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M2 Renal/Respiratory > Tubulointerstitial, Vascular, & Chronic Kidney Diseases - Regner > Flashcards

Tubulointerstitial, Vascular, & Chronic Kidney Diseases - Regner Flashcards

1
Q

Acute Interstitial Nephritis

Describe it briefly. What are its three main causes?

A

Acute Interstitial Nephritis

Inflammation of renal tubules & interstitium

Causes:

  1. Drug hypersensitivity (PCNs, NSAIDs, sulfonamides, rifampin)
  2. Infections
  3. Autoimmune diseases
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2
Q

Acute Interstitial Nephritis

How is it diagnosed?

A

Acute Interstitial Nephritis

  • Look for signs of hypersensitivity rxn:
    • Fever, arthralgia, maculopapular rash
    • Peripheral blood eosinophilia
  • Urinalysis can show:
    • Eosinophils
    • WBCs + WBC casts
    • RBCs
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3
Q

Acute Interstitial Nephritis

How is it treated?

A

Acute Interstitial Nephritis

  • Discontinue offending drug
  • Treat associated infections
  • Treat underlying cause in autoimmune disorders
  • Corticosteroids sometimes used
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4
Q

Acute Interstitial Nephritis

Describe the microscopic morphology

A

Acute Interstitial Nephritis

  • Renal interstitial inflammation and edema.
    • Tubule involvement (tubulitis)
    • Spares glomeruli and vessels
  • Lymphocytes, plasma cells, eosinophils
  • May see granulomas
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5
Q

Acute Pyelonephritis

  1. Describe it briefly. How does the condition reach the kidneys?
  2. What is its typical cause?
A

Acute Pyelonephritis

  1. Acute kidney inflammation due to bacterial infection
    • Urinary route
    • Hematogenous route
  2. Urinary tract pathogens
    • Often Gram negative bacilli
      • E. coli
      • Proteus
      • Enterobacter
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6
Q

Acute Pyelonephritis

Name five conditions that can predispose an individual to acute pyelonephritis.

A

Acute Pyelonephritis

  1. Urinary obstruction (congenital or acquired)
  2. Urinary tract instrumentation (catheter, etc.)
  3. Vesicoureteral reflux (backward urine flow)
  4. Pregnancy
  5. Diabetes
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7
Q

Multiple Myeloma

  1. Describe it.
  2. In what ways does it affect the kidneys?
  3. How does the kidney damage present in clinic?
A

Multiple Myeloma

  1. A cancer of plasma cells that typically produce excessive amounts of abnormal antibody fragments, esp. the Ig light chain.
  2. Myeloma cast nephropathy: ​Chronic renal failure (25% of pts) results from:
  • Direct tubular toxicity from Ig light chains
  • Tubular obstruction by casts
  • Interstitial inflammation
  1. Presents as an AKI
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8
Q

Multiple Myeloma

Name three predisposing factors that favor intrutubular precipitation of Ig light chains and cast formation?

A

Multiple Myeloma

  1. Hypercalcemia
  2. Volume depletion
  3. Nephrotoxins
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9
Q

Multiple Myeloma

  1. What is the typical age of presentation?
  2. What are typical presenting features?
  3. What is a useful diagnostic test for renal involvement (“cast nephropathy”)?
A

Multiple Myeloma

  1. Older, usually >40yrs
  2. Features:
    • Renal insufficiency & proteinuria
    • History of bone pain, fractures
    • Hypercalcemia
    • Monoclonal Ig light chains in blood or urine
  3. Renal biopsy followed by microscopy
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10
Q

Multiple Myeloma

What morphologic features of cast nephropathy are seen using:

  • Light microscopy?
  • Immunofluorescent microscopy?
  • Electron microscopy?
A

Multiple Myeloma

  • LM: Crystalline, FRACTURED casts in tubules with cellular reaction (looks like the cells try to wall off the light chain casts)
  • IF: May see light chain predominance (e.g. use anti-kappa chain Ab → lots of glowy stuff)
  • EM: Electron dense, fractured casts
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11
Q

Multiple Myeloma

How is it treated?

A

Multiple Myeloma

  • Acutely, to prevent tubular obstruction by casts:
    • Hydration
    • Urine alkalinization
  • Long term:
    • Chemotherapy
    • Stem cell transplantation
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12
Q

Name four types of renal vascular disease.

A
  1. Hypertensive nephrosclerosis
  2. Renovascular hypertension
  3. Atheroembolic disease
  4. Thrombotic microangiopathy
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13
Q

Hypertensive Nephrosclerosis

  1. In what context is this disease seen?
  2. What urinalysis finding is often present?
  3. What is the gross morphology?
  4. What is the microscopic morphology?
A

Hypertensive Nephrosclerosis

  1. Context: long-standing, poorly controlled HTN
  2. Urinalysis: proteinuria
  3. Gross: kidney has finely granular subscapular surface
  4. Light microscopy: glomerular sclerosis, tubular atrophy, interstitial fibrosis, arteriolar hyalinosis.
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14
Q

What is the renal microscopic morphology seen in Malignant Hypertension?

A
  • Mucoid intimal thickening of arteries (“onion skin”)
  • Glomerular capillary wrinkling
  • Duplication of GBM (also seen in Thrombotic Microangiopathy)
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15
Q

Renovascular Hypertension

  • What are the two main causes of this condition?
  • What other disease can be caused secondary to this condition?
    • How?
A

Renovascular Hypertension

  • Causes:
    1. Atherosclerosis
    2. Fibromuscular dysplasia
  • Can result in secondary systemic HTN
    • How: Decrease in renal blood flow causes activation of RAAS, stimulating vasoconstriction and fluid retainment
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16
Q

Renovascular Hypertension

When should you suspect this disease?

A

Renovascular Hypertension

  • Atypically early OR late onset HTN
  • Difficult to control HTN
  • Bruit in abdomen or flank
  • Renal failure after starting ACE-I
    • Kidney has become dependent on RAAS activation to obtain sufficient blood flow
17
Q

Renovascular Hypertension

Name a few methods useful for diagnosing this condition.

A

Renovascular Hypertension

  • Contrast CT
  • MRA (like MRI, but Angiography)
  • Renal arteriography
  • Doppler Ultrasound
  • Others
18
Q

Fibromuscular Dysplasia

  1. Who does it typically affect?
  2. Briefly describe the disease
  3. Which vessels are typically affected?
  4. What is the radiographic morphology of affected vessels?
A

Fibromuscular Dysplasia

  1. Younger women
  2. (Wiki) “A non-atherosclerotic, non-inflammatory vascular disease that causes abnormal growth within the wall of an artery”
  3. Often affected (~30% have two affected vascular beds):
    • Renal artery (60-75%, bilateral in 35%)
    • Cervicocranial arteries (25-30%)
    • Visceral and extremity arteries
  4. Alternating thinned media and thickened fibromuscular ridges, causing a “string of beads” appearance on radiography
19
Q

Renal Artery Stenosis

  • Name three ways it can be treated / managed.
A

Renal Artery Stenosis

  1. Surgical revascularization
  2. Angioplasty and stenting
  3. Medical management only
20
Q

Renal Cortical Infarction

  1. What is the gross morphology of this type of infarct?
  2. How does the infarct appear when the occlusion occurs:
    • In the renal artery?
    • In a smaller branch?
A

Renal Cortical Infarction

  1. Appearance:
    • Pale w/ hyperemic border
      • Hemorrhage & actue inflammation at edge
    • Coagulative necrosis
    • Later on, becomes fibrotic
  2. Occlusion:
    • Renal artery: Extensive parenchymal infarction
    • Smaller artery: Wedge-shaped infarct
21
Q

Atheroembolic Disease

  1. Describe the pathology. What is the typical emboli type?
  2. What is a common cause?
  3. Aside from the kidney microvasculature, what other sites are commonly infarcted by these emboli?
  4. What is a common blood and urine finding?
A

Atheroembolic Disease

  1. Disruption of atherosclerotic plaques - acute and subacute renal failure due to shower of cholesterol emboli
  2. Procedures that disrupts aortic plaques
  3. Other sites:
    • Bowel
    • Digits
    • Brain (stroke)
  4. Eosinophils found in blood or urine (due to activation of C5a - chemotaxis)
22
Q

Thrombotic Microangiopathy (TMA)

Name 4 conditions that often cause TMA

A

Thrombotic Microangiopathy (TMA)

Causes:

  • Microangiopathic hemolytic anemia
    • Subtype of hemolytic anemia - hemolysis occurs in small vessles due to endothelial pathology)
    • Seen in SLE, HUS (Hemolytic uremic syndrome)
      • ​HUS often secondary to intestinal E. coli infection
  • Thrombocytopenia
  • TTP (Thrombotic Thrombocytopenic purpura)
    • (Wiki) defective zinc metalloprotease causes abnormal proteolosis of VWF - VWF pieces unfold & aggregate
  • Renal failure
23
Q

Thrombotic Microangiopathy (TMA)

Describe the pathogenesis of TMA

A

Thrombotic Microangiopathy (TMA)

Thrombosis formation in capillaries and arterioles causes endothelial injury & activation, platelet aggregation

24
Q

CKD

  • What are four major causes of CKD?
  • At approximately what GFR can the kidneys no longer function to maintain life?
A

CKD

  • Causes:
    1. Diabetes (#1 cause of CKD in the US)
    2. HTN
    3. Glomerulonephritis
    4. Cystic Diseases
  • GFR < 10 ml/min
25
Q

CKD

In CKD, kidney size is usually, but not always, reduced. Name four conditions in which CKD can occur with normal-sized or large kidneys.

A

Normal or large kidney size with CKD:

  1. Diabetes
  2. Amyloidosis
  3. HIV
  4. Cystic kidney diseases
26
Q

CKD

Name some potential consequences of CKD.

A

CKD

Major Consequences

  1. Anemia (Epo deficiency)
  2. Hypertension (reduced excretion ability & RAAS activation)
  3. Secondary Hyperparathyroidism
    • Decreased renal synthesis of Vitamin D3 causes hypocalcemia, increasing PTH
    • Increased phosphorus retention also increases PTH

Other Consequences

  1. Metabolic acidosis
    • Decreased ammonium secretion, retention of phosphates & sulfates
  2. Hyperkalemia
  3. Disturbed sodium/water balance
  4. Coagulopathy (platelet dysfunction)
  5. Sensorimotor neuropathy
27
Q

CKD

Decreased urea excretion in CKD leads to chronic ______.

What are the symptoms of this?

A

Chronic uremia

Symptoms:

  • Lethargy & fatigue
  • Day-night sleep reversal (huh. neat.)
  • Anorexia, nausea, & vomiting
  • Pruritis
  • Restless legs syndrome
  • Uremic pericarditis
28
Q

CKD

How is CKD treated?

A

CKD

To treat CKD, control its causes:

  • control HTN (ACE-I, ARB)
  • control blood glucose
  • control hyperlipidemia
  • smoking cessation

And correct its consequences:

  • Reduce proteinuria
  • Correct anemia
  • Correct acidosis
  • Dietary restrictions if needed

Once severe (GFR < 10 ml/min), dialysis or transplant will likely be necessary.

M2 Renal/Respiratory (30 decks)

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