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Renal II Exam 2 > Robbins - Tubular and Interstitial Diseases > Flashcards

Robbins - Tubular and Interstitial Diseases Flashcards

1
Q

What are the 2 main mechanisms for acute tubular injury/ATI?

A

Ischemia

&

Direct toxicity - endogenous and exogenous

  • endogenous: hemoglobin, monoclonal light chains, bile/bilirubin
  • exogenous: drugs, radiocontrast soln., heavy metals, CCl4/solvents
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2
Q

Ischemic ATI is often due to what?

A

period of inadequate blood flow to organs/hypovolemic shock

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3
Q

Nephrotoxic ATI is often due to what? What can lead to both ischemic and toxic ATI?

A
  • endogenous: hemoglobin, monoclonal light chains, bile/bilirubin
  • exogenous: drugs, radiocontrast soln., heavy metals, CCl4/solvents

Combinations of toxic and ischemic ATI can occur - transfusion blood type mismatch, hemolytic crisis, skeletal mm injuries –> myoglobinuria

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4
Q
A
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5
Q

What are the critical factors in pathogenesis of ATI?

A

tubular injury

persistent and severe disturbances in blood flow

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6
Q

What is the pathogenesis behind tubule cell injury in ATI?

A

Tubule cells sensitive to toxins and ischemia - high rate of metabolism, transport many things

Insult causes loss of cell polarity - memb proteins redist.

-results in increased Na+ to DCT, causes vasoconstriction via tubuloglomerular feedback

Injured cell invites leukocytes

Tubule cells slough off BM and occlude tubule

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7
Q

Injured tubule cells eventually detach from BM, what are the effects of this?

A

Luminal obstruction

increased intratubular pressure

decreased GFR

glomerular filtrate can leak back into interstitium and cause edema, increased interstitial pressure, and further damage to the tubule

= decreased GFR

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8
Q

What is the pathogenesis behind disturbances in blood flow in ATI?

A

Ischemic renal injury = hemodynamic alterations that cause reduced GFR

  • intrarenal vasoconstriction (reduced glom. blood flow and O2 delivery to TAL and PCT in medulla)
  • influenced by RAS and NO production by endothelials
  • possible mesangial contraction
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9
Q

What systems are implicated behind ischemic injury with ATI?

A

RAS

  • increased NA+ delivery to distal tubule (tubuloglomerular feedback)

Sublethal endothelial injury

  • increased endothelin - vasoconstricts
  • decreased NO and prostaglandins
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10
Q

What gross morphological findings help indicate that ATI is possibly reversible?

A

Patchiness of tubular necrosis

Maintenance of BM - depends on capacity of injured epithelials to proliferate

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11
Q

What are some major morphological findings associated with ATI?

A

Focal tubular epithelial necrosis

rupture of BM - tubulorrhexis

occlusion of tubular lumens by casts - eosinophilic, with Tamm-Horsfall proteins

Interstitial edema

Regenerating epithelium - dark nuclei

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12
Q

What are some morphological findings associated with toxic ATI?

A

acute tubular injury, esp. in PCTs

tubular necrosis

Specific findings can point to toxicity:

  • HgCl - large acidophilic inclusions
  • CCl4 - neutral lipid accumulation with fatty change and necrosis
  • Ethylene glycol - ballooning with degeneration of PCT, calcium oxalate crystals
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13
Q

What are the 3 parts of the clinical phase of ATI?

A

Initiation

Maintenance

Recovery

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14
Q

What are the characteristics of the initiation phase of ATI?

A

~36 hours, after injury/insult

  • slight decrease in urine output –> transient decrease in blood flow and GFR
  • slight increase in BUN
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15
Q

What are the characteristics of the maintenance phase of ATI?

A

oliguria - 40-400mL/day

salt and water overload

rising BUN

hyperkalemia

metabolic acidosis

uremic syndrome

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16
Q

What are the characteristics of the recovery phase of ATI?

A
  • increased urine –> 3L/day
  • large amounts of Na+, K+ and water lost

hypokalemia

vulnerable to infection

tubular fxn, conc. ability restored

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17
Q

What is the prognosis of ATI?

A

95% of people who do not succumb to initial toxic event recover

50% of people with shock or multi-organ failure do not recover

18
Q

How is tubulointerstitial nephritis characterized?

A

inflammatory injuries to tubules and interstitium

insidious in onset, marked by azotemia

19
Q

Acute tubulointerstitial nephritis is characterized by what?

A

rapid clinical onset

interstitial edema

leukocytic infiltration of interstitium and tubules

tubular injury

20
Q

Chronic tubulointerstitial nephritis is characterized by what?

A

Infiltration with mononuclear leukocytes

interstitial fibrosis

tubular atrophy

21
Q

How do you distinguish tubulointerstitial nephritis from glomerular disease?

A

No nephritic/nephrotic syndrome

Defects in tubular fxn

  • metabolic acidosis, polyuria, nocturia, salt wasting, defects in tubular wasting
22
Q

What are some major categories of causes for tubulointerstitial nephritis?

A

Infections

Toxins

Metabolic Disease

Physical Factors

Neoplasms

Immunological Reations

Vascular Diseases

23
Q

What is the 2nd most common cause of acute kidney injury?

A

drug and toxin-induced tubulointerstitial nephritis

(first is pyelonephritis)

24
Q

What are 3 ways toxins and drugs trigger kidney injury?

A
  1. interstitial immunological rxn - hypersensitivity nephritis
  2. cause acute tubular injury - ie CCl4/ethylene glycol
  3. Cumulative subclinical injury to tubules, creating chronic renal insufficiency (!)
25
Q

What drugs can trigger acute drug-induced interstitial nephritis?

A

Synthetic PCNs - methicillin, ampicillin

Other synthetic ABs - rifampin

thiazide diuretics

NSAIDs

allopurinol, cimetidine

26
Q

What is the clinical picture of drug-induced interstitial nephritis?

A

2-40 days (~15 days) aft drug exposure

  • fever, eosinophilia, rash (25%), renal abnormalities
  • hematuria, mild proteinuria, leukocyturia
  • rising serum creatine or acute kidney injury in 50% older patients
27
Q

What is the pathogenesis of acute drug-induced interstitial nephritis?

A

late phase Type I hypersensitivty rxn

  • or -

T-cell mediated/Type IV rxn

Drugs turn to haptens, bind tubules, become immunogenic –> IgE binding, or T-cell mediated response

28
Q

Why is it important to recognize acute drug-induced interstitial nephritis?

A

Remove offending drug to start recovery

recovery can take several months, irreversible damage can occur

40% of cases are idiopathic

29
Q

What are some clinical features of acute drug-induced interstitial nephritis?

A

papillary necrosis

  • compression or obstruction of small vessels in medulla leading to ischemia
  • can be excreted, causing gross hematuria or renal colic

Clinical features - Gross pee, pain.

30
Q

What conditions do you see papillary necrosis for?

A

analgesic nephropathy

DM

urinary tract obstruction

sickle cell disease/trait

  • compression of renal medulla small vessels, or microvascular disease
31
Q

What are the NSAID-related renal syndromes?

A

Acute kidney injury - lack of vasodilation via prostaglandins, esp. with other kidney problems or volume depletion

Acute hypersensitivity intersitial nephritis

Acute interstiital nephritis and Minimal Change Disease - hypersensitivty rxn to glomeruli and interstitium, podocytes collateral damage

Membranous nephropathy - correllated, no clear pathology

32
Q

Hyperuricemic disorders can cause nephropathies. Name 3.

A
  1. Acute Uric Acid Nephropathy
  2. Chronic Urate Nephropathy
  3. Nephrolithiasis
33
Q

What is the pathogenesis behind acute uric acid nephropathy?

A

ppt of uric acid crystals in renal tubules -> nephrons obstructed -> acute renal failure

Likely to occur in ind. with leukemia - lymphomas undergoing chemo

  • cells lyse, release uric acid, ppt in acidic pH in collecting tubules
  • definitive proof that life is a bitch - got cancer? How about some kidney stones too?
34
Q

What is the pathogenesis behind chronic urate nephropathy?

A

THE GOUT!!

  • gouty nephropathy, with people wiht protracted forms of hyperuricemia

Monosodium urate crystals deposit in acidic distal tubules, collecting ducts

  • bifringent crystals that evoke mononuclear cells, giant cells
  • complex called tophus

Eventual tubular defects, nephropathy

35
Q

What problems can cause hypercalcemia? This is renal, why do we care?

A

Hypercalcemia - hyper-PTH, mult myeloma, Vit D intoxication, excess Ca++ intake, metastatic cancer

Leads to formation of calcium stones in kidneys - nephrocalcinosis

36
Q

What problems does nephrocalcinosis cause?

A

Extensive nephrocalcinosis can lead to tubulointerstitial disease, renal insufficiency

Tubular acidosis

salt-losing nephritis

slowly progressive renal insufficiency

kidney stones, secondary pyelonephritis

37
Q

What is acute phosphate nephropathy from?

A

CaPO4 crystals in tubules

from oral phosphate soln for colonoscopy

renal insufficiency for several weeks aft

38
Q

What is myeloma kidney? Why would hematopoietic tumors affect the kidney?

A

Kidneys get clogged with tiny proteins, assorted tumor-related crap

tubulointerstitial problems - hypercalcemia, ureteral obstruction

Also:

therapy - irradiation, hyperuricemia, chemo

infection aft bone marrow transplant

39
Q

What factors (previously called tumor crap) contribute to renal damage with myeloma kidney?

A

Bence-Jones proteinuria, cast nephropathy

Amyloidosis

Light chain deposition disease

Hypercalcemia, hyperuricemia

40
Q

What is the pathogenesis of Bence-Jones proteinuria?

A

a type of light chain proteinuria

light chain Ig’s directly toxic to endothelials

Light chain Ig’s combine with Tamm Horsfall proteins that obstruct tubular lumens

Occurs in 70% of people with mult myeloma - significant light chain proteinuria

41
Q

What is hepatorenal syndrome?

A

Impairment of renal function in patients with acute or chronic liver disease

  • high serum bilirubin leads to bile cast formation
  • casts can start in distal nephron and grow in proximal tubule, directly toxic and destroys nephron

Tubular bile casts are yellow-green to pink

42
Q
A

Renal II Exam 2 (8 decks)

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