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
Describe the progression of chronic pyelonephritis
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
What are the microscopic findings of chronic pyelonephritis?
"Thyroidization" of the tubules Tubule cells become dilated and the flow to them decreases No PMNs invading, but there are lymphocytes
27
Xanthogranulomatous Pyelonephritis | What kind of infection is it associated with? What is it commonly mistaken for?
Proteus infection, which could also cause a staghorn calculus May mimic a tumor
28
Acute Drug-Induced Interstitial Nephritis | Clinical Presentation
Rash | Acute renal failure
29
Acute Drug-Induced Interstitial Nephritis | Pathogenesis
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
Acute Drug-Induced Interstitial Nephritis | Prognosis
Good in acute | Renal failure in chronic
31
Acute Drug-Induced Interstitial Nephritis | Treatment
Stop taking the drug!
32
What is the mechanism of NSAIDs that may cause acute hypersensitivity interstitial nephritis?
NSAIDs inhibit prostaglandin synthesis
33
Acute Drug-Induced Interstitial Nephritis due to NSAIDs is very similar to what disease?
MCD Interstitial nephritis Foot process effacement
34
What is the compound in Chinese herbs that may induce tubulointerstitial nephritis?
Aristolochic acid
35
In Chinese herb induced Acute Interstitial Nephritis, what is seen on renal biopsy?
Interstitial fibrosis with atrophy and loss of tubules
36
Urate Nephropathy | Pathogenesis of Acute and Chronic forms
Acute - tubular and epithelial uric acid crystal buildup Chronic - also includes interstitial involvement
37
Urate Nephropathy | What do you see on H&E stain in the chronic form?
Inflammatory reaction, frequently with giant cells (tophi)
38
Multiple Myeloma | What is the primary pathological problem?
Plasma cell malignancy creating excess Ig or light chain The proteins circulate in blood and are filtered through the GBM
39
Multiple Myeloma | Where do the proteins tend to precipitate? What can this lead to?
Distal tubules Multiple Myeloma could cause uric acid buildup, hypercalcemia, light chain casts, acute renal failure
40
Arterionephrosclerosis | What is the pathological problem?
Benign HTN leads to thickening and sclerosis of arterial walls (hyaline arteriosclerosis)
41
How will Malignant HTN effect the kidneys?
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
What are some issues/symptoms that can be seen from renal artery stenosis?
``` Pain Livedo reticularis (vascular rash) Renal infarct (white) ```
43
What is the basic lesion in all thrombotic microangiopathy diseases?
Endothelial injury
44
3 basic symptoms of Thrombotic Microangiopathy
Microangiopathic hemolytic anemia Thrombocytopenia Renal Failure
45
What is the typical pathogenesis of HUS in children?
STEC (Shiga toxin producing E coli) infection, often ingested in undercooked ground beef
46
What is the typical pathogenesis of HUS in adults?
Endothelial injury due to atypical uncontrolled complement activation
47
What is the typical pathogenesis of TTP?
Excess platelet activation from lack of ADAMTS13 enzyme to get rid of vWF multimers in blood
48
What will lab tests reveal in Thrombotic Microangiopathy?
Thrombocytopenia | Schistocytes in peripheral blood smears
49
What is seen on H&E stain in Thrombotic Microangiopathy?
Lots of bright red/pink due to fibrin thrombi Mesangium is dilated and destroyed in the disease process
50
What is the treatment for Thrombotic Microangiopathy?
Supportive Care for underlying disease May use eculizumab antibodies against complement C5 in atypical HUS