Pathophysiology of AKI

Question 1

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

Answer 1

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

Question 2

What are the classifications of AKI based on its onset?

Answer 2

Community-acquired and hospital-acquired.

Question 3

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

Answer 3

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

Question 4

What are the phases of AKI?

Answer 4

Initiation, extension, maintenance, repair.

Question 5

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

Answer 5

International Renal Interest Society (IRIS) AKI grading scheme.

Question 6

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

Answer 6

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

Question 7

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

Answer 7

biomarkers.

Question 8

What are the three primary etiologies of AKI?

Answer 8

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

Question 9

What is pre-renal azotemia?

Answer 9

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

Question 10

What is the main cause of pre-renal azotemia?

Answer 10

Dehydration and hypovolemia.

Question 11

What is intrinsic renal AKI characterized by?

Answer 11

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

Question 12

What is acute tubular necrosis?

Answer 12

Tubular damage that results from ischemic or nephrotoxic insults.

Question 13

What is post-renal AKI caused by?

Answer 13

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

Question 14

True or False: AKI is irreversible.

Answer 14

False; AKI allows the potential for renal recovery.

Question 15

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

Answer 15

Phase 1—initiation.

Question 16

What occurs during the extension phase of AKI?

Answer 16

Continued hypoxia and inflammatory responses propagate kidney damage.

Question 17

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

Answer 17

Cells undergo repair, migration, apoptosis, and proliferation.

Question 18

What happens during the repair phase of AKI?

Answer 18

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

Question 19

What are some systemic consequences of severe AKI?

Answer 19

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

Question 20

What is the relationship between AKI and CKD?

Answer 20

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

Question 21

What is the significance of minimizing CKD following AKI?

Answer 21

It prevents impaired blood flow autoregulation and worsened renal function.

Question 22

What are the consequences of CKD following AKI?

Answer 22

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

Question 23

What initiates the AKI-to-CKD transition?

Answer 23

Failed or incomplete recovery from AKI.

Question 24

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

Answer 24

Tubule atrophy and renal fibrosis (tubulointerstitial fibrosis).

Question 25

What is the normal pathway of tubular healing following AKI?

Answer 25

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

Question 26

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

Answer 26

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

Question 27

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

Answer 27

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

Question 28

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

Answer 28

False.

Question 29

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

Answer 29

New acute injury or other mechanisms of progression.

Question 30

What happens if AKI occurs on top of underlying CKD?

Answer 30

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

Question 31

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

Answer 31

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

Question 32

What aspects of AKI pathophysiology should be researched further?

Answer 32

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