AKI Pathology

acute kidney injury

-sudden and rapid deterioration of kidney function (over hours to days)

-accumulation of nitrogen-based waste products in blood, including BUN and creatinine

-electrolyte imbalances

-accumulation of water

azotemia

accumulation of nitrogen based products

yes often

Is acute kidney injury reversible?

diabetes, htn, advanced age

What are the risk factors for acute kidney injury?

reduction in urine output

What is usually the first indicator of acute kidney injury?

oliguria

< 500 mL/day

anuria

< 50 mL/day

AKI KDIGO Criteria:

-Urine volume <0.5 mL/kg/h for at least 6 hrs, or

-Increase in SCr by ≥0.3 mg/dL within 48 hrs, or

-Increase in SCr to ≥ 1.5 times baseline within the prior 7 days

acute kidney disease (AKD)

AKI that extends beyond 7 days

chronic kidney disease (CKD)

AKI that extends beyond 90 days

continum

AKI and CKD are a ________ of each other.

pre-renal AKI

before the kidney -> primarily vasculature related

intrinsic AKI

within the kidney

post-renal AKI

downstream of the kidney -> ureter, bladder

hypoperfusion of the renal parenchyma

What is pre-renal AKI caused by?

systemic arterial hypotension

-↓ in intravascular volume (hemorrhage, excessive vomiting/diarrhea, dehydration, extensive burns, diuretics)

-↓ effective circulating blood volume

prerenal AKI

-decreased blood flow to kidney

-decreased glomerular capillary hydrostatic pressure

-decreased net filtration pressure

-decreased filtration

acute tubular necrosis (ATN)

What is the most common type of intrinsic AKI?

Acute tubular necrosis

results from renal ischemia or nephrotoxins

phases of tubule damage (acute tubular necrosis)

1) initiation

2) extension

3) maintenance

4) recovery

initiation

initial ischemic event causes renal tubular epithelial cell injury (not necessarily necrosis)

extension

continued hypoxia with inflammatory response

maintenance

GFR reaches lowest point and then cellular repair processes start (migration, dedifferentiation, proliferation)

recovery

tubule cells are regenerated

interstitial damage: acute interstitial nephritis (AIN)

-Idiosyncratic delayed hypersensitivity immune reaction caused by medications, infections, autoimmune diseases

-Characterized by tubular and interstitial inflammation, and edema with inflammatory lesions (T lymphocytes, monocytes, macrophages)

-T-cells → proinflammatory molecules → → destructive fibrogenic process (interstitial fibrosis, ischemia, and tubular atrophy

renal vasculature damage

-Large atheroemboli / thromboemboli occlude the larger kidney vessels

-Microvascular damage and inflammation of smaller vessels

glomerular damage

Circulating immune complexes deposit in the glomeruli and cause an inflammatory reaction (e.g., lupus nephritis, IgA nephropathy)

causes of intrinsic AKI

-tubule damage: acute tubular necrosis (ATN)

-interstitial damage: acute interstitial nephritis (AIN)

-renal vasculature damage

-glomerular damage

sepsis-associated acute kidney injury (SA-AKI)

-Occurrence of AKI within 7 days of sepsis onset

-One of the most common causes of AKI

-Multiple contributing mechanisms both post renal and intrinsic

post-renal AKI

-Caused by obstruction of urine flow downstream from the kidney

-Urine accumulates above the obstruction → increased pressure upstream

bladder outlet obstruction

What is the most common cause of post-renal AKI?

AKI consequences if untreated

-ATN with sloughing of the tubular epithelial cells

-cellular debris occludes the tubular lumen

-increased intratubular pressure offsets perfusion pressure

-decreased or abolished net filtration pressure

-decreased GFR

short term AKI consequences

-Hyperkalemia

-Metabolic acidosis

-Hyperphosphatemia

-Pulmonary and/or peripheral edema

-Azotemia (altered mental status)

long term consequences of AKI

-Nephron loss, fibrosis and CKD

-Cardiovascular disease

-Death

typical causes of prerenal AKI

dehydration, HF, NSAIDs, ACEis

typical causes of intrinsic AKI

ischemia (ATN), toxins, inflammation (AIN)

typical causes of postrenal AKI

stones, BPH, tumors