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Renal Week 2 > Tubulointerstitial Disease II > Flashcards

Tubulointerstitial Disease II Flashcards

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1
Q

What is AKI (ARF) defined as?

A

rise in Pcr of at least 0.3mg/dL over a 48 hr period and/or

-rise in Pcr of at least 1.5 baseline within the 7 previous days

and a urine volume less than 0.5ml/kg per hour for 6 hours

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2
Q

Acute tubular necrosis is usually due to what?

A

shock (profound hypotension and ischemia)

can be septic shock where you are hypotensive but at the same time you get intense renal vasoconstriction

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3
Q

What is the difference between fraction excretion of Na in pre-renal vs acute tubular necrosis?

A

pre-renal: less than 1%
acute tubular necrosis: 2+%

in ATN, the tubules aren’t functioning so it makes sense that Na excretion would increase

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4
Q

What is the difference between urine SG in pre-renal vs acute tubular necrosis?

A

SG in ATN would be the same are plasma (1.010) because the kidney has lost the ability to concentrate or dilute the urine

while in pre-renal it is greater than 1.010

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5
Q

What is the difference between Usom in pre-renal vs acute tubular necrosis?

A

pre-renal: 500+

ATN: 300 (same as plasma- cant dilute or concentrate)

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6
Q

What is the difference between plasma BUN/creatinine ratio in pre-renal vs acute tubular necrosis?

A

pre-renal: 20+

ATN: less than 10-15

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7
Q

What is the difference between Una in pre-renal vs acute tubular necrosis?

A

pre-renal: less than 20

ATN: 40+

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8
Q

When are hyaline casts seen?

A

physiologic in highly concentrated urine (no injury needed). Granular casts do need some kind of pathology

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9
Q

What things cause acute TIN of the proximal tubules?

A

antibiotics (aminoglycosides)
MM (light chains)
lymphoproliferative disorders

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10
Q

What things cause chronic TIN of the proximal tubules?

A

heavy metals

cystinosis

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11
Q

What things would suggest proximal tubule dysfunction?

A

things that are normally reabsorbed in the PT are found in the urine:

  • glucose (with normal Pglu- not diabetes)
  • LMW proteins (B2 microglobulins)
  • uric acids, phosphates (so low blood levels)
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12
Q

What things cause acute TIN of the distal tubules?

A
  • antibiotics
  • analgesics
  • NSAIDS
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13
Q

What things cause chronic TIN of the distal tubules?

A

-hypercalcemia
-obstructive uropathy
amyloidosis
-sickle hemoglobinopathy

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14
Q

What things would suggest distal tubule dysfunction?

A
  • metabolic acidosis
  • hyperkalemia
  • low Pna
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15
Q

What is acute interstitial nephritis?

A

immune mediated hypersensitivity reaction to an antigen (drug or infection)

not dose dependent- more unpredictable idiosyncratic (does tend to recur with re-exposure)

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16
Q

What would be a clinical sign of damage to the medulla?

A

impaired urine concentrating ability (decreased Na reabsorption)

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17
Q

What are some antigens that have been known to stimulate acute interstitial nephritis (AIN)?

A
  • altered tubular BM, secreted tubular proteins, or non-renal proteins (immune complexes)
  • molecular mimicry by bacterial infection
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18
Q

What cells mediate AIN?

A

T cells (cell mediated) for the most part and antibodies can play a part in methicillin induced AIN

often see eosinophils in the urine here

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19
Q

What does the massive inflammation caused by AIN cause?

A

activates fibroblasts and matrix proliferation mediated by TGF-b release that causing chronic interstitial scarring

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20
Q

How does AIN present?

A

Usually within 3 weeks of starting a new drug you will see sudden onset of renal insufficiency that is accompanied by fever, rash, flank pain from swollen kidneys, and little hematuria

GFR will be impacted as well

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21
Q

What is the hallmark of AIN on urinalysis?

A

sterile pyuria (mostly neutrophils) and eosinophiluria

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22
Q

Is there much proteinuria with AIN?

A

No, that would be more suggestive of a glomerular disease

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23
Q

What are the most common drugs to induce AIN?

A

-synthetic penicillins (methicillin, ampicillin)
-rifampin, ciprofloxacin,
diuretics (thiazides)
-NSAIDs
-Proton pump inhibitors, Allopurinol, cimetidine

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24
Q

Note: NUMERICALLY (aka by number of instances) PPIs are the most common just because of how often they are used being OTC. But this is a fairly uncommon event

A

Note: NUMERICALLY (aka by number of instances) PPIs are the most common just because of how often they are used being OTC. But this is a fairly uncommon event

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25
What is unique about the AIN induced by NSAIDs?
People with NSAID induced AIN also see changes in their BM and will get nephrotic range proteinuria (hematuria rare) Can cause chronic interstitial scarring with prolonged use
26
How can NSAIDs cause renal failure?
they prevent the formation of prostaglandins that help dilate the afferent arterioles to maintain GFR in volume depletion
27
What are some bacterial causes of AIN?
- Corynebacterium diptheriae - Legionella - E. Coli
28
What are some viral causes of AIN?
- CMV - EBV - Hantavirus basically all the big ones
29
What are some immune causes of AIN?
- acute rejection of renal transplant - SLE - sarcoidosis
30
How are aminoglycosides nephrotoxic?
the drug is + charged and freely filtered and is reabsorbed by megalin in the PT via endocytosis and there is can concentrate and lead to cell damage and necrosis and loss of function no inflammation here (direct)
31
So what are some signs of amino glycoside nephrotoxicity?
Manifestations of PT dysfunction- renal glycosuria, increase serum creatinine (lowered GFR) can also harm distal- K+ and Mg++ wasting,
32
T or F. Aminoglycoside nephrotoxicity is a non-inflammatory process
T. The urine will show minimal proteinuria (not glomerular), not many cells, but granular casts will be present
33
Is amino glycoside nephrotoxicity reversible?
Yes, it is very dose-dependent and can be reversed when the drug is stopped (dose and use dependent)
34
How are IV/arterial contrasts nephrotoxic (Note: PO contrasts are not nephrotoxic)?
- vasoconstricts and makes the medulla, which doesn't receive much blood flow anyways, susceptible to ischemia and - the contrast itself is directly nephrotoxic Rare if individual is healthy with normal GFR
35
Response of kidney to IV/arterial contrasts
short term (30 min) increase in RBF followed by more prolonged period of renal artery vasoconstriction and reduced RBF and shunting of medullary blood flow to the cortical segments
36
Timeframe for increases in Pcr with contrasts?
increases within 48-72 hrs, peaks at 3-5 days, and returns within 7-10 days
37
When is nephrotoxicity via contrast media a problem?
only in patients with compromised renal function and in diabetics
38
T or F. IV contrast agents tend to produce a non-oliguric AKI/ARF
T. And urinalysis tends to be normal because it is a non-inflammatory process (like aminoglycosides)
39
What things can cause papillary necrosis?
Sickle cell (even with trait sometimes) Obstructive uropathy Diabetes mellitus Analgesics SODA
40
Analgesic abuse nephropathy is associated with what? 2 things
phenacetin- drugs accumulate and are highly concentrated in the renal medullary interstitium and Uri-Epithelia cancer
41
How does analgesic abuse nephropathy present?
slow progressive impairment of renal function with signs of tubular dysfunction (more hyperkalemia and normal anion gap metabolic acidosis) cant concentrate urine
42
Atristolochic nephropathy
a chronic direct interstitial nephritis that is mostly isolated to the cortex and causes extensive interstitial fibrosis and tubular atrophy caused by atristolochic acid
43
Is Atristolochic nephropathy inflammatory in nature?
No, cellular infiltration of the interstitium is rare
44
Are the glomeruli affected in Atristolochic nephropathy?
No, they are spared and immune deposits are not observed These findings suggest that the primary lesions may be centered in the vessel walls, thereby leading to ischemia and interstitial fibrosis Mechanism: The drug forms covalent adducts with DNA.
45
How does Atristolochic nephropathy present?
- slowly progressive renal insufficiency - unremarkable urine sediment - proteinuria low (less than 1g/d) because it is tubular in nature
46
What cancers is Atristolochic nephropathy associated with?
cellular atypia and urothelial (transitional cell) carcinoma of the renal pelvis, ureter, and bladder
47
Ingestion of aristolochic acid has also been identified as the cause of ____ _______.
Balkan nephropathy
48
How does Balkan nephropathy present?
- Slowly progressive renal insufficiency - Urine sediment usually unremarkable Proteinuria usually low
49
What are the three renal syndromes caused/related to urate?
-acute uric acid nephropathy (tumor lysis syndrome) - chronic urate nephropathy - uric acid nephrolithiasis (kidney stones)
50
What causes TLS?
Acute kidney injury caused by overproduction of uric acid in patients with lymphoma, leukemia, myeloproliferative diseases, and tumor cell lysis syndrome after chemotherapy.
51
What happens to all of the uric acid produced by TLS or tumors?
They enter the tubules and precipitate in the DT and act like an obstruction
52
How is TLS blocked?
fluids to promote increased flow and xanthine oxidase inhibitors such as Allopurinol or Rasburicase to degrade uric acid
53
What pathologies promote hypercalcemia?
- hyperPTH - MM - vitamin D overload
54
What does hypercalcemia do to kidneys?
deposition of calcium in the interstitial area to generate inflammation that lead to tubular scarring
55
What is the early kidney sign of hypercalcemia?
impaired ability to concentrate urine
56
The earliest damage caused by hypercalcemia is what?
is to the tubular epithelial cells in the form of mitochondrial distortion and other signs of cell injury. Subsequently, calcium deposits appear within the mitochondria, cytoplasm, and basement membrane. Calcified cellular debris may obstruct tubular lumens and cause obstructive atrophy of nephrons and secondary interstitial fibrosis and inflammation.
57
How does hypercalcemia progress in the kidneys?
With further damage, a slowly progressive renal insufficiency develops.
58
When can acute phosphate nephropathy occur?
Extensive accumulations of calcium phosphate crystals in tubules can occur in patients consuming high doses of oral phosphate solutions in preparation for colonoscopy. Only bad with preexisting kidney disease Patients typically only partially recover renal function. These colon preps are now off the market
59
Why do the calcium phosphate crystals precipitate in these states?
These patients are not hypercalcemic, but excess phosphate load, perhaps complicated by dehydration, causes marked precipitation of calcium phosphate, typically presenting as renal insufficiency several weeks after the exposure.
60
What is the MOI of PKD?
can be AD or AR AD PCKD is the most common genetic kidney disease, accounts for 5-10 % of ESRD patients *Very high penetrance*, leads to progressive CKD during adulthood, usually at 40+ yo
61
What is PKD associated with?
intra-cranial aneurysms Not associated with higher risk of renal cancer
62
What can happen to the cysts in PKD?
Cysts can hemmorrhage (gross hematuria and flank pain) and can become infected cysts can form in other organs as well
63
What mutations are associated with PKD? Where are these in the genome?
Mutation of polycystin 1 or polycystin 2 (part of cilia) PKD1 on chromosome 16 (account for 80-90% of patients) PKD2 on chromosome 4
64
Signs of PKD?
early satiety. Use ultrasound to ID
65
PKD Cysts develop early, age 20 -30 yr of age Hypertension is common Progressive increase number and size of cysts over time Kidney size and volume steadily increasing due to cysts
Normal anatomy becomes distorted Leading to CKD and ultimately to ESRD Bland urinalysis (because not glomerular in nature), unless having hematuria Minimal proteinuria (usually)
66
How well do PKD respond to renal transplantation?
Extremely well. Does not recur in kidney transplants
67
How does MM affect the kidneys?
B2 micro globulin light chains are filtered into the kidneys at a rate too high to reabsorb and eventually will cause damage to the PT causing a Falconi like presentation

Renal Week 2 (13 decks)

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