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Pathophysiology - Urinary Tract > Tubulointerstitial Diseases > Flashcards

Tubulointerstitial Diseases Flashcards

1
Q

What are tubulointerstitial diseases?

A

Heterogenous disorders with tubular intersitial injury, includes acute tubular necrosis/injury, and acute or chronic tubulointerstitial nephritis

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2
Q

What is the most common cause of acute renal failure?

A

Acute tubular necrosis / acute tubular injury

ATN / ATI

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3
Q

What are the two broad etiologies of ATN/ATI?

A

Ischemic

Nephrotoxic

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4
Q

What occurs in the pathogenesis of ATN/ATI? Is the damage irreversible?

A

Cells become injured and lose their functions. They are sloughed off and form necrotic plugs (brown, granular casts). Furthermore, loss of cell polarity leads to increased Na+ reabsorption in PCT -> increased Na delivery to macula densa -> further vasoconstriction of afferent arteriole and ischemia.

They may be regenerated if basement membrane stays intact.

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5
Q

What do the cells look like in mild vs severe cases of ATN/ATI?

A

Mild - reversible changes - cellular swelling, loss of brush border and polarity, blebbing, cell detachment

Severe- irreversible changes - necrosis of cells which slough into the lumen, leaving bare basement membranes

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6
Q

Give the causes of ATN/ATI within the ischemic category.

A

hypotension, shock, sepsis, hemorrhage, or heart failure

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7
Q

Give the causes of ATN/ATI within the nephrotoxic category.

A

Exogenous: aminoglycosides**, heavy metals like lead, cisplatin, ethylene glycol, radiocontrast agents.

Endogenous: myoglobinuria (crush injury), hemoglobinuria, monoclonal light chains (Bence-Jones protein), urate

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8
Q

What are the different patterns of damage between ischemic type vs toxic type ATN/ATI?

A

Ischemic - focal / patch necrosis, especially affecting proximal tubules, and TALH

Toxic type - far more diffuse damage to same areas

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9
Q

What is tubulointerstitial nephritis / what are its two forms?

A

Renal diseases characterizes by inflammatory injury to renal tubules and interstitium, typically sparing the glomerulus

  1. Acute form - generally reversible
  2. Chronic form - generally progressive insults that lead to atrophy and fibrosis over years
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10
Q

What are the typical causes of acute tubulointerstitial nephritis (ATIN)?

A

Drug reaction - penicillins, sulfa drugs (TMP/SMX, thiazide/loop diuretics, NSAIDs, proton pump inhibitors)

Systemic infections - i.e. mycoplasma

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11
Q

What is the pathogenesis of drug-related acute tubulointerstitial nephritis (acute intersitial nephritis)?

A

Drug acts as a hapten to illicit an immune response / hypersensitivity (probably Type I / IV)

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12
Q

What will ATIN show pathologically?

A

All the signs of a Type I/IV hypersensitivity in the interstitium and tubules

Lymphocytes, macrophages, eosinophils** (most characteristic of drug hyperreactivity), neutrophils

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13
Q

What are the clinical features of ATIN?

A

About 15 days after drug exposure, patient has fever, rash, eosinophilia, pyuria, and hematuria.

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14
Q

What is the prognosis of ATIN?

A

Resolves with cessation of the drug, but may progress to renal papillary necrosis

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15
Q

What are the metabolic and electrolyte changes most characteristic of kidney failure (tubular issue)?

A

Metabolic acidosis - continued production of acids which cannot be excreted

Hyperkalemia - inability to secrete potassium in the DCT

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16
Q

What is chronic tubulointersitial fibrosis (CTIN)?

A

Chronic tubular insults over years causing interstitial inflammation and fibrosis, and tubular atrophy with dysfunction.

Gradual loss of renal function over years.

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17
Q

What causes chronic tubulointersitial fibrosis (CTIN)?

A

Infections, reflux or obstructive nephropathy, autoimmune disorders (SLE, Sjogren’s syndrome, sarcoidosis), metabolic diseases, chronic toxin exposures

18
Q

What does it mean when CTIN is symmetric and bilateral?

A

CTIN is most often due to metabolic nephropathies or toxins - i.e. drugs, heavy metals, or chronic exposure to uric acid / oxalate crystals

-> will affect both sides equally

19
Q

What is reflux or obstructive nephropathy?

A

Reflux nephropathy - damage caused by prolonged vesicoureteral reflux -> recurrent acute pyelonephritis infections

Obstructive nephropathy - chronic urinary tract obstruction leads to urine buildup and damage (i.e. due to kidney stones, BPH, or cervical carcinoma)

20
Q

What is the cause of unequal or unilateral CTIN?

A

Diseases which can affect one side only: reflux nephropathy or chronic urinary tract obstruction

21
Q

What is seen in urinary sediment in ATIN vs glomerulonephritis?

A

ATIN - eosinophils

GN - RBC’s and RBC casts

22
Q

What are the common causative organisms of most bacterial UTIs?

A

E. coli, most common

Staphylococcus saphrophyticus, in sexual active young women

Proteus, Klebsiella, enterobacter

23
Q

What tends to be the cause of UTIs in immunocompromised patients, especially if transplant recipients?

A

Adenovirus - hemorrhagic cystitis

BK virus, a polyomavirus - hemorrhagic cystitis

CMV

24
Q

What are the clinical features of a cystitis?

A

Suprapubic pain, dysuria, frequency, urgency, with systemic symptoms usually absent

25
Q

What do urinalysis, dipstick, and culture show for bacterial cystitis?

A

urinalysis - >10 WBC/hpf, with urine often cloudy

dipstick - leukocyte esterase and nitrite positive (bacterial)

Culture - >100,000 CFU / mL

26
Q

What are the two broad routes of infection for acute pyelonephritis, and which is most common?

A
  1. Hematogenous - i.e. bacteremia in septic patients, or infected emboli from endocarditis
  2. Ascending infection - 95% of cases -> colonization of urethra / bladder with ascend up ureter
27
Q

What are some conditions which increase the risk of UTI becoming acute pyelonephritis?

A
  1. Obstruction of urine flow at any level - BPH, neurogenic bladder in diabetes, urethral stricture
  2. Vesicoureteral reflux
  3. Instrumentation of GU tract / indwelling catheter
  4. Pregnancy - gravid uterus obstructs one or both ureters
  5. Immune dysfunction states - AIDS, diabetes, steroids
  6. Age and sex
28
Q

What are the clinical features of acute pyelonephritis?

A

Flank pain and fever, with lab findings similar to cystitis, as well as systemic leukocytosis (systemic findings)

29
Q

Who tends to get the most UTI’s before age 1? Why?

A

Males - because congenital anomalies of urinary tract are more frequent in male infants, with problems of urethral valves and ureteral valves.

30
Q

Who tends to get the most UTI’s between ages 1-50 years old and why?

A

Women - short urethra, lack of antibacterial prostatic secretions, and trauma during sexual intercourse “honeymoon cystitis”

31
Q

Who tends to get UTI’s over age 50 years?

A

Men once again - due to benign prostatic hyperplasia -> urinary stasis

32
Q

What are the possible structural underlying causes of vesicoureteral reflux?

A
  1. Deficiency in longitudinal muscle of the ureter which causes ureter to enter bladder without sufficient tunneling -> does not close during detrussor contraction
  2. Congenital para-ureteral diverticulum -> dilatation disallows bladder contraction
  3. Inflammation of bladder wall, making it stiff.
33
Q

How does acute pyelonephritis appear grossly?

A

Streaks of yellow pus extending up from the renal pyramids and medulla into the cortex
-> affects the cortex, with gray-white abscesses

34
Q

What does acute pyelonephritis look like microscopically / what is spared?

A

Intense neutrophilic interstitial / tubular infiltrate, with marked tubular destruction

-> glomeruli and vessels are relatively spared

35
Q

Who does Candida albicans cause UTI of?

A

Diabetic and immunosuppressed patients

36
Q

What are the possible complications of acute pyelonephritis (other than chronic pyelonephritis due to repeated episodes)?

A
  1. Renal papillary necrosis - sloughing off into renal pelvis, causing further obstruction
  2. Perinephric abscess - infection breaking through renal capsule and spreading to perinephric soft tissues
  3. Pyonephrosis - infection is so severe kidney is literally transformed into a bag of pus
  4. Urosepsis - bloodstream infection
37
Q

How does renal papillary necrosis appear pathologically?

A

Coagulation necrosis (ischemic) with sharply demarcated edges undergiong inflammation

38
Q

What is the cause of chronic pyelonephritis and how does it appear grossly?

A

Repeated bouts of acute pyelonephritis

Appears as severe scarring of renal parenchyma, calyces, and pelvis. This leads to blunted calyces. Cortex will be thinned by numerous broad scars

39
Q

What are the underlying conditions which predispose to chronic pyelonephritis? What will intrarenal reflux cause?

A

Vesicoureteral reflux and chronic obstructing kidney stones.

Intrarenal reflux caused by very bad vesicoureteral reflux will cause scarring at upper and lower poles of the kidney.

40
Q

How will chronic pyelonephritis appear microscopically?

A

Tubules contain eosinophilic casts resembling thyroid tissue -> thyroidization of tubules.

Everything else will be scarred and fibrosed -> glomerulosclerosis and interstitial fibrosis, with tubular atrophy (obviously)

Pathophysiology - Urinary Tract (14 decks)

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