Tubular and Interstitial Pathology Flashcards

1
Q

What are the types of Tubulo-Interstitial Nephritis (TIN)?

A
  • Primary: infectious (most common kidney diseases), non-infectious (drug and toxin-induced, metabolic, neoplastic)
  • Secondary: associated with other diseases (glomerulonephritis, vascular, cystic, etc.)
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2
Q

inflammation affecting the tubules, interstitium, and renal pelvis; can be acute and chronic

A

pyelonephritis

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3
Q

What are the pathways of infection in infectious TIN?

A
  • hematogeneous infection (from obstruction, immunosuppression, diabetes, septicemia, endocarditis; common agents are Staph, E. coli, and fungi)
  • ascending infection (from reflux, obstruction, other abnormality of urinary tract; common agents are E. coli, Proteus, and Enterobacter)
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4
Q

What is the prognosis for pyelonephritis?

A

good for acute onset; renal failure for chronic

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5
Q

What are clinical features associated with acute pyelonephritis?

A

sudden onset, costovertebral angle pain,, fever, malaise, frequency/urgency

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6
Q

Which bacteria are the main etiologic agents (85%) of pyelonephritis?

A

gram (-) rods, including E. coli, Proteus, Klebsiella, and Enterobacter

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7
Q

Pathology associated with acute pyelonephritis?

A
  • patchy interstitial suppurative inflamm. (PMNs in tubules and interstitium)
  • tubular necrosis of medulla
  • perinephric abscess
  • papillary necrosis
  • pyonephrosis (sac of pus)
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8
Q

What are risk factors for papillary necrosis?

A
  • analgesics
  • diabetes
  • sickle cell anemia
  • obstruction
  • tuberculosis
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9
Q

Viral pyelonephritis is caused by which virus?

A

polyoma virus

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10
Q

What are the features of chronic pyelonephritis?

A
  • chronic TIN
  • many cases bacterial in origin
  • insidious onset w/ scarring
  • gradual renal insufficiency
  • pyuria and proteinuria on UA
  • polyuria and nocturia (due to loss of conc. ability)
  • contracted kidneys and deformed calyces on X-ray
  • reflux nephropathy
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11
Q

What is seen on histology with chronic pyelonephritis?

A

interstitial lymphocytes but no PMNs; glomerular sclerosis, dilated tubules (“thyroidization”)

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12
Q

a type of chronic pyelonephritis mimicking malignancy

A

xanthogranulomatous pyelonephritis

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13
Q

What are some causes of xanthogranulomatous pyelonephritis?

A

Proteus and obstruction

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14
Q

What is seen on histology with acute drug-induced interstitial nephritis?

A

interstitial inflammation, abundant eosinophils, edema

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15
Q

What is the classic clinical presentation of acute drug-induced interstitial nephritis?

A
  • rash (25%)

- acute renal failure (50%), esp. older patients

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16
Q

What are some of the etiologic agents of acute drug-induced interstitial nephritis?

A

synthetic antibiotics, diuretics, NSAIDs

17
Q

Which types of tubulointerstitial nephritis are not infectious nor drug-induced?

A
  • Metabolic (urate, oxalate, hypercalcemia)

- Neoplastic (multiple myeloma)

18
Q

What is the immune mechanism behind drug-induced TIN?

A
  • idiosyncratic (NOT dose-related)
  • hypersensitivity
  • IgE-mediated
  • pos. skin test to drug hapten
19
Q

What is the etiology of ATI?

A
  • ischemic tubular injury

- toxic injury

20
Q

What are the ischemic, toxic, and combined causes of ATI?

A
  • ischemic: BP drop, severe trauma, acute pancreatitis
  • toxic: drugs (abx), contrast dyes, poisons (heavy metal), organic solvents
  • combined (mismatched blood transfusion, hemolytic crises, skeletal muscle injury, intratubular casts)
21
Q

What is the difference b/t acute and chronic urate nephropathy?

A
  • acute: patients with leukemia/lymphoma who are on chemo (tumor lysis syndrome - releases urate deposits)
  • chronic: “gouty”; associated w/ tophi (urate crystals + surrounding inflamm. rxn)
22
Q

What is a major cause of oxalate nephropathy?

A

ethylene glycol (antifreeze) intoxication

23
Q

Chronic oxalate nephropathy can happen after which type of surgery?

A

bariatric surgery (because it causes malabsorption)

24
Q

What are some other potential causes of oxalate nephropathy aside from antifreeze intoxication?

A

primary (hereditary), enteric, Vit. B6 deficiency, excessive ingestion of Vit. C, diet rich in oxalic acid

25
Q

What is the typical clinical presentation of a patient with ATI?

A
  • rapid reduction of renal function and urinary output (oliguria)
  • “non-oliguric” in 50% of ATI cases
  • uremia
  • signs of fluid overload
  • electrolyte imbalances and acdidosis
26
Q

Which part of the tubule usually undergoes necrosis first with acute tubular injury?

A

proximal tubules

27
Q

What is the prognosis for ATI?

A

fairly good, as it is reversible; treatment is mostly supportive

28
Q

Why is there polyuria during the recovery phase of ATI?

A

because the glomerular filtrate cannot be adequately reabsorbed by the damaged tubular epithelium

29
Q

What are the risk factors/etiology for renal calculi?

A

infection, urinary stasis, immobility, hypercalcemia, increased uric acid, increased urinary oxalate level