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FA: random > Renal > Flashcards

Renal Flashcards

1
Q

Differentiate cyst location in dysplastic kidney dz, PKD, Medullary cystic kidney dz

A

dysplastic => renal parenchyma & abnormal tissue

PKD=> bilateral enlarged kidneys w/ cysts in cortex & medulla

medullary => medullary collecting ducts w/ parenchymal fibrosis leading to shrunken kidneys

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2
Q

How does the ARPKD present?

A

baby w/ portal HTN due to congenital hepatic fibrosis

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3
Q

How does ADPKD present?

A

young adult w/ HTN, hematuria, progressive renal failure w/ FHx of death due to berry aneurysm rupture or chronic renal failure

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4
Q

What is the timeline & hallmark of acute renal failure?

A

azotemia (high BUN & Cr) w/in days often w/ oliguria

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5
Q

What is the cause of pre renal ARF? what are the assoc labs?

A

decreased Q to kidneys so decreased GFR;
BUN:Cr > 15
tubular fxn intact so FENa < 1% & urine osm > 500 mOsm/kg

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6
Q

What is cause of post renal azotemia?

A

obstruction of urinary tract downstream decreasing GFR (backup), azotemia & oliguria

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7
Q

Differentiate the timeline of early & long-standing post renal obstruction

A

early increase in pressure leads to BUN:Cr > 15
FENa < 1% & urine osm > 500mOsm

long term causes tubular damage causing BUN:Cr < 15
FENa > 2% & urine osm < 500mOsm

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8
Q

what is the MCC of acute renal failure?

A

intrarenal azotemia => injury & necrosis of tubular epithelial cells

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9
Q

What will be seen on urinalysis during ATN?

A

brown, granular casts in urine
serum BUN:Cr < 15
FENa > 2%
urine osm < 500 mOsm

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10
Q

What are the clinical features of ATN?

A

oliguria w/ brown granular casts
BUN:Cr < 15
Hyperkalemia (decresed renal fxn) w/ metabolic acidosis

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11
Q

Describe ATN if ischemia is the cause. What is the most susceptible part of kidney?

A

decreased Q so often preceded by pre renal azotemia =>

proximal tubule & medullary segment of thick ascending limb are most susceptible

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12
Q

What are nephrotoxic agents to the kidney that may lead to ATN?

A 
MC is aminoglycosides;
heavy metals (lead);
myoglobinuria (crush injury to muscle);
ethylene glycol;
radiocontrast dye (CT scan);
urate (tumor lysis syndrome or high gout)
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13
Q

How will you know if someone ingested ethylene glycol?

A

oxalate crystals in urine

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14
Q

What are ways to avoid tumor lysis syndrome causing ATN?

A

hydration & allopurinol prior to CTX

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15
Q

If ATN occurs, how is it treated and can the pt recover? what is the timeframe?

A

Reversible => supportive dialysis due to severe electrolyte imbalances

oliguria can present for 2-3wks before recovery due to tubular cells regenerating

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16
Q

Why does it take 2-3wks for oliguria to remit?

A

tubular cells are stable cells so takes time to re-enter the cell cycle & regenerate

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17
Q

What causes acute interstitial nephritis? How is it treated? What happens if it is not?

A

Drug induced HSR causing infrarenal azotemia typically from NSAIDs, penicillin & diuretics
Resolves w/ drug stoppage;
if Rx is not pulled then renal papillary necrosis may occur

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18
Q

How does acute interstitial nephritis present?

A

oliguria, fever & rash varying from days to weeks (any time) after using a Rx => eosinophils MAY be in urine

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19
Q

How does renal papillary necrosis present? What are the common causes?

A 
gross hematuria w/ flank pain
causes=>
Chronic analgesic pain (phenacetin or aspirin use);
DM;
Sickle cell disease OR trait;
Severe acute pyelonephritis
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20
Q

Define nephrotic syndrome & the 4 possible results

A

proteinuria > 3.5g/day

hypoalbuminemia - pitting edema;
hypogammaglobulinemia - increased infection risk;
hyper coagulable state - due to loss of AT-3;
hyperlipidemia & hypercholesterolemia - fatty casts in urine

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21
Q

How does the MCC of nephrotic syndrome in children present on H&E? EM? IF? urinalysis?

A

H&E: normal glomeruli;
EM: effacement of foot processes
IF: no IC deposits so negative IF

Urinalysis has selective proteinuria w/ loss of albumin but not Ig loss

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22
Q

What cancer is minimal change disease associated with? why?

A

Hodgkin lymphoma due to massive increase of cytokines from RS cells

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23
Q

What is the response to treatment of minimal change disease?

A

excellent response to steroids due to damage caused by cytokines from T cells

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24
Q

What is the MCC of nephrotic syndrome in Hispanics & AA?

A

Focal segmental glomerulosclerosis (FSGS)

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25
Q

What is FSGS associated with?

A

HIV; heroin use; sickle cell disease

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26
Q

How does FSGS appear on H&E? EM? IF?

A

HE: focal & segmental pink sclerosis
EM: effacement of foot processes
IF: no IC deposits = neg IF

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27
Q

What is the response to Tx in FSGS?

A

poor response to steroids leading to chronic renal failure

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28
Q

What is the MCC of nephrotic syndrome in caucasian adults?

A

membranous nephropathy

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29
Q

What is membranous nephropathy assoc w/?

A

HBV, HCV;
solid tumors;
SLE (usually diffuse proliferative GN);
Rx (NSAIDs & penicillamine)

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30
Q

How does membranous nephropathy appear on H&E? EM? IF?

A

HE: thick glomerular BM
EM: subepithelial deposits w/ ‘Spike & dome” appearance
IF: IC deposits so granular IF

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31
Q

What is the response to Tx of membranous nephropathy?

A

poor response to steroids causing chronic renal failure

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32
Q

How does membranoproliferative glomerulonephritis present on H&E? EM? IF?

A

HE: thick glomerular BM often w/ “tram-track” appearance
EM: 2 types based on location of deposits (sub endothelial or intramembranous)
IF: IC deposition = granular IF

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33
Q

What is the response to Tx of membranoproliferative GN?

A

poor response to steroids leads to chronic renal failure

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34
Q

Describe the pathophys of renal disease in diabetes mellitus

A

high glucose leads to NEG of vascular BM causing HYALINE ARTERIOSCLEROSIS (thick wall damages lumen) =>
glomerular EFFERENT arteriole constriction leads to hyperfiltration causing microalbuminuria =>
nephrotic syndrome w/ sclerosis of mesangium => formation of Kimmelstiel Wilson nodules (dense sclerosis)

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35
Q

What is the response to Tx of diabetic nephrotic syndrome? why?

A

ACE like hyaline arteriosclerosis causes efferent constriction so ACE inhibitors slow dz progression

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36
Q

How does amyloidosis affect the kidney? How can it be proven to be the cause?

A

MC systemic organ in systemic amyloidosis=>
amyloid deposits in mesangium causing nephrotic syndrome

Apple-green birefringence under polarized light after Congo red stain

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37
Q

If minimal change disease does not respond to steroids, what is the progression?

A

FSGS

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38
Q

Based on the location of any IC deposition, differentiate the the types of nephrotic syndrome

A

Membranous = sub epithelial deposits (S&D)

Type I MPGN = subendothelial

Type II MPGN = dense deposits in intramembranous portion of glomerulus

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39
Q

Type I MPGN is assoc with what?

A

HBV & HCV

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40
Q

Differentiate how HBV & HCV can cause nephrotic syndrome

A

Membranous nephropathy has sub epithelial deposits w/ spike & dome

type I MPGN has subendothelial deposits

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41
Q

Type II MPGN is assoc w/ what? Describe how it gets its appearance on EM

A

assoc w/ C3 nephritic factor => autoAb stabilizes C3 convertase leading to over activation of complement, inflammation, & LOW circulating C3

binds to intramembranous portion of BM in kidney causing tram-track appearance

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42
Q

Define nephritic syndrome

A 
glomerular inflammation & bleeding =>
limited proteinuria (<3.5g/day);
oliguria & azotemia;
salt retention w/ periorbital edema progressing to HTN;
RBC casts & dysmorphic RBC in urine
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43
Q

If nephritic syndrome is suspected, how can it be confirmed?

A

Bx showing hyper cellular & inflamed glomeruli

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44
Q

What causes the damage in nephritic syndrome?

A

IC deposition activates complement leading to C5a attracting neutrophils which cause the damage

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45
Q

Differentiate the 2 types of nephritic syndrome that occurs after infections

A

both occur after infection

post-strept GN arises after GAS of skin or pharynx but can be occur after nonstrept organism as well

IgA nephropathy (Berger dz) occurs after mucosal infection such as gastroenteritis

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46
Q

What is the virulence factor that must be present in organism to cause PSGN?

A

nephritogenic strains must carry M protein virulence factor

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47
Q

When & how will patient w/ PSGN present?

A

2-3wks after infxn w/ hematuria (cola colored), oliguria, HTN & periorbital edema

usually kids but can be in adults

48
Q

What is the appearance of PSGN on HE? EM? IF?

A

HE: hypercellular, inflamed glomeruli
EM: subepithelial humps
IF: granular = IC deposits

49
Q

What is the Tx for PSGN?

A

supportive only bc progression is self limited w/ only 1% of kids going to renal failure
but
25% of adults develop rapidly progressive GN (RPGN)

50
Q

What is the timeline for RPGN?

A

nephritic syndrome to renal failure in wks to months

51
Q

How does RPGN appear on HE? IF?

A

HE: crescents in Bowman space

IF is variable depending on underlying cause

52
Q

What does a linear pattern on IF assoc w/ RPGN mean? How will it present? why? who is most likely to have this dz?

A

Goodpasture syndrome => anti-BM Ab

Ab against collagen in glomerular (hematuria) & alveolar (hemoptysis) BM

classically is young, adult males

53
Q

What does a granular pattern on IF in presentation of RPGN?

A

PSGN or diffuse proliferative GN

54
Q

What is significant about diffuse proliferative GN?

A

antigen-Ab complex deposition usually sub endothelial

MC type of renal disease in SLE

55
Q

differentiate the types of renal dz seen in SLE. What is significant about renal dz in SLE?

A

MC COD in SLE

membranous nephropathy is nephrotic w/ granular IF but SUBEPITHELIAL deposits (S&D)

DPGN is nephritic w/ granular IF w/ antigen-Ab complexes but are SUBENDOTHELIAL deposits

56
Q

If a pt presents w/ crescents in Bowman space & negative IF w/ hematuria & slight proteinuria, what should the next test be? What is the Ddx?

A

C-ANCA => Wegener granulomatosis

P-ANCA => microscopic polyangiitis & Churg Strauss

57
Q

What differentiates the P-ANCA assoc nephritic syndromes?

A

Churg Strauss has 3 things:
Granulomatous inflammation;
eosinophilia;
asthma

58
Q

What is the MC nephropathy worldwide? present on IF? profession

A

IgA nephropathy

IgA IC deposits in mesangium of glomeruli

may slowly progress to renal failure

59
Q

How does the IgA nephropathy present typically?

A

kid w/ episodic gross or microscopic hematuria w/ RBC casts following mucosal infection (gastroenteritis) causing IgA to increase then deposit in mesangium

60
Q

What is an inherited nephritic syndrome? Where is the defect? how does it present?

A

XLR defect in type IV collagen causing thinning & splitting of glomerular BM

presents w/ isolated hematuria, sensory hearing loss, ocular disturbances

61
Q

How does cystitis present?

A

dysuria, urinary freq, urgency, suprapubic pain

NO SYSTEMIC SIGNS

62
Q

What are the lab findings in cystitis? what is the gold standard of Dx of cystitis?

A

urinalysis: cloudy urine > 10WBC/hpf
dipstick: (+) leukocyte esterase (pyruria) & nitrites (bacteria convert nitrates to nitrites)

GOLD STANDARD=> culture: >100k cfu

63
Q

Name the 5 MCC of cystitis

A 
E. coli (80% in ALL population groups)
Staph saprophyticus (in sex, active female but E. coli is #1)
Kleb pneumoniae;
Proteus mirabilis;
Enterococcus faecalis
64
Q

If pt presents w/ cystitis Sx & ammonia scented urine, what is the cause?

A

Proteus mirabilis => alkaline urine w/ ammonia scent

65
Q

If urinalysis is done w/ urethritis Sx but urine culture is negative, what is most likely cause? what is the dominating sign of urethritis?

A

Dysuria is dominant sign of urethritis => sterile pyruria due to Chlamydia trachomatis or N. gonorrhoeae

66
Q

Patient w/ fever, flank pain, WBC casts & leukocytosis along with cystitis Sx has what? what are the MCC?

A

pyelonephritis from ascending infection from =>
E. coli (90%)
Klebsiella species
Enterococcus faecalis

67
Q

Why does pyelonephritis cause flank pain?

A

inflammation of the capsule of the kidney

68
Q

Define chronic pyelonephritis. What is common causes?

A

interstitial fibrosis & atrophy of tubules due to multiple bouts of acute pyelonephritis

MCC are vesicoureteral reflux in kids;
obstruction in adults such as BPH or cervical CA

69
Q

Chronic pyelonephritis assoc w/ vesicoureteral reflux leads to what w/in the kidney?

A

cortical scarring w/ blunted calyces;

scarring at both poles is characteristic

70
Q

Describe the H&E stain of chronic pyelonephritis. what does it resemble?

A

atrophic tubules w/ eosinophilic proteinaceous material resembling thyroid follicles => waxy casts in urine

71
Q

What are the risk factors of nephrolithiasis? how does it present?

A

risks are high [ ] of solute in urinary filtrate along w/ low urine volume

presents as colicky pain w/ hematuria & unilateral flank tenderness

72
Q

what is the cause & Tx of the MC type of kidney stone?

A

Ca+ oxalate &/or Ca+ phosphate stone =>
usually idiopathic hypercalciuria but other causes must be worked up

Tx is hydrochlorothiazide => Ca+ sparing diuretic

73
Q

What autoimmune dz is assoc w/ Ca+ oxalate &/or Ca+ phosphate stones?

A

Crohn dz

74
Q

What is MCC & Tx of the 2nd most common type of kidney stone?

A

Ammonium Mg+ phosphate stone =>
infection w/ urease-positive organisms (Proteus vulgaris or Klebsiella) causes alkaline urine leading to stone

Tx is surgical removal bc of size & ABx to eradicate the pathogen

75
Q

What 2 types of stones can form stag horn calculi? where do they form? what can they cause?

A

Ammonium Mg+ phosphate & cysteine stones can cause staghorn calculi in the renal calyces=>

nidus for UTI

76
Q

Name some risk factors for the only radiolucent kidney stone. who is it MC seen in?

A

hot, arid climates w/ low urine volume & acidic pH;

MC in pt w/ gout but also in hyperuricemia

77
Q

Who is likely to have hyperuricemia & more uric acid stones besides gout pt? Tx in these pt

A

Dz w/ high nuclear turnover such as leukemia or myeloproliferative d/o

Tx is hydrate & alkalinize the urine (KHCO3); allopurinol can also be given

78
Q

What is a rare cause of nephrolithiasis MC seen in kids? what is it assoc w/?

A

cysteine stone => cystinuria

genetic defect of tubules resulting in decreased reabsorption of cysteine

79
Q

What are MCC of chronic renal failure?

A

DM, HTN, glomerular dz

80
Q

Clinical features of chronic renal failure

A 
uremia; 
HTN (salt & water retention);
hyperkalemia w/ anion gap metabolic acidosis;
anemia;
hypocalcemia;
renal osteodystrophy
81
Q

What is Tx for chronic renal failure?

A

dialysis or renal transplant

82
Q

How will a patient’s kidney on dialysis present grossly? Is any increase risk of dz assoc?

A

cysts develop w/in shrunken end-stage kidneys during dialysis => increase risk for renal cell CA

83
Q

Uremia from chronic renal disease causes what?

A

azotemia results in nausea, anorexia, pericarditis, platelet dysfxn (inh adhesion & aggregation), encephalopathy w/ asterixes, urea crystals deposit in skin

84
Q

Anemia from chronic renal disease is due to what?

A

decreased EPO production by renal peritubular interstitial cells

85
Q

hypocalcemia in chronic renal disease is due to what?

A

decreased alpha-1-hydroxylation of vitamin D by proximal renal tubule cells & hyperphosphatemia

86
Q

Renal osteodystrophy in chronic renal dz is due to what?

A

secondary hyperPTH causing osteitis fibrosis cystica from elevated PTH leading to Ca+ resorption causing “burn out” of bone;
osteomalacia => cannot mineralize bone;
osteoporosis => slow degradation of Ca+

87
Q

What makes up a angiomyolipoma? What is it assoc w/?

A

Hamartoma of blood vessels, smooth muscle & adipose tissue

Tuberous sclerosis

88
Q

Renal cell carcinoma arises from what tissue? what is the triad of Sx?

A

kidney tubules

hematuria, palpable mass, flank pain => all 3 rarely occur together

89
Q

In renal cell CA, what systemic Sx may be present? what can it produce?

A

fever, weight loss, paraneoplastic syndrome

EPO can cause polycythemia;
renin causes HTN;
PTHrP leading to hypercalcemia;
ACTH causing Cushing’s

90
Q

Staging of renal cell CA is based on what?

A

T => size & involvement of renal vein (risk of hematogenous spread to lungs & bone)

N=> spread to retroperitoneal lymph nodes

91
Q

An enlargement of the pampiniform venous plexus in the scrotum is seen on exam due to cancer. What side is it on and why?

A

Left sided varicocele due to involvement of left renal vein by CA blocking drainage of left spermatic vein leading to varicocele

Right spermatic vein drains directly in to IVD

92
Q

How does renal cell CA present grossly & microscopically?

A

gross: yellow mass
micro: clear cytoplasm

93
Q

Renal cell CA Tumors can be hereditary or sporadic but all share what in common? describe the further pathogenesis

A

loss of VHL (3p) tumor suppressor gene leading to increased IGF-1 to promote growth & increased HIF transcription factor causing more VEGF & PDGF to be produced

94
Q

Differentiate sporadic & hereditary renal cell CA

A

sporadic in adult male smokers w/ single tumor in upper pole of kidney

hereditary in younger adults often bilateral w/ FHx of VHL dz => increase risk of hemangioblastoma of cerebellum & renal cell CA

95
Q

Define a Wilms tumor

A

malignant kidney tumor made of blastema (immature kidney mesenchyme), primitive glomeruli & tubules, & stromal cells

MC in 3yr old kids

96
Q

How do Wilms tumors present?

A

large, unilateral flank mass w/ hematuria & HTN (due to renin secretion)

97
Q

In syndromic cases, what mutation is present? differentiate the 2 diseases in which this mutation is present

A

WT1 mutation

WAGR syndrome=> Wilms tumor, Aniridia, Genital abnormalities, mental/motor Retardation

Beckwith-Wiedemann syndrome=> Wilms tumor, neonatal hypoglycemia, organomegaly (including tongue)

98
Q

Define urothelial (transitional cell) CA

A

MC lower urinary tract cancer typically in bladder but can also arise from renal pelvis, ureter, or urethra

99
Q

Give the major risks of urothelial CA

A

1) cigarette smoke;

naphthylamine (smoke);
azo dyes (hair dressers);
cyclophosphamide or phenacetin use

100
Q

How does urothelial CA present & how is it treated?

A

older adults w/ painless hematuria

Rx only due to “field defect” from multifocal & high recurrence

101
Q

Describe the 2 paths of urothelial CA pathways

A

Flat => starts high grade w/ EARLY p53 mutations & invades early

Papillary => starts low grade w/ papillary growth (finger-like projections) then progresses to high grade before invading => may have LATE p53 mutations

102
Q

What must occur for squamous cell CA to be present? What are the MC risk assoc?

A

background of squamous metaplasia due to normal bladder not having squamous epithelium

chronic inflammation is MC risk factor =>
chronic cystitis in older woman;
Schistosoma hematobium infxn in young, Egyptian male;
long standing nephrolithiasis

103
Q

Define adenocarcinoma of lower urinary tract

A

malignant proliferation of glands involving bladder

104
Q

Describe how adenocarcinoma arises

A

urachal remnant => tumor develops at dome of bladder;
cystitis glandularis forming columnar metaplasia;
exstrophy (congenital failure to form caudal portion of anterior abdominal & bladder walls)

105
Q

What is the glomerular filtration barrier composed of?

A

fenestrated capillary endothelium => size barrier;

fused basement membrane w/ heparan sulfate => negative charge barrier

epithelial layer consisting of podocyte foot processes

106
Q

What is the urine crystal in the MC kidney stone?

A

envelope or dumbbell shaped

107
Q

What is the pH of the urine in Ammonium Mg+ phosphate kidney stone? what does the urine crystal look like?

A

high pH

coffin lid

108
Q

Differentiate the different types of Calcium kidney stones based on pH

A

high pH => calcium phosphate

low pH => Calcium oxalate

109
Q

What is the pH of the urine in a person producing uric acid stone? what does the stone look like?

A

low pH

Rhomboid or rosettes

110
Q

What is the pH of the urine in a person producing cystine stone? what does the stone look like?

A

low pH

Hexagonal

111
Q

Define hydronephrosis. What are some of the causes of the pathology?

A

distention/dilation of renal pelvis & calyces causes by
UT obstruction (stones, BPH, cervical cancer, injury to ureter),
retroperitoneal fibrosis (post surg),
vesicoureteral reflux

112
Q

Where does dilation take place in hydronephrosis? what does it ultimately lead to?

A

Dilation occurs proximal to site of pathology BUT only impairs renal fxn if bilateral or only one kidney

leads to compression atrophy of renal cortex & medulla

113
Q

Define renal oncocytoma. How does it present?

A

benign epithelial cell tumor w/ large eosinophilic cells w/ abundant mitochondria w/o perinuclear clearing

Painless hematuria, flank pain, abdominal mass

Tx w/ nephrectomy

114
Q

Acute infectious hemorrhagic cystitis is caused by what?

A

adenovirus (nonenveloped, dsDNA)

115
Q

Describe the 3 stages of acute tubular necrosis

A

1) inciting event
2) Maintenance => oliguric lasting 1-3wks w/ risk of HYPERkalemia, metabolic acidosis
3) Recovery phase => polyuric, BUN & Cr fall w/ risk of HYPOkalemia

FA: random (15 decks)

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