Pathophysiology of Acute Kidney Injury (AKI)
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Questions and Answers

Which of the following statements about DAMPs and PAMPs is true?

  • PAMPs originate from damaged tissues.
  • Neither DAMPs nor PAMPs interact with pattern recognition receptors.
  • DAMPs are released only from pathogens.
  • Both DAMPs and PAMPs act as danger signals to the immune system. (correct)

M1 macrophages are associated with anti-inflammatory responses.

False (B)

What are the two main phenotypes of macrophages?

M1 and M2

DAMPs and PAMPs interact with _____ in the innate immune system to signal an immune response.

<p>pattern recognition receptors (PRRs)</p> Signup and view all the answers

Match the macrophage phenotype with its corresponding function:

<p>M1 = Pro-inflammatory response M2 = Tissue repair and regeneration Activated Macrophages = Removal of damaged particles M-CSF Production = Supports anti-inflammatory activity</p> Signup and view all the answers

What is a consequence of ischemia leading to ATP depletion?

<p>Activation of intracellular lipases (B)</p> Signup and view all the answers

Apoptosis is a chaotic process characterized by the rupture of the plasma cell membrane.

<p>False (B)</p> Signup and view all the answers

What type of macrophages are involved in the inflammation during the early phase of acute kidney injury (AKI)?

<p>M1 macrophages</p> Signup and view all the answers

Reperfusion leads to the production of ________ species which can cause lipid peroxidation.

<p>reactive oxygen</p> Signup and view all the answers

Match the cellular responses to their descriptions in epithelial injury:

<p>Necrosis = Chaotic process with plasma membrane rupture Apoptosis = Highly regulated and not inflammatory Sublethal injury = Disruption of cytoskeletal network and cell detachment</p> Signup and view all the answers

Which of the following is NOT a consequence of intracellular lipase activation?

<p>Increased ATP production (D)</p> Signup and view all the answers

Systemic inflammation can lead to acute kidney injury (AKI).

<p>True (A)</p> Signup and view all the answers

What is the role of M2 macrophages in the context of ischemic injury?

<p>Anti-inflammatory and facilitate recovery</p> Signup and view all the answers

What does DAMPs stand for?

<p>Damage-Associated Molecular Patterns (D)</p> Signup and view all the answers

Macrophage infiltration is associated with scarring and fibrosis in kidney injuries.

<p>True (A)</p> Signup and view all the answers

What is the role of TGFβ in kidney injury?

<p>It promotes fibrosis and contributes to maladaptive repair.</p> Signup and view all the answers

The innate immune response is activated during _____ injury.

<p>acute</p> Signup and view all the answers

Match the type of macrophage with its function during kidney injury:

<p>M1 = Pro-inflammatory response M2 = Wound healing response M2 (pro-fibrotic) = Progression to chronic kidney disease Macrophage infiltration = Correlates with scarring and fibrosis</p> Signup and view all the answers

What cellular response can lead to stress-induced senescence in tubular epithelial cells?

<p>G2/M cell-cycle arrest (C)</p> Signup and view all the answers

Macrophages only have a pro-inflammatory role in kidney injury.

<p>False (B)</p> Signup and view all the answers

What type of receptors are TLRs and NLRs?

<p>Pattern recognition receptors</p> Signup and view all the answers

The _____ response helps clear cellular debris and promotes tissue repair.

<p>adaptive</p> Signup and view all the answers

What is the primary consequence of maladaptive repair following kidney injury?

<p>Progression to chronic kidney disease (CKD) (B)</p> Signup and view all the answers

What is the primary mortality rate for dogs with acute kidney injury (AKI)?

<p>39% (B)</p> Signup and view all the answers

Community-acquired AKI presents with early detection due to frequent monitoring.

<p>False (B)</p> Signup and view all the answers

Name one of the syndromes included in the definition of acute kidney injury (AKI) in human medicine.

<p>Sepsis</p> Signup and view all the answers

In veterinary medicine, AKI is defined as sudden renal parenchymal injury leading to generalized kidney failure to meet __________ demands.

<p>excretory</p> Signup and view all the answers

Match the type of AKI with its description:

<p>Community-acquired AKI = Delayed presentation after initial insult outside of the hospital Hospital-acquired AKI = Early detection through frequent monitoring of renal markers</p> Signup and view all the answers

Which of the following options is NOT associated with an increase in mortality in AKI?

<p>Excellent renal function (B)</p> Signup and view all the answers

Ischemia-reperfusion injury is one of the common mechanisms of kidney injury.

<p>True (A)</p> Signup and view all the answers

What is the odds ratio for survival when AKI is present?

<p>0.2</p> Signup and view all the answers

Which of the following is a mechanism involved in sepsis-induced acute kidney injury (AKI)?

<p>Inflammation and microcirculatory dysfunction (D)</p> Signup and view all the answers

Ischemia-reperfusion injury leads to the production of reactive oxygen species (ROS).

<p>True (A)</p> Signup and view all the answers

What type of injury is characterized by altered renal hemodynamics and direct tubular epithelial toxicity?

<p>Nephrotoxic AKI</p> Signup and view all the answers

Inflammatory cytokines such as _____ and TNF-a are involved in the ischemia-reperfusion injury cascade.

<p>IL6</p> Signup and view all the answers

Match the type of acute kidney injury with its associated characteristic:

<p>Ischemia-reperfusion injury = Triggers inflammatory cascade Sepsis-induced AKI = Microcirculatory dysfunction Nephrotoxic AKI = Direct tubular toxicity AKI in general = Involves complex interplay of mechanisms</p> Signup and view all the answers

Which factor is not typically associated with nephrotoxic acute kidney injury?

<p>Severe systemic infection (D)</p> Signup and view all the answers

Maladaptive repair after acute kidney injury can lead to chronic kidney disease (CKD).

<p>True (A)</p> Signup and view all the answers

Name one potential consequence of the inflammatory cascade triggered by ischemia-reperfusion injury.

<p>Cell death</p> Signup and view all the answers

What is the primary cause of pre-renal AKI?

<p>Renal hypoperfusion (C)</p> Signup and view all the answers

Intrinsic renal AKI is caused by a response to renal hypoperfusion.

<p>False (B)</p> Signup and view all the answers

Name the phase of AKI where uremic effects dominate.

<p>Maintenance</p> Signup and view all the answers

The imbalance in __________ delivery to renal tissue can lead to ischemic injury.

<p>oxygen</p> Signup and view all the answers

Match the type of AKI with its characteristics:

<p>Pre-renal AKI = Response to renal hypoperfusion Intrinsic renal AKI = Parenchymal injury Post-renal AKI = Impaired urine flow Maintenance phase = Uremic effects dominate</p> Signup and view all the answers

Which of the following best describes the term 'adaptive repair' in AKI?

<p>Is regulated and supports recovery following injury (D)</p> Signup and view all the answers

DAMPs primarily recruit leukocytes during the late phase of AKI.

<p>False (B)</p> Signup and view all the answers

What cellular event occurs due to ATP depletion during ischemia?

<p>Loss of ionic gradients</p> Signup and view all the answers

Ischemia can lead to the production of reactive oxygen species (ROS), resulting in __________ damage.

<p>lipid peroxidation</p> Signup and view all the answers

Which of the following mediators is released during the early phase of inflammation in AKI?

<p>M1 macrophages (B)</p> Signup and view all the answers

The recovery phase of AKI guarantees complete renal function restoration.

<p>False (B)</p> Signup and view all the answers

Identify one key characteristic of tubular dysfunction in AKI.

<p>Intratubular obstruction</p> Signup and view all the answers

Reperfusion injury is primarily associated with the production of __________ species.

<p>reactive oxygen</p> Signup and view all the answers

Match the phenomenon with its description:

<p>Necrosis = Chaotic and inflammatory cell death Apoptosis = Regulated programmed cell death Sublethal injury = Cellular dysfunction without death Reperfusion injury = Caused by restoration of blood flow</p> Signup and view all the answers

What is the primary function of M1 macrophages during the first 24-48 hours after injury?

<p>Clear damaged pathogenic particles (D)</p> Signup and view all the answers

M2 macrophages are primarily responsible for the initial inflammatory response in acute kidney injury.

<p>False (B)</p> Signup and view all the answers

What do DAMPs and PAMPs signal to in the immune system?

<p>innate immune receptors</p> Signup and view all the answers

The _______ feedback mechanism involves solute delivery to the macula densa.

<p>tubulo-glomerular</p> Signup and view all the answers

Match the macrophage type with its role during kidney injury:

<p>M1 macrophages = Pro-inflammatory response M2 macrophages = Tissue repair Pro-fibrotic M2 = Progression to chronic kidney disease Macrophage infiltration = Scarring and fibrosis</p> Signup and view all the answers

Which factors are involved in the tubulo-glomerular feedback mechanism?

<p>Chloride and renin (D)</p> Signup and view all the answers

Maladaptive repair leads to inflammation, fibrosis, and chronic kidney disease (CKD).

<p>True (A)</p> Signup and view all the answers

What is the role of KIM-1 in tubular epithelial cells?

<p>Macrophage chemotaxis</p> Signup and view all the answers

M-CSF is produced by _______ after kidney injury.

<p>proximal tubular cells</p> Signup and view all the answers

Which cytokines are released by M1 macrophages?

<p>IL-1, IL-6, IL-12, TNF (B)</p> Signup and view all the answers

Chronic kidney disease (CKD) primarily develops due to immediate cell death following acute injury.

<p>False (B)</p> Signup and view all the answers

Name one consequence of tubule cell stress-induced senescence.

<p>Maladaptive repair and fibrosis</p> Signup and view all the answers

The initial response to injury is characterized by the activation of ______ macrophages.

<p>M1</p> Signup and view all the answers

Match the macrophage phase with its function:

<p>M1 macrophage = Acute injury phase M2 macrophage = Wound healing phase Pro-fibrotic M2 = CKD progression phase</p> Signup and view all the answers

Flashcards

DAMPs

Damage-associated molecular patterns released from injured tissues.

M1 Macrophages

Activated immune cells that are pro-inflammatory, removing damaged tissue and pathogens in the first 24-48 hours of injury.

M2 Macrophages

Anti-inflammatory immune cells promoting tissue repair and regeneration.

PAMPs

Pathogen-associated molecular patterns released by pathogens.

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Tubular Leakage

Loss of integrity of tubules (small tubes), allowing substances that shouldn't be in the urine to leak into the urine.

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Kidney Injury

Damage to the kidney, triggering cellular stress response and potential activation of cell death pathways.

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AKI

Acute Kidney Injury; a potential result of kidney injury.

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Macrophages (M1)

Pro-inflammatory macrophages involved in the acute injury phase.

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Macrophages (M2)

Wound-healing and pro-fibrotic macrophages; subacute or repair phase

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Tubular Epithelial Cells

Cells lining kidney tubules, affected by and involved in CKD progression.

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KIM-1

A protein expressed by tubular epithelial cells, which can lead to the recruitment of more macrophages

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Fibrosis

Excessive scarring or tissue deposition in the kidney, contributing to CKD.

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Maladaptive repair

A dysfunctional repair process contributing to CKD from the initial injury

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Ischemia-induced cell injury

Ischemia, or reduced blood flow, leads to ATP depletion, disrupting ionic gradients, causing cell swelling, and activating intracellular enzymes, ultimately damaging mitochondria and producing harmful substances like eicosanoids.

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Reperfusion injury

Reestablishing blood flow after ischemia can cause further injury, primarily due to the generation of reactive oxygen species (ROS), leading to lipid peroxidation, protein damage, and DNA damage.

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Sublethal injury to renal tubular cells

Damage that doesn't kill the cell, but disrupts the cell's structure and function, affecting the cytoskeleton, polarization, brush border, cell adhesion, and attachment to the basement membrane.

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Apoptosis

A regulated, programmed form of cell death that is not inflammatory, involving very specific cellular processes.

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Inflammation and AKI

Inflammation, including leukocyte recruitment, is a key contributor to Acute Kidney Injury (AKI). Resident inflammatory cells are activated at first, followed by a recruitment of other immune cells, like neutrophils and macrophages. Systemic inflammation can extend the damage.

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AKI in Veterinary Practice

Acute kidney injury (AKI) is increasingly recognized in animals, especially dogs with septic peritonitis. It is associated with increased mortality and is often detected through advanced monitoring and care, such as renal replacement therapies.

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AKI Mortality Rate

The mortality rate for animals with AKI is significantly higher (39%) compared to those without AKI (9%). The odds of survival are reduced by 40% for every 0.1 mg/dL increase in creatinine.

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Why is AKI a Continuum?

AKI encompasses a range of severity, from mild renal insult to complete kidney failure. The spectrum of damage includes functional and structural changes in the kidneys.

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Community-Acquired AKI

AKI that develops outside the hospital setting, often with delayed recognition due to initial injury occurring before presentation.

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Hospital-Acquired AKI

AKI that develops during hospitalization, often detected through frequent monitoring of renal markers.

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Why 'Acute Kidney Injury' Instead of 'Acute Renal Failure'?

The shift to 'acute kidney injury' emphasizes the functional aspect of kidney damage. Markers like GFR and surrogates of GFR help assess the extent of kidney function.

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Causes of AKI

AKI can result from various conditions, including sepsis, cardiorenal syndrome, urinary tract obstruction, ischemia-reperfusion injury, and nephrotoxicity.

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AKI: Functional Definition

AKI is defined by changes in kidney function, as measured by GFR, creatinine, cystatin C, SDMA, and urine specific gravity.

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Ischemia-Reperfusion Injury (IRI)

Damage to kidney tissue caused by a lack of blood flow followed by its restoration. Occurs primarily in the outer medulla and cortico-medullary junction due to high oxygen demand and poor perfusion in these areas.

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Pre-renal AKI

A type of AKI where the kidney is not damaged but is unable to function properly due to inadequate blood supply.

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Intrinsic Renal AKI

A type of AKI where the kidney itself is damaged, either in the tubules, filters, or other structures.

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What triggers IRI's inflammatory cascade?

Reperfusion after ischemia activates various pro-inflammatory mechanisms, increasing the damage:

  • Pro-inflammatory cytokines (IL-6, TNF-α) are released.
  • Adhesion molecules (ICAM-1) are expressed.
  • Leukotriene pathway (5-LO) is activated.
  • Leukocytes infiltrate and activate.
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Post-renal AKI

A type of AKI where urine is blocked from leaving the body, leading to kidney damage.

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AKI & Sepsis

Sepsis leads to AKI through multiple pathways:

  1. Ischemia reperfusion injury: Microcirculatory problems (endothelial damage) and decreased blood flow.
  2. Inflammation: Release of PAMPs and DAMPs activates immune cells.
  3. Metabolic reprogramming: Cells prioritize survival over function, leading to impaired organ function.
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AKI & Nephrotoxic Agents

The kidneys are susceptible to toxins due to their high blood supply, filtration function, concentration of substances, and reabsorption process. Nephrotoxic agents can cause AKI by:

  • Altering blood flow (NSAIDS, ACEi, ARBs)
  • Triggering inflammation (acute eosinophilic interstitial nephritis)
  • Directly damaging tubular cells (ethylene glycol, aminoglycosides)
  • Damaging blood vessels (antineoplastics)
  • Causing blockage in tubules (sulfonamides, oxalate, melamine)
  • Inducing osmotic stress (mannitol, HES)
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AKI Phases: Initiation

The initial stage of AKI where the kidney is first injured, often through blood loss, sepsis, or drugs.

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AKI & Inflammation

Inflammation plays a crucial role in AKI. It recruits leukocytes to the injured area, amplifying damage. It's a double-edged sword – inflammation can accelerate injury but is also necessary for repair.

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AKI Phases: Extension

The stage of AKI where the initial injury continues to worsen, extending the damage to the kidneys.

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AKI & Adaptive Repair

Following AKI, the kidney can either repair itself successfully (adaptive repair) or develop chronic problems (maladaptive repair). Adaptive repair restores function, while maladaptive repair leads to CKD.

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AKI Phases: Maintenance

The stage of AKI where the kidneys are significantly damaged and can't function properly, leading to waste buildup in the body.

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AKI & CKD

Maladaptive repair in AKI can lead to chronic kidney disease (CKD). This means the initial injury is not fully resolved and the kidney function continues to decline over time.

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AKI Phases: Recovery

The stage of AKI where the kidneys may start to heal and function again, but some damage may be permanent.

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AKI & Maladaptive Repair

Maladaptive repair in AKI can lead to fibrosis, a process of excessive scarring in the kidney. This impairs kidney function and contributes to CKD progression.

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Microvascular Imbalance in AKI

An imbalance between blood vessel dilation and constriction in the kidneys, leading to poor blood flow and oxygen supply to the kidney cells.

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Tubular Dysfunction in AKI

Damage to the tiny tubules in the kidney, causing them to lose their ability to filter waste and control fluid balance.

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Cell Death in AKI

The death of kidney cells due to injury, which can either be through a messy process (necrosis) or a more orderly process (apoptosis).

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Adaptive Repair in AKI

The body's attempt to repair the damaged kidney cells, which can result in full recovery or lead to permanent damage.

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Why is the kidney vulnerable to ischemia despite high blood flow?

Kidneys, despite receiving a significant amount of blood, are highly sensitive to ischemic injury due to their high metabolic demands and unique structure. They rely heavily on oxygen, and even a short interruption in blood flow can cause significant damage.

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Endothelial Injury in AKI

Damage to the cells that line the inside of blood vessels, leading to leakage, inflammation, and disruptions in blood flow regulation.

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ATP Depletion in AKI

A shortage of energy in kidney cells due to reduced blood flow, ultimately disrupting their function and leading to cell damage.

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DAMPs and PAMPs

Molecules released by damaged cells (DAMPs) or pathogens (PAMPs) that trigger an immune response by interacting with pattern recognition receptors (PRRs).

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Macrophage Phenotypes

Macrophages have different roles depending on the stage of injury. M1 macrophages are pro-inflammatory and active during the initial 24-48 hours. M2 macrophages are anti-inflammatory and promote tissue repair and regeneration.

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Tubulo-Glomerular Feedback (TGF)

A mechanism where changes in the filtered fluid detected by specialized cells (macula densa) in the kidney tubules influence the blood flow to the glomeruli, ultimately regulating filtration rate.

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TGF & Proximal Tubular Dysfunction

When the proximal tubules are damaged, more solutes reach the macula densa, leading to vasoconstriction of afferent arterioles, reducing blood flow and glomerular filtration rate (GFR).

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TGF - Afferent Vasoconstriction

The afferent arteriole (incoming blood vessel to the glomerulus) constricts in response to signals from the macula densa, reducing blood flow and GFR.

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Macrophages & Scarring

Macrophage infiltration in the kidney is associated with scarring (fibrosis), leading to a decline in kidney function.

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KIM-1 & Macrophages

KIM-1, a protein expressed by damaged tubular epithelial cells, attracts macrophages to the injured site, contributing to inflammation and potentially fibrosis.

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Tubular Epithelial Cell Stress

Injured tubular epithelial cells can undergo cell cycle perturbation, leading to the release of pro-inflammatory and pro-fibrotic factors, contributing to maladaptive repair.

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Senescence & Maladaptive Repair

Senescent cells, which are damaged and no longer divide, can contribute to inflammation and fibrosis, promoting maladaptive repair and CKD progression.

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Tubular Repopulation

The kidney can regenerate after injury through proliferation of existing cells and potentially the activation of stem or progenitor cells.

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Progenitor Cells & Repair

Progenitor cells, which can differentiate into various kidney cell types, may contribute to kidney regeneration following injury.

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Open Question: Tubular Repopulation Source

It isn't clear whether tubular repopulation comes primarily from existing tubular cells or from progenitor cells. Likely, both contribute to the process.

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Study Notes

Pathophysiology of Acute Kidney Injury (AKI)

  • AKI is defined by a rapid increase in serum creatinine, decrease in urine output, or both.
  • AKI is not a single disease, but a collection of syndromes including sepsis, cardiorenal syndrome, and urinary tract obstruction.
  • AKI can be community or hospital acquired.
  • Community acquired AKI is triggered outside the hospital, with a delay in presentation of a few days.
  • Hospital acquired AKI occurs during the period of hospital treatment, and includes frequent monitoring of kidney function markers for early detection.
  • In dogs with septic peritonitis, AKI occurs in 40% of cases and is associated with decreased survival odds.
  • Mortality rate in dogs with AKI is 39%, versus 9% in dogs without AKI.

Outline: Pathophysiology of AKI

  • Definition: Detailed description of AKI
  • General pathophysiology of injury: Includes ischemia-reperfusion injury, sepsis, and toxic nephrosis as underlying causes.
  • Renal repair: Describes the body's response to repair damage.
  • Specific pathophysiology: A breakdown of specifics regarding different causes of AKI.
    • Ischemia-reperfusion, sepsis, toxic nephrosis

AKI: Why a new name?

  • Functional definition: Uses functional markers such as GFR (glomerular filtration rate) surrogates (creatinine, cystatin C, SDMA), and USG (urine specific gravity).
  • Lesional definition: Focuses on injury markers such as urine sediment, casts, renal glucosuria, uGGT (urinary gamma glutamyl transferase), and uNAG (urinary N-acetyl-glucosaminidase).

Pathophysiology - Historical Classification

  • Pre-renal AKI: Physiologic response to renal hypoperfusion, without tubular injury.
  • Intrinsic renal AKI: Parenchymal injury (glomerular, tubular, vascular, interstitial).
  • Post-renal AKI: Impaired flow of urine (obstruction, rupture).

General Pathophysiology – The Phases of AKI

  • I - Initiation: Kidney injury initiation.
  • II - Extension: Progression of injury.
  • III - Maintenance: Kidney function maintained in the face of extensive damage.
  • IV - Recovery: Functional recovery with complete return or chronic kidney disease.

Pathophysiology - Five Characteristics

  • Microvascular imbalance: Imbalance in vasodilatory and vasoconstrictive factors.
  • Tubular dysfunction: Involves obstruction within the tubules.
  • Cell death: Apoptosis and necrosis.
  • Inflammation: Causes of inflammation are explored.
  • Adaptive and maladaptive repair: Body's repair mechanisms in the context of damage.

Endothelial Injury (Microvascular Events)

  • Dysbalance between vasodilatory and vasoconstrictive mediators.
  • Energy deprivation of endothelium.
  • Increased permeability and edema.
  • Release of cytokines, chemokines, adhesion molecules.

(Micro-)Vascular Imbalance in AKI

  • Imbalance in vasodilatory/vasoconstrictive factors.
  • Mismatch between oxygen and nutrient delivery.
  • Often regional, not generalized.
  • Kidney not a primary organ.

Definition of AKI (hum)

  • Fast increase in serum creatinine.
  • Decreased urine output

Definition of AKI (vet)

  • Spectrum of diseases with sudden onset renal parenchymal injury.
  • Generalized failure of the kidney to meet excretory, metabolic, and endocrine demands of the body.
  • Rapid hemodynamic, filtration, tubulointerstitial, or outflow injury.

Interstitial Events (Inflammation, Edema)

  • Injury (Ischemia) → ATP depletion.
  • HIF gene upregulation.
  • Generation of ROS.
  • Inflammation and recruitment of leukocytes.

Inflammation - Central Role for Macrophages

  • Biphasic phenotypes:
    • M1 pro-inflammatory: Active during the first 24-48 hours of injury, triggered by DAMPs/PAMPs to eliminate pathogen particles.
    • M2 anti-inflammatory: Starts after the initial pro-inflammatory phase. Involved in tissue repair.

Tubulo-Glomerular Feedback

  • Proximal tubular dysfunction → increased solute delivery to the macula densa.
  • Afferent vasoconstriction and decreased SN-GFR.
  • This contributes to oliguria.

Ischemia-Reperfusion Injury (IRI)

  • IRI triggers an inflammatory cascade.
  • Pro-inflammatory cytokines are activated.
  • Inflammatory molecules are expressed.
  • Leukocyte infiltration and activation.
  • Generation of reactive oxygen species.

Sepsis-Induced AKI

  • Combination of mechanisms including ischemia-reperfusion injury, microcirculatory dysfunction, inflammation and metabolic reprogramming.

Kidney predisposed to toxic injury

  • High blood supply.
  • Filtration and tubular concentration
  • Tubular reabsorption

Take home messages

  • AKI involves a complex interplay of multiple mechanisms in systemic diseases.
  • Inflammation is central, even without infection.

Kidney Repair

  • Adaptive repair: restores normal cell function and homeostasis; lost epithelial cells are replaced via proliferation.
  • Maladaptive repair: occurs with prolonged or severe injury and results in scarring, inflammation, fibrosis, and CKD progression.

Epithelial-to-mesenchymal transition

  • Transition from epithelial cells to mesenchymal cells.
  • Occurs in response to inflammation, ischemia and reperfusion.
  • Results in accumulation of fibrotic scar tissue.

Antifibrotic strategies

  • Therapies targeting the mechanisms causing fibrogenesis.

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Related Documents

2024 HD Academy Pathophysiology of AKI PDF

Description

This quiz explores the pathophysiology of Acute Kidney Injury (AKI), including its definitions, causes, and implications for both community and hospital-acquired cases. It covers various syndromes related to AKI and the impact on survival rates in affected dogs. Test your knowledge on this critical topic in veterinary medicine.

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