CRP- Renal > Interstitial Nephritis > Flashcards

Interstitial Nephritis Flashcards

(47 cards)

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1
Q

What makes up most of the kidney cortex?

A

PCTs

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2
Q

Does the collecting duct system have a separate embryological origin?

A

YES

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3
Q

What is the role of the interstitial cells?

A
  • production of erythropoeitin

- conversion of vitamin D to its active form (allows GI tract to absorb calcium from diet).

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4
Q

What will you see with someone who has ACUTE interstitial nephritis?

A

someone who has acute renal failure

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5
Q

What are the causes of ACUTE renal failure?

A
  • acute tubular necrosis (50%)
  • acute interstitial nephritis
  • pre-renal azotemia
  • contrast nephropathy
  • urinary tract obstruction
  • glomerulonephritis or vasculitis
  • atheroemboli
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6
Q

** What is ACUTE interstitial nephritis?

A

an inflammatory lesion of the kidney marked by intense accumulation of PMNs, eosinophils, and lymphocytes induced by immunologic injury.

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7
Q

** What is CHRONIC interstitial nephritis?

A

a fibrosis of the renal tubulointerstitium from immunologic or toxic injury

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8
Q

What is the difference between acute tubular necrosis and acute interstitial nephritis?

A

acute tubular necrosis= ischemic or toxic injury to the tubular epithelial cells that causes them to leave the basement membrane and block the renal tubule.

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9
Q

How does ACUTE interstitial nephritis typically present?

A

sudden deterioration in kidney function and typically occurs in hospitalized pts.
*This is important to distinguish from acute tubular necrosis because its very dangerous to biopsy a pt in this state so we must rely on our clinical intuition.

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10
Q

*** What are the causes of acute interstitial nephritis?

A
  • DRUGS= NSAIDs and antibiotics (sulfa drugs, rifampin, fluoroquinolones, PPIs..).
  • This occurs bc the body recognizes these drugs as foreign and forms antibodies against these antigens, and these antibodies cross-react with the innocent by-standing kidney.
  • INFECTION= legionella, leptospirosis, cytomegalovirus, streptococci…
  • AUTOIMMUNE= SLE, tubulointerstitial nephritis and uveitis.
  • METABOLIC= oxalate (metabolite of ethylene glycol), which in addition to metabolic acidosis, also causes acute renal damage. Also uric acid (from nucleotide breakdown; often from leukemia treatment).
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11
Q

Do common urinary tract infections from gram negative bacteria (i.e. E. coli) cause acute renal failure?

A

NO

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12
Q

What will you see with metabolic causes of acute interstitial nephritis?

A

tubular oxalate crystals or uric acid crystals

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13
Q

What is pyelonephritis?

A

tubular interstitial nephritis secondary to urinary tract infection.

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14
Q

*** What are the clinical clues to help you make the diagnosis of ACUTE interstitial nephritis?

A
  • urinalysis= pyuria (pus; WBCs in the urine) or eosinophilia.
  • renal function= acute rise in BUN and creatinine.
  • systemic= eosinophilia, fever, rash, malaise
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15
Q

What is the therapy for ACUTE interstitial nephritis?

A
  • remove inciting agent

- consider anti-inflammatories or immunosuppressives

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16
Q

What would you find in a biopsy of someone who has CHRONIC renal failure (elevated serum creatinine for weeks/months)?

A
  • scarring, fibrosing low level of inflammatory process. Most will be due to CHRONIC INTERSTITIAL NEPHRITIS. This will be due to either HTN, chronic ischemia, or toxic nephropathies.
  • a few will have glomerulonephritis.
  • less will have cystic disease
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17
Q

What will CHRONIC interstitial nephritis actually look like on histology?

A

almost like the thyroid due to what looks similar to colloid in the tubules.

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18
Q
  • What is important to remember about CHRONIC tubulointerstitial nephritis?
A

it is the final common pathway for all disorders causing renal failure and may represent a specific series of disorders originating with a toxic, metabolic, or immune injury to the renal tubules and interstitium.

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19
Q

What is the relationship between inulin clearance (GFR) and interstitial fibrosis?

Study These Flashcards
A

as you increase the amount of interstitial fibrosis, you decrease GFR :(

20
Q

What is the mechanisms of renal fibrosis in CHRONIC tubulointersitial nephritis?

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A

tubular injury leads to recruitment/activation of fibroblasts and also due to epithelial transformation to fibroblasts (EPITHELIAL-MESENCHYMAL TRANSFORMATION).
*This is the holy-grail to target, because if we can prevent the fibrosis, we prevent the problem.

21
Q

*** How can you tell someone has CHRONIC interstitial nephritis clinically?

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A
  • declining GFR
  • loss of tubular functions= decreased NH4 production (acidosis), decreased EPO (anemia), disordered medulla (polyuria), and decreased vitamin D activation (osteodystrophy).
  • slowly developing uremia
  • no proteinuria (bc this is not a glomerular problem)
  • HTN
22
Q

What are the causes of CHRONIC interstitial nephritis?

Study These Flashcards
A
  • chronic pyelonephritis
  • heavy metal poisoning (lead or cadmium)
  • hypercalcemia and hypercalciuric disorders
  • sarcoidosis (granulomatous inflammation)
  • analgesic abuse
  • cystic diseases
23
Q
  • What is CHRONIC pyelonephritis?
Study These Flashcards
A

this is chronic interstitial nephritis, characterized by renal scarring with distortion of the CALYCES and RENAL PELVIS. Not necessarily urinary tract infection related.
*AKA this is just another name for CHRONIC interstitial nephritis. It simply implies the pathology, NOT the etiology (cause).

24
Q

What is xanthogranulomatous pyelonephritis?

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A

result of chronic obstruction and a chronic PSEUDOMONAS infection.

25
What conditions can lead to calcium deposition in the kidney (nephrocalcinosis)?
- hyperparathyroidism - multiple myeloma - vitamin D overdose - metastatic bone disease
26
What cystic diseases are associated with interstitial nephritis?
- Adult polycystic kidney disease (PKD)
27
What is the therapy for CHRONIC interstitial nephritis?
Nothing we can do
28
What do we see in pts who have chronic renal failure?
- secondary hyperparathyroidism (SHPT) - adynamic bone disease - mixed osteodystrophy - vascular clacification
29
**What are the problems of chronic renal failure?
1. vitamin D deficiency 2. cannot excrete phosphate appropriately, causing serum phosphate to rise (hyperphosphatemia). This actually causes a DROP in serum calcium. Fibroblast growth factor (FGF) 23, which impairs calcium and phosphorus metabolism.
30
What is hyperparathyroid renal bone disease important?
- increased risk of bone fractures (bc PTH take calcium from the bones to increase serum calcium). - increased risk of vascular and soft tissue calcification.
31
**** So to review, what is the pathogenesis of hyperparathyroidism in chronic kidney disease?
- reduced phosphorus excretion= increased FGF23 and hyperphosphatemia (high phosphate in the blood). Hyperphosphatemia causes hypocalcemia (low calcium in the blood), which increases PTH secretion. FGF23 blocks active vitamin D synthesis, which also contributes to hypocalcemia, also leading to increased PTH secretion. Thus, the net effect is HYPERPARATHYROIDISM. The price of this is decreased bone mass, due to increased bone resorption.
32
What other facors may aggravate hyperparathyroidism?
chronic proliferation of the parathyroid gland, leading to nodularity.
33
What happens to the calcium sensing receptor of the parathyroid gland in chronic kidney disease?
it is poorly expressed, augmenting hyperparathyroidism, bc the gland is unable to respond to how much calcium is in the blood (aka it lacks its negative feedback, if the serum calcium is able to get to normal levels).
34
What does the vitamin D receptor do on the parathyroid gland and what happens to it in chronic kidney disease?
it helps to suppress the parathyroid gland, but is not found in the nodules of a hyperparathyroid gland. Thus giving vitamin D will not help to shut down the parathyroid, bc it lacks these receptors. AKA it is hard to shut down the parathyroid when it is overactive.
35
**** What is the most common bone disorder associated with chronic kidney disease?
hyperparathyroidism
36
*** What is the key to pathogenesis in of hyperparathyroidism?
hyperphosphatemia (by suppressing calcium levels and stimulating FGF-23 production) and vitamin D deficiency (a result of FGF-23 and damage to the kidney where vitamin D is activated).
37
**** What is the importance of FGF-23 accumulation in chronic kidney disease (CKD)?
links high phosphate and low active vitamin D
38
**** Do we normally have FGF-23 in our bodies?
YES it comes from bone and NORMALLY causes phosphate excretion, but in CHRONIC KIDNEY DISEASE, the kidney is damaged and can't get rid of this; hence HYPERphosphatemia.
39
Is vascular calcification very common in pts with chronic kidney disease?
YES
40
**** What is the pathogenesis of vascular calcification?
renal disease, causing decreased phosphate excretion, leading to hyperphosphatemia and FGF-23 accumulation. Together these lead to reduced vitamin D levels. Hyperphosphatemia subsequently leads to calcium and phosphate deposition in vessels (aka even though calcium and phosphate deposition is normal in bone deposition, when phosphate is too high, it can actually turn vascular tissue into bone tissue)!! This will lead to cardiac disease.
41
Where does the vessel calcification occur in CKD?
medial (tunica media) calcification, opposed to intimal calcification seen in atherosclerosis.
42
What are the organ consequences due to vessel calcification?
- cardiac failure secondary to vascular stiffness and increased afterload. - calcific arteriopathy= necrotic areas of skin due to small vessel occlusion.
43
**** How do we treat chronic kidney disease?
- EARLY ON we try giving activated vitamin D to offset the falling vitamin D levels, but regulating an endocrine gland is very difficult, bc this could cause too much calcium to flood the system. - LATER ON when the patient is already on dialysis, we attempt to: 1. control hyperphosphatemia 2. restore vitamin D 3. directly suppress PTH secretion if 1 and 2 fail. 4. surgically reduce parathyroid mass if 3 fails. - for low turnover bone disease: 1. avoid over-suppression of PTH 2. avoid excess calcium loading
44
How do we control (decrease) the serum phosphorus (between 4 and 5)?
- increase vegetables in diet because plant phosphorus is phytate, which is a bigger molecule and LESS absorbable than animal derived phosphorus. - prevent phosphorus absorption during a meal via phosphate-binding drugs.
45
How do phosphate binders work and what are they?
a cation binds phosphorus (a trivalent substance that is easily bound) and then prevents its absorption. - aluminum hydroxide - calcium carbonate - calcium acetate - Sevelamer hydrochloride (best but expensive) - ferric citrate * These drugs only work when taken with a meal, bc duh, they are preventing the phosphorus in the food we are eating from being absorbed.
46
What is a big problem with phosphate binders?
- adherence is poor bc you have to take so many pills. - heavy metal loading bc these are all also heavy metals. - some cause calcium loading - cost
47
How do we treat renal osteodystrophy?
Cinacalcet (calcimimetic)= drug that binds and changes the configuration of the calcium receptor on the parathyroid gland, thus fooling the parathyroid into thinking there are adequate amounts of calcium, so it doesn't produce excess PTH. *VERY GOOD DRUG
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