Renal Flashcards

1
Q

IgA nephropathy (berger)
post infections nephropathy
goodpastures
and vasculitis

are all exmaples of what

A

AGN

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2
Q

glomerular nephritis this is most commonly seen after Group A strep infection

A

post infectious

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3
Q

MCC of AGN worldwide

A

Berger’s IgA

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4
Q

what type of infections would we expect to led to berger’s dz

A

respiratory or GI

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5
Q

10 year old boy is seen with facial edema and dark cloudy urine 3 weeks following infection as well as oliguria

how would you dx him

A

most likely post infectious AGN

dx with antistreptolysin (ASO) titers and low serum complement c3

Tx is supportive

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6
Q

pt comes in 2 days following URI and is seen with hematuria, RBC casts and edema, as well as azotemia

what would be the official dx test

A

most likely IgA nephropathy given resent URI

dx with IgA mesangial deposits on immunostaining

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7
Q

this is a type of glomerulonephritis seen associated with anti-GBM antibodies that attack the basement membrane in the kidney and lung

how would you dx

A

good pastures

linear IgG deposits

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8
Q

what are the clinical manifestations of AGN

A

hematuria is the hallmark cola colored
edema in 85% due to decreased onctoic pressure and increase Na retention

HTN in 80% secondary to H20 retention

fever abdominal pain and flank pain due to renal capsule expansion
5. oliguria as a result of AKI

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9
Q

what is the nonspecific manner to dx AGN

A

UA with hematuria, RBC casts, dysmporphic RBC, proteinuria usually less than 3g, and a high specific gravity

elevated BUN and elevated Cr

renal biopsy is the gold standard but this is not needed in post strep as it is supportive tx

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10
Q

DVT and frothy urine are characteristic of this type of kidney injury

A

nephrotic syndrome

fatty casts and more than 3.5 g of protein

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11
Q

minimal change disease is a type of

A

nephrotic syndrome seen in children

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12
Q

what types of AKI are reversible

A

prerenal and postrenal

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13
Q

this is the most common type of AKI seen as a result of a decrease in renal perfusion

what is the tx

A

prerenal

nephrons are structurally intact and is usually corrected by volume repletion

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14
Q

BPH is a common cause of this type of AKI

A

post renal

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15
Q

what are the different types of intrinsic kidney injury we see

A

ATN
AIN
AGN
vascular

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16
Q

prolonged pre-renal hypotension, hypovolemia or post-op can result in what type of kidney injury

A

ischemica ATN

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17
Q

exogenous cause of nephrotoxic intrinsic AKI

A

AG (10-265), contrast dye, cyclosporin medications

18
Q

endogenous causes of intrinsic ACT

A

Gout seen as cyrstal precipitation, myglobinuria (rhabdomylosis), lymphoma and leukemia, Bence-Jones multiple myeloma

19
Q

MC type of intrinsic kidney dz

A

endogenous nephrotoxic

20
Q

what would we suspect in a pt with epithelial muddy brown casts

21
Q

what would we expect to see in the UA of a pt with ATN

A

low specific gravity b/c they are unable to concentrate urine do to tubular cell damage
muddy brown casts

22
Q

wbc casts are paohtgonomic for

A

AIN

also seen with increase IgE

23
Q

AIN is usually the result of

A

drug allergy 70%
PCN, NSAIDS, sulfa, cephalosporins, ciprofloxacin, rifampin, allopurinol.

15% due to infection
autoimmune 6%
idiopathic 8%

24
Q

clinical manifestations of AIN

A

fever eosinophilia, maculopapular rash, arthralgia

remember this is hypersensitivity

25
With what AKI would you expected to see a low FeNa
prerenal | holding onto sodium
26
why would we see a decreased BUN
``` pregnancy fluid overload liver failure negative nitrogen balance nephrotic syndrome ```
27
what are the three hallmarks of glomerular injury
protein uria lipiduria edema
28
what are the clinical signs of glomerular kidney injury
HTN | edema
29
MCC of chronic renal failure in the US
inflammatory injury
30
this is focal scarring of some glomeruli that is idiopathic but associated with hypoxia and HIV
focal segmental sclerosis
31
how to you differentiate focal segmental sclerosis from minimal change dz
HTN is not seen in MCD and you also see reduced renal function in focal segmental sclerosis
32
what is the MCC of ESRD and what is the pathophysiology
DM this is why we try to protect pts with an ACE inhibitor to decreased GFR and blood pressure through preventing the conversion of agiontensin I from the liver to agiotensin II
33
second most common caused of ESRD
HTN
34
Third MCC of ESRD
infection
35
this hormone acts on principle cells and increased NA/ resorption K secretion
aldosterone we see a loss of sodium with addison's because of hypo-aldosterone
36
this hormone is the most powerful sodium retainer
angiotensin II
37
which hormone on RAS increases water resorption
ADH
38
how does sympathetic activation work on the renal tubules
reduces GFR
39
what types of pathogens do we want to consider in a pt with an ascending UTI and stones
klebsiella or proteus
40
struvite stones are formed from what
Mg ammonium and phosphate and may form staghorn calculi in the renal pelvis due to era-splitting organisms