Tubulointerstitial, Vascular, & Chronic Kidney Diseases - Regner Flashcards Preview

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

Flashcards in Tubulointerstitial, Vascular, & Chronic Kidney Diseases - Regner Deck (28):
1

Acute Interstitial Nephritis

Describe it briefly. What are its three main causes?

Acute Interstitial Nephritis

Inflammation of renal tubules & interstitium

Causes:

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

2

Acute Interstitial Nephritis

How is it diagnosed?

 

Acute Interstitial Nephritis

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

3

Acute Interstitial Nephritis

How is it treated?

Acute Interstitial Nephritis

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

4

Acute Interstitial Nephritis

Describe the microscopic morphology

Acute Interstitial Nephritis

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

5

Acute Pyelonephritis

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

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

6

Acute Pyelonephritis

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

Acute Pyelonephritis

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

7

Multiple Myeloma

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

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

3. Presents as an AKI

8

Multiple Myeloma

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

Multiple Myeloma

  1. Hypercalcemia
  2. Volume depletion
  3. Nephrotoxins

9

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")?

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

10

Multiple Myeloma

What morphologic features of cast nephropathy are seen using:

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

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

11

Multiple Myeloma

How is it treated?

Multiple Myeloma

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

12

Name four types of renal vascular disease.

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

13

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?

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.

14

What is the renal microscopic morphology seen in Malignant Hypertension?

  • Mucoid intimal thickening of arteries ("onion skin")
  • Glomerular capillary wrinkling
  • Duplication of GBM (also seen in Thrombotic Microangiopathy)

 

15

Renovascular Hypertension

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

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

16

Renovascular Hypertension

When should you suspect this disease?

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

Renovascular Hypertension

Name a few methods useful for diagnosing this condition.

Renovascular Hypertension

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

18

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?

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

Renal Artery Stenosis

  • Name three ways it can be treated / managed.

Renal Artery Stenosis

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

20

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?

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

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?

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

Thrombotic Microangiopathy (TMA)

Name 4 conditions that often cause TMA

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

Thrombotic Microangiopathy (TMA)

Describe the pathogenesis of TMA

 

Thrombotic Microangiopathy (TMA)

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

24

CKD

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

CKD

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

25

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.

Normal or large kidney size with CKD:

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

26

CKD

Name some potential consequences of CKD.

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

CKD

Decreased urea excretion in CKD leads to chronic ______.

What are the symptoms of this?

Chronic uremia

Symptoms:

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

28

CKD

How is CKD treated?

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.

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