Pathophysiology of AKI Flashcards
What is the definition of Acute Kidney Injury (AKI)?
Injury to the renal parenchyma, with or without a decrease in kidney function.
What are the classifications of AKI based on its onset?
Community-acquired and hospital-acquired.
What is the time frame for diagnosing AKI based on serum creatinine increase?
An increase in serum creatinine by ≥0.3 mg/dL from baseline within 48 hours.
What are the phases of AKI?
Initiation, extension, maintenance, repair.
What grading system is used for AKI in small animal patients?
International Renal Interest Society (IRIS) AKI grading scheme.
What is the clinical description of AKI Grade I according to IRIS?
Non-azotemic AKI, with documented AKI and oliguria/anuria.
Fill in the blank: AKI can be diagnosed by documentation of acute decrease in kidney function or increase in kidney injury _______.
biomarkers.
What are the three primary etiologies of AKI?
- Volume-responsive (pre-renal) * Intrinsic renal * Post-renal.
What is pre-renal azotemia?
A decrease in GFR due to decreased renal perfusion pressure without damage to the renal parenchyma.
What is the main cause of pre-renal azotemia?
Dehydration and hypovolemia.
What is intrinsic renal AKI characterized by?
Damage to the renal structures: tubules, glomeruli, interstitium, intrarenal blood vessels.
What is acute tubular necrosis?
Tubular damage that results from ischemic or nephrotoxic insults.
What is post-renal AKI caused by?
Acute obstruction of urinary flow due to urinary tract obstruction or uroabdomen.
True or False: AKI is irreversible.
False; AKI allows the potential for renal recovery.
During which phase of AKI does renal blood flow decrease significantly?
Phase 1—initiation.
What occurs during the extension phase of AKI?
Continued hypoxia and inflammatory responses propagate kidney damage.
What is the main event in the maintenance phase of AKI?
Cells undergo repair, migration, apoptosis, and proliferation.
What happens during the repair phase of AKI?
Cellular regeneration, differentiation, and repair of the renal tissue occurs.
What are some systemic consequences of severe AKI?
- Accumulation of uremic toxins * Fluid retention * Coagulation disturbances * Anemia * Metabolic acidosis * Hyperkalemia.
What is the relationship between AKI and CKD?
AKI is a risk factor for the development of CKD, and CKD is a risk factor for AKI.
What is the significance of minimizing CKD following AKI?
It prevents impaired blood flow autoregulation and worsened renal function.
What are the consequences of CKD following AKI?
Impaired blood flow autoregulation, glomerular hypertension, glomerulosclerosis, tubulointerstitial fibrosis, worsened renal function, shortened survival time post-AKI, and more intensive chronic management.
What initiates the AKI-to-CKD transition?
Failed or incomplete recovery from AKI.
What does the AKI-to-CKD transition lead to?
Tubule atrophy and renal fibrosis (tubulointerstitial fibrosis).
What is the normal pathway of tubular healing following AKI?
Cell dedifferentiation and proliferation, followed by redifferentiation and recovery of normal cell structure.
What occurs in a subpopulation of dedifferentiated, proliferating tubules during recovery from AKI?
They undergo pathologic growth arrest, fail to redifferentiate, and become atrophic.
What is the result of disturbed interactions between peritubular capillary endothelium and pericyte-like fibroblasts?
Myofibroblast transformation, proliferation, fibrosis, capillary disintegration, and rarefaction.
True or False: Fibrosis is intrinsically progressive and extends into regions of healthy renal parenchyma.
False.
What triggers the progression of renal disease following the AKI-to-CKD transition?
New acute injury or other mechanisms of progression.
What happens if AKI occurs on top of underlying CKD?
Injured tubules heal poorly and cause disproportionately severe scarring with loss of peritubular capillaries.
What therapeutic opportunity exists regarding the AKI-to-CKD transition?
Modulating the AKI-to-CKD transition to decrease the extent of CKD post-AKI.
What aspects of AKI pathophysiology should be researched further?
Strategies for earlier identification of AKI, improving tubular recovery rates, and modulating the AKI-to-CKD transition.
