Pathophysiology of AKI Flashcards

1
Q

What is the definition of Acute Kidney Injury (AKI)?

A

Injury to the renal parenchyma, with or without a decrease in kidney function.

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2
Q

What are the classifications of AKI based on its onset?

A

Community-acquired and hospital-acquired.

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3
Q

What is the time frame for diagnosing AKI based on serum creatinine increase?

A

An increase in serum creatinine by ≥0.3 mg/dL from baseline within 48 hours.

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4
Q

What are the phases of AKI?

A

Initiation, extension, maintenance, repair.

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5
Q

What grading system is used for AKI in small animal patients?

A

International Renal Interest Society (IRIS) AKI grading scheme.

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6
Q

What is the clinical description of AKI Grade I according to IRIS?

A

Non-azotemic AKI, with documented AKI and oliguria/anuria.

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7
Q

Fill in the blank: AKI can be diagnosed by documentation of acute decrease in kidney function or increase in kidney injury _______.

A

biomarkers.

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8
Q

What are the three primary etiologies of AKI?

A
  • Volume-responsive (pre-renal) * Intrinsic renal * Post-renal.
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9
Q

What is pre-renal azotemia?

A

A decrease in GFR due to decreased renal perfusion pressure without damage to the renal parenchyma.

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10
Q

What is the main cause of pre-renal azotemia?

A

Dehydration and hypovolemia.

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11
Q

What is intrinsic renal AKI characterized by?

A

Damage to the renal structures: tubules, glomeruli, interstitium, intrarenal blood vessels.

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12
Q

What is acute tubular necrosis?

A

Tubular damage that results from ischemic or nephrotoxic insults.

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13
Q

What is post-renal AKI caused by?

A

Acute obstruction of urinary flow due to urinary tract obstruction or uroabdomen.

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14
Q

True or False: AKI is irreversible.

A

False; AKI allows the potential for renal recovery.

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15
Q

During which phase of AKI does renal blood flow decrease significantly?

A

Phase 1—initiation.

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16
Q

What occurs during the extension phase of AKI?

A

Continued hypoxia and inflammatory responses propagate kidney damage.

17
Q

What is the main event in the maintenance phase of AKI?

A

Cells undergo repair, migration, apoptosis, and proliferation.

18
Q

What happens during the repair phase of AKI?

A

Cellular regeneration, differentiation, and repair of the renal tissue occurs.

19
Q

What are some systemic consequences of severe AKI?

A
  • Accumulation of uremic toxins * Fluid retention * Coagulation disturbances * Anemia * Metabolic acidosis * Hyperkalemia.
20
Q

What is the relationship between AKI and CKD?

A

AKI is a risk factor for the development of CKD, and CKD is a risk factor for AKI.

21
Q

What is the significance of minimizing CKD following AKI?

A

It prevents impaired blood flow autoregulation and worsened renal function.

22
Q

What are the consequences of CKD following AKI?

A

Impaired blood flow autoregulation, glomerular hypertension, glomerulosclerosis, tubulointerstitial fibrosis, worsened renal function, shortened survival time post-AKI, and more intensive chronic management.

23
Q

What initiates the AKI-to-CKD transition?

A

Failed or incomplete recovery from AKI.

24
Q

What does the AKI-to-CKD transition lead to?

A

Tubule atrophy and renal fibrosis (tubulointerstitial fibrosis).

25
Q

What is the normal pathway of tubular healing following AKI?

A

Cell dedifferentiation and proliferation, followed by redifferentiation and recovery of normal cell structure.

26
Q

What occurs in a subpopulation of dedifferentiated, proliferating tubules during recovery from AKI?

A

They undergo pathologic growth arrest, fail to redifferentiate, and become atrophic.

27
Q

What is the result of disturbed interactions between peritubular capillary endothelium and pericyte-like fibroblasts?

A

Myofibroblast transformation, proliferation, fibrosis, capillary disintegration, and rarefaction.

28
Q

True or False: Fibrosis is intrinsically progressive and extends into regions of healthy renal parenchyma.

A

False.

29
Q

What triggers the progression of renal disease following the AKI-to-CKD transition?

A

New acute injury or other mechanisms of progression.

30
Q

What happens if AKI occurs on top of underlying CKD?

A

Injured tubules heal poorly and cause disproportionately severe scarring with loss of peritubular capillaries.

31
Q

What therapeutic opportunity exists regarding the AKI-to-CKD transition?

A

Modulating the AKI-to-CKD transition to decrease the extent of CKD post-AKI.

32
Q

What aspects of AKI pathophysiology should be researched further?

A

Strategies for earlier identification of AKI, improving tubular recovery rates, and modulating the AKI-to-CKD transition.