AKI Flashcards
What is AKI
It’s acute/ abrupt decline in kidney function leading to increased serum creatinine or decreased urine output or both
How quickly does AKI develop?
Over hours to days with progressive elevated BUN creatinine and potassium with or without oligouria
What is Azotemia?
Elevation of serum creatinine and BUN related to inability of renal system to filter waste
What is uraemia ?
Decrease of n renal function to point where symptoms begin to develop in multiple body systems
Elevated BUN and Cr causes anorexia, vomiting, purities, or itchiness and neurological changes
Manifestations due to accumulation of waste products in blood and electrolytes imbalance and inflammation
Oligouria
Urine output less than 30ml/hr or less
Or less than 400ml/day
What are the 3 categories of AKI?
Pre-renal
Intra-renal
Post renal
Pre- renal AKI is what
Decreased renal perfusion and filteration
What is pre-renal AKI related to?
It’s related to factors that reduces renal blood flow leading to decreased glomerular perfusion and filtration
Hypovolemia, decreased cardiac output as well as vascular obstruction can cause pre-renal AKI
How do the body auto compensate if perfusion is low
With Decrease circulatory volume auto regulatory mechanisms that increase angiotensin II, aldosterone, norepinephrine and anti diuretic hormones (ADH) to try to preserve blood flow to essential organ
Pre-renal Azotemia is associated with what?
Decrease excretion of sodium
Increased salt and water retention
Decreased urine output
What are the causes of AKI
Vasoactive meds- ACE-I, ARBs, epinephrine, dopamine
NSAIDs
Radioconstrast agents
What’s the mode of action of medication that cause AKI?
The vasoconstriction meds- ACE-I, ARBs, epinephrine, dopamine
NSAIDs and radiocontrast agents cause renal vasoconstriction leading to hypoperfusion of the glomeruli
True or false?
AKI associated with pre-renal is reversible
True
Intra- renal causes of AKI
Glumerulonephritis
Vascular causes- renal vein thrombosis or renal infraction
Interstitial disease
What is nephrotic syndrome
Sequela of glumeronepritis
Expression of 3.5g or more protein in urine per day
Acute tubular necrosis is due to what?
Ischemia- disruption of glomerular base membrane and patchy destruction of tubular epithelium
Nephrotoxin: necrosis of tubular epithelium cells which slough off and plug renal tubules
Pathophyology of acute tubular necrosis
Hypovolemia & decrease renal blood flow
Activate RAAS resulting in constriction of peripherial arteries and renal after ent arteioles
Decreased blood flow = decrease glumerullar capillary pressure and decreased GFR and tubular dysfunction contributing to oliguria
Ischemia = decrease permeability of glumerular cells
Damaged nephron leads to development of edema and collection of necrotic cells
Necrotic cells decrease glumerular filtration and increase pressure within the tubules
Glumerular leak blood
Decrease fluid flow within the tubules
Ultimately leads to oliguria
Under what condition is acute tubular necrosis reversible
If Ischemia is not prolonged
Basement membrane is not destroyed
Tubular epithelium regenerate
What are the causes of post renal AKI?
Obstruction of urine flow
Back up of urine into renal pelvis which impairs kidney function
Most common cause for d Post renal causes of AKI
Prostatic hyperplasia
Prostate cancer
Renal calculi
Trauma
Extrarenal turmors
Post renal cause of AKI account to what percentage
5%
Post renal AKI is almost always treatable if identified before permanent kidney damage
What are the 4 stages of AKI
Initiation phase
Extension phase
Maintenance phase
Recovery phase
If patient does not recover, they develop CKD
What’s the xtics of initiation phase
Increased serum creatinine
Increase BUN
Decrease urine output
Extension phase
Progressive Ischemia
Inflammation
