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Renal > TubuloInterstitial Disease and PCKD > Flashcards

TubuloInterstitial Disease and PCKD Flashcards

1
Q

How does the protein loss associated with tubulointerstitial disease differ from the nephrotic protein loss?

A

TIN predominantly loses LMW proteins like B2-microglobulin instead of albumin

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2
Q

TIN can have isolated tubular defects and urinary concentrating defects. What would be the clinical presentations of those?

A 
Tubular defects:
glycosuria
proteinuria
aminoaciduria
K wasting OR retention
RTA

Urinary concentrating defects:
polyuria
nocturia

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3
Q

What is the effect of TIN on urinary Na, urine concentration and body volume?

A

It enhances Na wasting, the urine is dilute and the body volume is depleted

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4
Q

What metablic disorder is often associated with TIN?

A

NG metabolic acidosis due to defective ammoniagenesis in the tubules

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5
Q

You do a urinalysis and see RBC, RBC casts, proteinuria and granular casts. What is the likely cause of the disease : nephritic, nephrotic or interstitial?

A

Nephritic

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6
Q

You do urinalysis and see heavy proteinuria, fatty casts, oval bodies, and free fat droplets. Is this nephrotic, nephritic or interstitial?

A

Nephrotic

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7
Q

You do urinalysis and see WBC casts, sterile pyuria, eosinophiluria, low grade proteinuria, hematuria. Nephritic, nephrotic or interstitial?

A

Interstitial

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8
Q 
Primary Na retention
Low urinary Na
hypertension
CHF
edema
severe reduction in GFR

Nephritic, nephrotic, interstitial?

A

Nephritic

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9
Q 
Secondary Na retention
low urinary Na
\+/- hypertension
edema
less severe reduction in GFR

Nephritic, nephrotic, interstitial?

A

nephrotic

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10
Q

impaired urine concentration
hyperkalemia
RTA (type IV)
Na wasting

Nephritic, Nephrotic, interstitial ?

A

Interstitial

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11
Q

What if Fanconi syndrome?

A

The clinical presentation of myeloma where there is disruption of the proximal tubule resulting in:

  1. RTA
  2. Glycosuria
  3. Phopsphate wasting, Uricosuria
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12
Q

What is the functional defect of a proximal tubule defect in Interstitial renal disease?
What is the syndrome?

A

Decreased reabsorption of HCO3, glucose, aminoacids, phosphate, uric acid

=

Fanconi syndrome

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13
Q

What are the functional defects of distal nephron interstitial renal disease?

A

decreased Na reabsorption, impaired K and H excretion –> RTA 4

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14
Q

What are the functional defects of the loop in interstitial renal disease?

A
  1. decreased Na reabsorption leading to salt wasting.

2. nephrogenic DI

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15
Q

What are the functional defects of the interstitium in TIN?

A

decreased epo—> anemia

decreased gradient so can’t concentrate urine

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16
Q

What is the most common cause of acute interstitial nephritis (non-infectious)?
How does it manifest?

A

Acute-Allergic drug reaction - a hypersensitivity reaction to a medication like antibiotic, NSAID, diuretic

The patient gets a rash, pruritis, eosinophilia and fever [ABSENT RESPONSE W NSAIDS]

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17
Q

What are indications for biopsy when acute allergic TIN is suspected?

A
  1. diagnostic uncertainty
  2. advanced kidney failure
  3. lack of spontaneous recovery after drug removal
18
Q

How is acute allergic TIN treated?

A
  1. withdraw inciting medication
  2. corticosteroids if there is aggressive disease (worsening azotemia).

If biopsy shows acute inflammation in the absence of chronic damage, cortico will be more effective

19
Q

What does the urinary sediment for acute allergic TIN show?

A

RBC, WBC, WBC casts

20
Q

How does acute TIN from NSAIDs differ from TIN from antibiotics or diuretics?

A

NSAIDs will not have rash, fever etc but will have large amounts of proteinuria.
It looks like MCD with concurrent tubulointerstitial inflammation

21
Q

What two renal syndromes are NSAIDs associated with?

A
  1. ATN when the patient has decreased EABV

2. TI renal disease with nephrotic proteinuria

22
Q

What are clinical signs of chronic TIN?

What is seen in the urine?

A

It is a syndrome of CKD that progressed to ESKD where older women are at highest risk

  1. polyuria
  2. nocturia

Urine will have bland sediment, low urine protein (and the proteins will be LMW like b2 microglobulin, tamm-horsfall, and light chains)

23
Q

What is seen on ultrasonography and biopsy for chronic TIN?

A

Ultrasonography- atrophic echogenic kidneys with CKD

Biopsy-

  1. lymphocytic infiltrate
  2. fibrosis in interstitium
  3. tubular atrophy
  4. arteriosclerosis
  5. global glomerulosclerosis
24
Q

What drugs cause chronic TIN?

A

Chinese herbs, lithium, cyc A, ANALGESICS

25
Q

What are the metabolic situations that can cause chronic TIN?

A

uric acid/oxalate deposition
chronic hypokalemia (which upregulates ammoniagenesis)
nephrocalcinosis

26
Q

What immunologic situations cause chronic TIN?

A

Sjogrens, SLE

27
Q

What are the two most prominent histologic features of analgesic nephropathy?

A
  1. vascular lesions
  2. papillary necrosis

Due to prolonged ingestion of analgesic mixtures (phenacetin and aspirin)

28
Q

The findings of analgesic nephropathy are relatively non-specific. (they present like any other chronic TIN). So what are the frequent findings that point in this direction?

A
  1. women 30-70
  2. questioning of chronic back pain/ headaches
  3. soreness
29
Q

What is the pathogenesis by which lead causes chronic TIN?

A

Lead is reabsorbed in the proximal tubule and accumulates in the proximal tubule cells.

The histological findings show intranuclear inclusion bodies with lead-protein complexes

30
Q

A patient presents with classic symptoms of chronic TIN. (glycosuria, dilute urine, etc). However, they have hyperuricemia, hypertension and gout. what does this make you suspicious of?

A

Lead nephropathy because it is the only one with hyperuricemia

31
Q

A patient presents with chronic TIN. They have type 1 RTA and nephrogenic diabetes insipidus. They have dry eyes and dry mouth. What is suspected?

A

Sjogren’s syndrome

32
Q

What is myeloma kidney?

A

Cast nephropathy which refers to acute or chronic renal failure resulting from filtration of toxic light chains leading to tubular injury (direct) and intratubular cast formation (obstruction)

33
Q

Why does volume depletion increase the likelihood of light chain nephropathy?

A

It is a TIN that damages tubules and forms intratubular casts.
If there is volume depletion, there will be slower flow allowing the concentration of light chain to increase promoting aggregation

34
Q

What would you see in the interstitium in a patient with cast nephropathy?

A

Macrophages with formation of giant cells

35
Q

What test confirms multiple myeloma?

A

SSA test will precipitate non-albumin proteins including light chains

36
Q

Which part of the tubule is most -affected by myeloma-related kidney disorders?

A

Proximal—> fanconi syndrome

37
Q

What gene is mutated in ADPKD1 and 2?

Which presents earlier/is more severe?

A

ADPKD1- mutated polycystin (plasma protein in most cystic epithelia) on chrom 16

ADPKD2 - mutated polycystin 2 (ca cell signaling)

ADPKD1 presents earlier

38
Q

A patient presents with flank pain, abdominal mass, gross hematuria. they frequently present with UTIs and uric acid stones.
They are hypertensive. Their parent had kidney problems. What is a suspicion?

A

PKD

39
Q

Where else can cysts form with ADPKD?
What is the effect on the heart?
What is the usual cause of death for a person with ADPKD?

A

Liver, pancreas spleen

Heart- hypertrophied LV, MVP

bursting berry aneurysm in the circle of willis

40
Q

ARPKD presents at what age? Describe the cysts.

A

It presents early in childhood. There is a high rate of infant mortality
There are many oval cysts that run parallel to each other and perpendicular to the poles of the kidney

41
Q

What two situations will have BUN/Cr ratios over 20?

A
  1. Pre-renal

2. Acute GN

Renal (11 decks)

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