Acute Kidney Injury, Tubulointerstitial Nephritis, Vascular Diseases Flashcards

1
Q

What is the clinical presentation of Acute Tubular Injury?

A
Reduction in renal function
Oliguria
Uremia (retention of metabolic waste that is not eliminated)
Fluid overload
Electrolyte abnormalities
Acidosis
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2
Q

Pathogenesis of Acute Tubular Injury

A

Some tubular injury occurs or there is a disturbance in blood flow

Causes intrarenal vasoconstriction, low GFR, less O2 and nutrient delivery to cells

Toxic injury to tubular cells

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3
Q

What type of Acute Tubular Injury tends to alter the PCT more?

A

Toxic type

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4
Q

Where is cast formation most commonly seen?

A

DCT of the nephron

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5
Q

How would you describe the necrosis seen is ischemic Acute Tubular Injury?

A

Patchy or focal

Seen in PCT, thick ascending limb

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6
Q

How do ischemic tubule cells looks differently from normal?

A

Basement membrane has many detached cells

High eosinophilia

Thinner epithelial lining because the cells are injured

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7
Q

What will lab tests reveal in Acute Tubular Injury? How is ATI typically diagnosed?

A

Renal failure

In reality, the diagnosis is usually based on clinical grounds

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8
Q

Prognosis and Treatment of Acute Tubular Injury

A

Reversible
3 phases: initiation, maintenance, recovery

Provide support, watch for HTN or cardiac failure
Monitor electrolytes

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9
Q

What are some causes of Ischemic ATI?

A

BP drop
Severe trauma
Acute pancreatitis

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10
Q

What are some causes of toxic ATI?

A

Drugs (antibiotics)
Contrast dyes
Poisons (heavy metal)
Organic solvents

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11
Q

What are some causes of combined ATI (ischemic + nephrotoxicity)?

A

Mismatched blood transfusion
Hemolytic crises (hemoglobinurea)
Skeletal muscle injury (myoglobinurea)
Intratubular casts

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12
Q

Describe the pathogenesis of antifreeze poisoning and what you’d see under the microscope.

A

Calcium oxalate is the toxic compound.

Early stage just affects the tubules, but later you will get an interstitial component too.

Calcium oxalate is very bright under polarized light

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13
Q

Describe mercury nephropathy

A

See acidophilic intracytoplasmic inclusions

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14
Q

Tubulointerstitial Nephritis

List the 3 major categories

A

Infectious
Drug induced
Other (metabolic or neoplastic)

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15
Q

What is the major factor in allowing bacteria to grow and travel up to the kidneys?

A

Urine retention

Anything obstructing the changing the unidirectional flow could facilitate growth of bacteria

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16
Q

Acute Pyelonephritis

What infections are the most common causes?

A

Gram Negative rods (E coli, Proteus, Klebsiella, Enterobacter)

Fungi or viruses in immunocompromised pts

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17
Q

Acute Pyelonephritis

What are some predisposing factors for infection?

A
Catheterization/Instrumentation
Urinary tract obstruction
Stones
Tumors
Enlarged prostate
Vesicoureteral reflux
Congenital abnormalities
Diabetes
Immune suppression/insufficiency
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18
Q

Acute Pyelonephritis

Clinical Presentation

A
Costovertebral angle pain
Fever
Malaise
Frequency/urgency
Urosepsis
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19
Q

What would you see under the microscope in Acute Pyelonephritis?

A

Suppurative inflammation (many PMNs) and formation of focal abscesses

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20
Q

Acute Pyelonephritis

Prognosis

A

Good for acute onset

Bad for chronic (renal failure)

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21
Q

Acute Pyelonephritis

Treatment

A

Antimicrobials against the causative agent

Correct any other predisposing factors

22
Q

What is papillary necrosis? How does one develop it?

A

Ischemia of the medullary tip leading to necrosis

Medulla normally receives a small blood supply, so it is susceptible to ischemia

23
Q

Predisposing factors for Papillary Necrosis

A
Analgesics
Diabetes
Sickle cell anemia
Obstruction
Tuberculosis
24
Q

Who is likely to get a viral interstitial nephritis?

A

Immunocompromised patients

25
Q

Describe the progression of chronic pyelonephritis

A

Mostly bacterial in origin
Gradual buildup of renal insufficiency

Loss of concentrating ability comes first, then patients may notice polyuria and nocturia

Often associated with chronic obstruction and reflux

26
Q

What are the microscopic findings of chronic pyelonephritis?

A

“Thyroidization” of the tubules

Tubule cells become dilated and the flow to them decreases
No PMNs invading, but there are lymphocytes

27
Q

Xanthogranulomatous Pyelonephritis

What kind of infection is it associated with? What is it commonly mistaken for?

A

Proteus infection, which could also cause a staghorn calculus

May mimic a tumor

28
Q

Acute Drug-Induced Interstitial Nephritis

Clinical Presentation

A

Rash

Acute renal failure

29
Q

Acute Drug-Induced Interstitial Nephritis

Pathogenesis

A

IgE and T cell mediated immune reaction to drug, often antibiotics, diuretics, or NSAIDs

Interstitial inflammation, abundant eosinophils and edema

This is NOT dose related. It is a hypersensitivity reaction.

Drugs act as haptens, covalently binding to cells and becoming imunogenic

30
Q

Acute Drug-Induced Interstitial Nephritis

Prognosis

A

Good in acute

Renal failure in chronic

31
Q

Acute Drug-Induced Interstitial Nephritis

Treatment

A

Stop taking the drug!

32
Q

What is the mechanism of NSAIDs that may cause acute hypersensitivity interstitial nephritis?

A

NSAIDs inhibit prostaglandin synthesis

33
Q

Acute Drug-Induced Interstitial Nephritis due to NSAIDs is very similar to what disease?

A

MCD
Interstitial nephritis
Foot process effacement

34
Q

What is the compound in Chinese herbs that may induce tubulointerstitial nephritis?

A

Aristolochic acid

35
Q

In Chinese herb induced Acute Interstitial Nephritis, what is seen on renal biopsy?

A

Interstitial fibrosis with atrophy and loss of tubules

36
Q

Urate Nephropathy

Pathogenesis of Acute and Chronic forms

A

Acute - tubular and epithelial uric acid crystal buildup

Chronic - also includes interstitial involvement

37
Q

Urate Nephropathy

What do you see on H&E stain in the chronic form?

A

Inflammatory reaction, frequently with giant cells (tophi)

38
Q

Multiple Myeloma

What is the primary pathological problem?

A

Plasma cell malignancy creating excess Ig or light chain

The proteins circulate in blood and are filtered through the GBM

39
Q

Multiple Myeloma

Where do the proteins tend to precipitate? What can this lead to?

A

Distal tubules

Multiple Myeloma could cause uric acid buildup, hypercalcemia, light chain casts, acute renal failure

40
Q

Arterionephrosclerosis

What is the pathological problem?

A

Benign HTN leads to thickening and sclerosis of arterial walls (hyaline arteriosclerosis)

41
Q

How will Malignant HTN effect the kidneys?

A

Acute phase will bring fibrinoid necrosis of the renal arteries and arterioles

Cause hyperplastic arteriosclerosis (“onion skin”) and smooth muscle hyperplasia

Will eventually lead to renal failure

42
Q

What are some issues/symptoms that can be seen from renal artery stenosis?

A
Pain
Livedo reticularis (vascular rash)
Renal infarct (white)
43
Q

What is the basic lesion in all thrombotic microangiopathy diseases?

A

Endothelial injury

44
Q

3 basic symptoms of Thrombotic Microangiopathy

A

Microangiopathic hemolytic anemia
Thrombocytopenia
Renal Failure

45
Q

What is the typical pathogenesis of HUS in children?

A

STEC (Shiga toxin producing E coli) infection, often ingested in undercooked ground beef

46
Q

What is the typical pathogenesis of HUS in adults?

A

Endothelial injury due to atypical uncontrolled complement activation

47
Q

What is the typical pathogenesis of TTP?

A

Excess platelet activation from lack of ADAMTS13 enzyme to get rid of vWF multimers in blood

48
Q

What will lab tests reveal in Thrombotic Microangiopathy?

A

Thrombocytopenia

Schistocytes in peripheral blood smears

49
Q

What is seen on H&E stain in Thrombotic Microangiopathy?

A

Lots of bright red/pink due to fibrin thrombi

Mesangium is dilated and destroyed in the disease process

50
Q

What is the treatment for Thrombotic Microangiopathy?

A

Supportive
Care for underlying disease

May use eculizumab antibodies against complement C5 in atypical HUS