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ACEM Primary Written > Renal: Pathology - Renal tubular and interstitial disease > Flashcards

Renal: Pathology - Renal tubular and interstitial disease Flashcards

1
Q

What are the causes of acute tubular necrosis?

A

INTO:
Ischaemia
acute tubulointerstitial Nephritis
Toxins
Obstruction

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2
Q

Three causes of ischaemia which may precipitate ATN

A
  1. Hypoperfusion
  2. Ischaemia of intrarenal vesels (e.g. in malignant HTN, microscopic polyangiitis)
  3. Thrombotic conditions (e.g. HUS, TTP, DIC)
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3
Q

Four types of toxins which can cause ATN

A
  1. Radiocontrast dye
  2. Radiation
  3. Myoglobin/haemoglobin
  4. Drugs (e.g. gentamicin)
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4
Q

What is the difference in the distribution of necrosis and casts in ischaemic vs nephrotoxic ATN?

A

Ischaemic: less necrosis than in toxic ATN, more patchy, mostly affecting the PST and TAL
Toxic: necrosis +++ in PCT and PST

Both: casts from DCT to collecting ducts

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5
Q

What are the histologic features of ischaemic vs nephrotoxic ATN?

A

Ischaemic: focal tubular epithelial necrosis with large skip areas, BM rupture, luminal occlusion
Toxic: may be non-specific, some distinctive patterns seen with certain drugs

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6
Q

Describe the three phases of ATN and the clinical features of each

A
  1. Initiation: lasts 36hrs, slight decrease in UO and increase in BUN
  2. Maintenance: sustained oliguria (40-400ml/day, with increased BUN, Na+ and H2O overload, hyperkalaemia, metabolic acidosis, uraemia, needs supportive management including dialysis
  3. Recovery: increased UO up to 3L/day (tubules damaged so increased water and electrolyte loss), increased risk of infection, hypokalaemia, normalisation of BUN and Cr
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7
Q

List 8 broad causes of tubulointerstitial nephritis with examples

A
  1. Infection: pyelonephritis
  2. Toxins: drugs, heavy metals
  3. Metabolic disease: nephrocalcinosis
  4. Physical factors: chronic urinary tract obstruction
  5. Neoplasms: MM
  6. Immunologic reactions: sarcoidosis, Sjogren syndrome, transplant rejection
  7. Vascular diseases
  8. Miscellaneous: Balkan nephropathy
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8
Q

List 8 drugs that may cause tubulointerstitial nephritis

A

SMART Nephrons Are Crying

Sulfonamides
Methicillin
Ampicillin
Rifampin
Thiazides
NSAIDs
Allopurinol
Colchicine

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9
Q

Outline the pathophysiological mechanism of ischaemic ATN

A
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10
Q

Dominant causative organisms in UTI

A

Gram negative (85%)
E. coli most common (followed by Proteus, Klebsiella, Enterobacter, S. faecalis)

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11
Q

Common haematogenous organisms causative of pyelonephritis

A

Staphylococcus
E. coli

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12
Q

Common causatives organisms in ascending UTI

A

E. coli
Proetus
Enterobacter

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13
Q

What % of otherwise normal children have vesicoureteral reflux?

A

1-2%

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14
Q

Three complications of acute pyelonephritis, a brief description of each, and in what circumstances they occur

A
  1. Papillary necrosis: in diabetics and with urinary tract obstruction, coagulative necrosis
  2. Pyonephrosis: with total or almost total obstruction; renal pelvis, calyses and ureters filled with pus
  3. Perinephric abscess: extension of supp
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15
Q

Histologic findings in acute pyelonephritis

A

Patchy interstitial suppurative inflammation, intratubular aggregates of neutrophils, tubular necrosis

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16
Q

8 predisposing factors for acute pyelonephritis

A
  1. Obstruction
  2. Instrumentation (e.g. IDC)
  3. Vesicoureteral reflux
  4. Pregnancy (4-6% of women develop bactiuria during pregnancy and 20-40% of these will develop symptomatic UTI if not treated)
  5. Gender and age (age 1-40 more common in women, more common in males with increasing age due to prostatic enlargement and instrumentation)
  6. Preexisting renal lesions
  7. Diabetes mellitus
  8. Immunosuppression / immunodeficiency
17
Q

What finding on urine sampling suggests pyelonephritis over lower UTI?

A

Pus casts (formed from neutrophils in tubules)

18
Q

What viral pathogen is of importance in causing pyelonephritis in kidney transplant recipients? How is it treated?

A

Polyomavirus
Treated with reduction in immunosuppression

19
Q

Define chronic pyelonephritis. What are its two forms and which is more common?

A

Chronic tubulointerstitial inflammation and renal scarring associated with pathologic involvement of calyces and pelvis
1. Reflux nephropathy (more common)
2. Chronic obstructive pyelonephritis

20
Q

What organism is xanthogranulomatous pyelonephritis associated with?

A

Proteus

21
Q

What is malignant nephrosclerosis?

A

Renal disease associated with malignant HTN

22
Q

What are the two major histologic features in blood vessels seen in malignant HTN?

A
  1. Fibrinoid necrosis of arterioles
  2. Onion-skinning (intimal thickening and fine concentric layering of collagen within interlobular arteries/arterioles: correlates well with renal failure)
23
Q

Describe the clinical presentation seen with typical HUS

A

Prodrome of flu-like symptoms or diarhoea
Sudden onset of bleeding manifestations (e.g. haematemesis, melaena), severe oliguria, and haematuria
Laboratory findings including microangiopathic haemolytic anaemia and thrombocytopaenia

24
Q

What organism causes typical HUS?

A

E. coli strains that produce Shiga-like toxin (usually strain O157:H7)

25
Q

Classical pentad of TTP

A
  1. Fever
  2. Neurologic symptoms
  3. Microangiopathic haemolytic anaemia
  4. Thrombocytopaenia
  5. Renal failure (thrombi seen in glomeruli)
26
Q

Gene affected in TTP

A

ADAMTS13: affects cleavage of vWF –> promotes platelet aggregation

27
Q

Inheritance pattern of polycystic kidney disease

A

AD

28
Q

What is the typical affected demographic in TTP

A

Women <40yo

29
Q

Five causes of atypical HUS

A
  1. Antiphospholipid syndrome (either primary or secondary to SLE)
  2. Complications of pregnancy (can occur 1 day to several months postpartum)
  3. Vascular renal disease (e.g. systemic sclerosis, malignant HTN)
  4. Chemotherapeutic and immunosuppressive drugs (e.g. cisplatin, cyclosporine, gemcitabine)
  5. Irradiation of kidney
30
Q

How is atypical HUS distinguished from TTP?

A

Atypical HUS shows normal levels of ADAMTS13

31
Q

Describe the pathophysiology of HUS

A

Shiga-like toxin induces endothelial injury –> endothelial activation–> platelet aggregation and intravascular thrombosis –> distal ischaemia

32
Q

Four risk factors for haematogenous route of infection in pyelonephritis

A
  1. Presence of ureteral obstruction
  2. Debilitated patients
  3. Immunosuppression
  4. Non-enteric organisms (e.g. staphylococci, certain fungi, viruses)

ACEM Primary Written (150 decks)

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