Renal Flashcards
(115 cards)
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
2
Q
How does the ARPKD present?
A
baby w/ portal HTN due to congenital hepatic fibrosis
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
4
Q
What is the timeline & hallmark of acute renal failure?
A
azotemia (high BUN & Cr) w/in days often w/ oliguria
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
6
Q
What is cause of post renal azotemia?
A
obstruction of urinary tract downstream decreasing GFR (backup), azotemia & oliguria
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
8
Q
what is the MCC of acute renal failure?
A
intrarenal azotemia => injury & necrosis of tubular epithelial cells
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
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
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
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)
13
Q
How will you know if someone ingested ethylene glycol?
A
oxalate crystals in urine
14
Q
What are ways to avoid tumor lysis syndrome causing ATN?
A
hydration & allopurinol prior to CTX
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
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
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
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
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
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
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
22
Q
What cancer is minimal change disease associated with? why?
A
Hodgkin lymphoma due to massive increase of cytokines from RS cells
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
24
Q
What is the MCC of nephrotic syndrome in Hispanics & AA?
A
Focal segmental glomerulosclerosis (FSGS)
25
What is FSGS associated with?
HIV; heroin use; sickle cell disease
26
How does FSGS appear on H&E? EM? IF?
HE: focal & segmental pink sclerosis
EM: effacement of foot processes
IF: no IC deposits = neg IF
27
What is the response to Tx in FSGS?
poor response to steroids leading to chronic renal failure
28
What is the MCC of nephrotic syndrome in caucasian adults?
membranous nephropathy
29
What is membranous nephropathy assoc w/?
HBV, HCV;
solid tumors;
SLE (usually diffuse proliferative GN);
Rx (NSAIDs & penicillamine)
30
How does membranous nephropathy appear on H&E? EM? IF?
HE: thick glomerular BM
EM: subepithelial deposits w/ 'Spike & dome" appearance
IF: IC deposits so granular IF
31
What is the response to Tx of membranous nephropathy?
poor response to steroids causing chronic renal failure
32
How does membranoproliferative glomerulonephritis present on H&E? EM? IF?
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
33
What is the response to Tx of membranoproliferative GN?
poor response to steroids leads to chronic renal failure
34
Describe the pathophys of renal disease in diabetes mellitus
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)
35
What is the response to Tx of diabetic nephrotic syndrome? why?
ACE like hyaline arteriosclerosis causes efferent constriction so ACE inhibitors slow dz progression
36
How does amyloidosis affect the kidney? How can it be proven to be the cause?
MC systemic organ in systemic amyloidosis=>
amyloid deposits in mesangium causing nephrotic syndrome
Apple-green birefringence under polarized light after Congo red stain
37
If minimal change disease does not respond to steroids, what is the progression?
FSGS
38
Based on the location of any IC deposition, differentiate the the types of nephrotic syndrome
Membranous = sub epithelial deposits (S&D)
Type I MPGN = subendothelial
Type II MPGN = dense deposits in intramembranous portion of glomerulus
39
Type I MPGN is assoc with what?
HBV & HCV
40
Differentiate how HBV & HCV can cause nephrotic syndrome
Membranous nephropathy has sub epithelial deposits w/ spike & dome
type I MPGN has subendothelial deposits
41
Type II MPGN is assoc w/ what? Describe how it gets its appearance on EM
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
42
Define nephritic syndrome
```
glomerular inflammation & bleeding =>
limited proteinuria (<3.5g/day);
oliguria & azotemia;
salt retention w/ periorbital edema progressing to HTN;
RBC casts & dysmorphic RBC in urine
```
43
If nephritic syndrome is suspected, how can it be confirmed?
Bx showing hyper cellular & inflamed glomeruli
44
What causes the damage in nephritic syndrome?
IC deposition activates complement leading to C5a attracting neutrophils which cause the damage
45
Differentiate the 2 types of nephritic syndrome that occurs after infections
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
46
What is the virulence factor that must be present in organism to cause PSGN?
nephritogenic strains must carry M protein virulence factor
47
When & how will patient w/ PSGN present?
2-3wks after infxn w/ hematuria (cola colored), oliguria, HTN & periorbital edema
usually kids but can be in adults
48
What is the appearance of PSGN on HE? EM? IF?
HE: hypercellular, inflamed glomeruli
EM: subepithelial humps
IF: granular = IC deposits
49
What is the Tx for PSGN?
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
What is the timeline for RPGN?
nephritic syndrome to renal failure in wks to months
51
How does RPGN appear on HE? IF?
HE: crescents in Bowman space
| IF is variable depending on underlying cause
52
What does a linear pattern on IF assoc w/ RPGN mean? How will it present? why? who is most likely to have this dz?
Goodpasture syndrome => anti-BM Ab
Ab against collagen in glomerular (hematuria) & alveolar (hemoptysis) BM
classically is young, adult males
53
What does a granular pattern on IF in presentation of RPGN?
PSGN or diffuse proliferative GN
54
What is significant about diffuse proliferative GN?
antigen-Ab complex deposition usually sub endothelial
MC type of renal disease in SLE
55
differentiate the types of renal dz seen in SLE. What is significant about renal dz in SLE?
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
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?
C-ANCA => Wegener granulomatosis
P-ANCA => microscopic polyangiitis & Churg Strauss
57
What differentiates the P-ANCA assoc nephritic syndromes?
Churg Strauss has 3 things:
Granulomatous inflammation;
eosinophilia;
asthma
58
What is the MC nephropathy worldwide? present on IF? profession
IgA nephropathy
IgA IC deposits in mesangium of glomeruli
may slowly progress to renal failure
59
How does the IgA nephropathy present typically?
kid w/ episodic gross or microscopic hematuria w/ RBC casts following mucosal infection (gastroenteritis) causing IgA to increase then deposit in mesangium
60
What is an inherited nephritic syndrome? Where is the defect? how does it present?
XLR defect in type IV collagen causing thinning & splitting of glomerular BM
presents w/ isolated hematuria, sensory hearing loss, ocular disturbances
61
How does cystitis present?
dysuria, urinary freq, urgency, suprapubic pain
NO SYSTEMIC SIGNS
62
What are the lab findings in cystitis? what is the gold standard of Dx of cystitis?
urinalysis: cloudy urine > 10WBC/hpf
dipstick: (+) leukocyte esterase (pyruria) & nitrites (bacteria convert nitrates to nitrites)
GOLD STANDARD=> culture: >100k cfu
63
Name the 5 MCC of cystitis
```
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
If pt presents w/ cystitis Sx & ammonia scented urine, what is the cause?
Proteus mirabilis => alkaline urine w/ ammonia scent
65
If urinalysis is done w/ urethritis Sx but urine culture is negative, what is most likely cause? what is the dominating sign of urethritis?
Dysuria is dominant sign of urethritis => sterile pyruria due to Chlamydia trachomatis or N. gonorrhoeae
66
Patient w/ fever, flank pain, WBC casts & leukocytosis along with cystitis Sx has what? what are the MCC?
pyelonephritis from ascending infection from =>
E. coli (90%)
Klebsiella species
Enterococcus faecalis
67
Why does pyelonephritis cause flank pain?
inflammation of the capsule of the kidney
68
Define chronic pyelonephritis. What is common causes?
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
Chronic pyelonephritis assoc w/ vesicoureteral reflux leads to what w/in the kidney?
cortical scarring w/ blunted calyces;
| scarring at both poles is characteristic
70
Describe the H&E stain of chronic pyelonephritis. what does it resemble?
atrophic tubules w/ eosinophilic proteinaceous material resembling thyroid follicles => waxy casts in urine
71
What are the risk factors of nephrolithiasis? how does it present?
risks are high [ ] of solute in urinary filtrate along w/ low urine volume
presents as colicky pain w/ hematuria & unilateral flank tenderness
72
what is the cause & Tx of the MC type of kidney stone?
Ca+ oxalate &/or Ca+ phosphate stone =>
usually idiopathic hypercalciuria but other causes must be worked up
Tx is hydrochlorothiazide => Ca+ sparing diuretic
73
What autoimmune dz is assoc w/ Ca+ oxalate &/or Ca+ phosphate stones?
Crohn dz
74
What is MCC & Tx of the 2nd most common type of kidney stone?
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
What 2 types of stones can form stag horn calculi? where do they form? what can they cause?
Ammonium Mg+ phosphate & cysteine stones can cause staghorn calculi in the renal calyces=>
nidus for UTI
76
Name some risk factors for the only radiolucent kidney stone. who is it MC seen in?
hot, arid climates w/ low urine volume & acidic pH;
| MC in pt w/ gout but also in hyperuricemia
77
Who is likely to have hyperuricemia & more uric acid stones besides gout pt? Tx in these pt
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
What is a rare cause of nephrolithiasis MC seen in kids? what is it assoc w/?
cysteine stone => cystinuria
genetic defect of tubules resulting in decreased reabsorption of cysteine
79
What are MCC of chronic renal failure?
DM, HTN, glomerular dz
80
Clinical features of chronic renal failure
```
uremia;
HTN (salt & water retention);
hyperkalemia w/ anion gap metabolic acidosis;
anemia;
hypocalcemia;
renal osteodystrophy
```
81
What is Tx for chronic renal failure?
dialysis or renal transplant
82
How will a patient's kidney on dialysis present grossly? Is any increase risk of dz assoc?
cysts develop w/in shrunken end-stage kidneys during dialysis => increase risk for renal cell CA
83
Uremia from chronic renal disease causes what?
azotemia results in nausea, anorexia, pericarditis, platelet dysfxn (inh adhesion & aggregation), encephalopathy w/ asterixes, urea crystals deposit in skin
84
Anemia from chronic renal disease is due to what?
decreased EPO production by renal peritubular interstitial cells
85
hypocalcemia in chronic renal disease is due to what?
decreased alpha-1-hydroxylation of vitamin D by proximal renal tubule cells & hyperphosphatemia
86
Renal osteodystrophy in chronic renal dz is due to what?
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
What makes up a angiomyolipoma? What is it assoc w/?
Hamartoma of blood vessels, smooth muscle & adipose tissue
Tuberous sclerosis
88
Renal cell carcinoma arises from what tissue? what is the triad of Sx?
kidney tubules
hematuria, palpable mass, flank pain => all 3 rarely occur together
89
In renal cell CA, what systemic Sx may be present? what can it produce?
fever, weight loss, paraneoplastic syndrome
EPO can cause polycythemia;
renin causes HTN;
PTHrP leading to hypercalcemia;
ACTH causing Cushing's
90
Staging of renal cell CA is based on what?
T => size & involvement of renal vein (risk of hematogenous spread to lungs & bone)
N=> spread to retroperitoneal lymph nodes
91
An enlargement of the pampiniform venous plexus in the scrotum is seen on exam due to cancer. What side is it on and why?
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
How does renal cell CA present grossly & microscopically?
gross: yellow mass
micro: clear cytoplasm
93
Renal cell CA Tumors can be hereditary or sporadic but all share what in common? describe the further pathogenesis
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
Differentiate sporadic & hereditary renal cell CA
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
Define a Wilms tumor
malignant kidney tumor made of blastema (immature kidney mesenchyme), primitive glomeruli & tubules, & stromal cells
MC in 3yr old kids
96
How do Wilms tumors present?
large, unilateral flank mass w/ hematuria & HTN (due to renin secretion)
97
In syndromic cases, what mutation is present? differentiate the 2 diseases in which this mutation is present
WT1 mutation
WAGR syndrome=> Wilms tumor, Aniridia, Genital abnormalities, mental/motor Retardation
Beckwith-Wiedemann syndrome=> Wilms tumor, neonatal hypoglycemia, organomegaly (including tongue)
98
Define urothelial (transitional cell) CA
MC lower urinary tract cancer typically in bladder but can also arise from renal pelvis, ureter, or urethra
99
Give the major risks of urothelial CA
1) cigarette smoke;
naphthylamine (smoke);
azo dyes (hair dressers);
cyclophosphamide or phenacetin use
100
How does urothelial CA present & how is it treated?
older adults w/ painless hematuria
Rx only due to "field defect" from multifocal & high recurrence
101
Describe the 2 paths of urothelial CA pathways
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
What must occur for squamous cell CA to be present? What are the MC risk assoc?
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
Define adenocarcinoma of lower urinary tract
malignant proliferation of glands involving bladder
104
Describe how adenocarcinoma arises
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
What is the glomerular filtration barrier composed of?
fenestrated capillary endothelium => size barrier;
fused basement membrane w/ heparan sulfate => negative charge barrier
epithelial layer consisting of podocyte foot processes
106
What is the urine crystal in the MC kidney stone?
envelope or dumbbell shaped
107
What is the pH of the urine in Ammonium Mg+ phosphate kidney stone? what does the urine crystal look like?
high pH
coffin lid
108
Differentiate the different types of Calcium kidney stones based on pH
high pH => calcium phosphate
low pH => Calcium oxalate
109
What is the pH of the urine in a person producing uric acid stone? what does the stone look like?
low pH
Rhomboid or rosettes
110
What is the pH of the urine in a person producing cystine stone? what does the stone look like?
low pH
Hexagonal
111
Define hydronephrosis. What are some of the causes of the pathology?
distention/dilation of renal pelvis & calyces causes by
UT obstruction (stones, BPH, cervical cancer, injury to ureter),
retroperitoneal fibrosis (post surg),
vesicoureteral reflux
112
Where does dilation take place in hydronephrosis? what does it ultimately lead to?
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
Define renal oncocytoma. How does it present?
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
Acute infectious hemorrhagic cystitis is caused by what?
adenovirus (nonenveloped, dsDNA)
115
Describe the 3 stages of acute tubular necrosis
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
