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Renal 2 > Path - Tubulointerstitial Disease 2 > Flashcards

Path - Tubulointerstitial Disease 2 Flashcards

1
Q

Acute renal dysfunction can be divided into what 3 categories?

A

Prerenal, intrinsic renal, post renal

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2
Q

Intrinsic acute kidney injury can be divided into what 3 subsets?

A

tubulointerstitial, glomerular, vasculature

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3
Q

Ways to identify AKI based on creatinine and/or urine volume status?

A
  • Increase in serum creatinine of at least 0.3 mg/dL over a 48 hour period and/or
  • rise in serum creatinine of ≥ 1.5x the baseline value within the 7 previous days
  • a urine volume ≤ 0.5 mL/kg per hour for 6 hours
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4
Q

Compare FENa in Prerenal AKI vs ATN

A

Prerenal AKI FENa <1%

ATN FENa > 2%

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5
Q

Compare urine Na+ concentration in prerenal AKI vs ATN?

A

Prerenal AKI <20 mEq/L

ATN > 40 mEq/L

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6
Q

Compare urine sp. gr in prerenal AKI vs ATN

A

Prerenal AKI >1.018 (high specific gravity)

ATN ~ 1.010 (isothenuric = inability to concentrate or dilute urine)

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7
Q

Compare urine osmolarity in prerenal AKI vs ATN

A

prerenal uOsm > 500 mOsm/kg

ATN ~300 (inability to concentrate or dilute urine)

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8
Q

Compare BUN/Cr ratio in prerenal AKI vs ATN

A

Prerenal AKI BUN/Cr >20

ATN <10-15 (cant reabsorb urea due to tubular injury)

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9
Q

Compare urine sediment in prerenal AKI vs ATN

A

prerenal AKI = hyaline casts

ATN = muddy brown granular casts

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10
Q

General concepts. What evidence points to a proximal tubular disorder?

A
  • Glucosuria with normal serum glucose
  • metabolic acidosis
  • K+ wasting
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11
Q

General concepts. What most likely can cause proximal tubular injury?

A

Drugs and heavy metals

Ex. aminoglycosides, cisplatin, Lead, cadmium

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12
Q

General concepts. What is most likely to cause interstitial injury? This causes what to occur?

A

Drugs, causing inflammation

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13
Q

General concept. What agents are most likely to cause distal tubular injury?

A

Amphotericin B, calcineurin inhibitors, lithium

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14
Q

General concept. What are some evidence of a distal tubular injury?

A
  • hyperkalemia
  • metabolic acidosis
  • concentrating defects
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15
Q

Do drugs commonly cause glomerular damage?

A

No, usually will be interstitial or tubular injury

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16
Q

Is drug indicued acute interstitial nephritis a dose dependent response?

A

No, it is idiosyncratic

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17
Q

General concept. If tubular cells are injured but glomerulus is unaffected, why does GFR even drop?

A

Tubular cell injury causes increased hydrostatic pressure in the tubule, which will increase filtration resistance

Remember, in homeostais, need intact vasculature, glomerulus, and tubular cells

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18
Q

Typical clinical presentation of acute interstitial nephritis?

A
  • Patient develops symptoms within 3 weeks of starting the new drug
  • sudden onset of renal insufficiency
  • Constitutional symptoms (fever, rash, flank pain, hematuria, sterile pyruia, eosinophiluria
  • Minimal proteinuria (due to intact glomerulus)
  • hemolysis, hepatitis (may also be present)
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19
Q

List some general constitutional symptoms of acute interstitial nephritis?

A

Think constitutional. Fever, rash, flank pain, hematuria, sterile pyuria (meaning no bacterial infection)

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20
Q

NSAID’s and AIN. What distinguishing feature do NSAIDs have that no other drug has?

A

NSAIDS can occasionally cause minimal change apperance (foot proccess effacement, nephrotic range proteinuria) in addition to other common symptoms in drug induced AIN

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21
Q

Mechanism of aminoglycoside nephrotoxicity? How do you combat this mechanism?

A

Aminoglycosides enter the tubular lumen by glomerular filtration. Proximal tubular cells will absorb large amounts of it, causing necrosis of these cells

  • Can overcome it by giving 1x high dose each day, you saturate the tubular cells, preventing any further uptake, but still have the same clinical effect that you want as if you were giving multiple times a day
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22
Q

What clinical manifestations are associated with aminoglycoside nephrotoxicity?

A

Progressive increase in serum creatinine

Renal K+ and Mg2+ wasting

Renal glucosuria

23
Q

In addition to aminoglycosides primarily affecting proximal tubule cells, where else can they cause nephrotoxicty. What disorder does this mimic?

A

aminoglycosides can affect thick ascending limb, resembling Barter’s syndrome

24
Q

Besides aminoglycosides, what else is very common in causing nephrotoxicity?

A

iodinated IV contrast

25
Q

Besides being tubular toxic, what other effect does IV contrast have in the kidney?

A

Can cause prolonged period of renal artery vasoconstriction

26
Q

IV contrast nephropathy is most common in what subset of patients?

A

Those with chronic kidney disease and/or diabetes mellitus. If you have both, you are at an even higher risk

27
Q

4 main causes of papillary necrosis?

A
  1. diabetes mellitus
  2. analgesic nephropathy
  3. sickle cell disease
  4. obstruction
28
Q

Is analgesic abuse nephropathy considered rapid or insiduous?

A

Slow progressive impairment of renal function

29
Q

Tubular dysfunction in analgesic nephropathy results in what clinical findings?

A

hyperkalemia, hyperchloremic renal tubular acidosis, nephrogenic DI, impaired sodium reabsorption

30
Q

Some patients with analgesic abuse nephropathy can progress to what type of cancer?

A

uro-epithelial cancer

31
Q

Aristolochic nephropathy is due to what?

A

aristolochic acid

32
Q

Aristolochic nephropathy was common where?

A
  1. Some herbal therapy from china that somehow had aristolochic acid in it
  2. Balkan’s
33
Q

Describe the pathology of an end stage interstial disease?

A

Interstitial fibrosis and tubular atrophy

- know these buzzwords to hint that patient has end stage renal disease

34
Q

Any chronic disease is associated with what type of casts?

A

Waxy casts. If you see waxy casts in U/A, tells you condition is chronic

35
Q

If patient that was exposed to aristolochic acid now develops hematuria (which wasn’t present before), what should you be thinking?

A

They have possibly developed urothelial cancer

36
Q

What 3 disorders are associated with uric acid?

A

Acute uric acid nephropathy, Chronic urate nephropathy, Uric acid nephrolithiasis

37
Q

Acute uric acid nephropathy is due to? How do you prevent this?

A

AKI caused by overproduction of uric acid in patients with rapidly progressing tumor lysis.

Give xanthine oxidase inhibitor (allopurinol) or uricase

38
Q

Chronic urate nephropathy may show what histologically?

A

birefringent needle like crystals either in tubular lumen or in the interstitum

39
Q

Uric acid nephrolithiasis. Describe xray findings? Describe CT findings?

A

Xray wont show it

CT will due to hyperdense region of uric acid stone

40
Q

What is the earliest functional defect in hypercalcemic nephropathy?

A

Inability to concentrate the urine

41
Q

List mechanisms by which hypercalcemia can injure renal tubule?

A
  1. Can cause vasoconstriction within the kidney
  2. Can lead to calcium oxolate crystallization within the tubular cell that can then migrate into the interstititum.

These ultimately can lead to interstitial fibrosis and atrophy (end renal disease)

42
Q

Describe how kidney handles hypercalcemia? What calcium sensor regulates this? Where is it located?

A

If you are hypercalcemic, you want kidneys to eliminate calcium. There is a calcium sensor/transporter on basolateral surface of thick ascending limb. When this sensor is activated, it downregulates Na/K/2Cl- transporter, making the gradient less favorable to reabsorb calcium, leading to increased hypercalciuria. This increases risk of kidney stones, therefore, there is a calcium sensor on apical side of collecting duct, will shut down AQ2, preventing H20 reabsorption, diluting the calcium and preventing risk of calcium stones.

43
Q

Acute phosphate nephropathy was commonly due to? Describe mechanism of this?

A

High doses of oral phosphate solutioins in preparation for colonoscopy.

Increased phosphate load, causing marked precipation of calcium phosphate. This typically presented as renal insufficiency several weeks after the exposure.

These type of colonoscopy preps are now off the market

44
Q

What is the most common genetic kidney disease?

A

Autosomal dominant polycystic kidney disease

45
Q

What vascular syndrome is associated with AD polycystic kidney disease?

A

intra-cranial aneurysms

46
Q

Earliest clinical finding in patients with AD polycystic kidney disease?

A

HTN

47
Q

Polycystin 1 is found on what chromosome?

A

Chromosome 16

48
Q

Polycystin 2 is found on what chromosome?

A

Chromosome 4

49
Q

Multiple myeloma results in increased filtration of what?

A

Light chains

50
Q

2 main pathogenic mechanisms of multiple myeloma? Where does each occur?

A

Direct tubular toxicity by light chains, occuring in the proximal tubule = fanconi syndrome

Intratubular cast formation, occuring in thick ascending limb = myeloma cast nephropathy

51
Q

What is the most common type of nephropathy associated with multiple myeloma?

A

Myeloma cast nephropathy

52
Q

In myeloma cast nephropathy, light chains bind with what?

A

Light chains (aka bence proteins) that have been filtered with bind with tamm-horsfall proteins, forming myeloma casts. These can lead to obstruction.

53
Q

What contributing factors increase risk of renal failure due to multiple myeloma?

A

High rate of light chain excretion (tumor load)

concurrent volume depletion

54
Q

Multiple myeloma causes what to occur with glomerulus?

A

Nothing, there is minimal glomerular abnormality, therefore very little if any proteinuria

Renal 2 (11 decks)

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