64
urothelial carcinoma
- in bladder usually - cigarette smoke, naphthylamine, azo dyes, cyclophosphamide or phenacetin - painless
65
two pathways of urothelial carcinoma
1. flat - starts as high grade (early p53) | 2. papillary - low grade to high grade to invasion
66
field defect
all of urothelium has been hit, tumors are multifocal and recur
67
risks of SCC
cystitis, schistosoma, low standing nephrolithiasis
68
where does adenocarcinoma of bladder come from
urachal remnant (dome of bladder), cystitis glandularis, exstrophy (no caudal portion)

Pathoma (11 decks)

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