Acute Kidney Injury Flashcards
Pre-renal failure
Renal hypoperfusion
2 major causes of hypoperfusion
1) True volume depletion
2) Decreased effective arterial blood volume (CHF, hepatic cirrhosis, sepsis)
GFR maintenance
Afferent arteriolar vasodilation
Efferent arteriolar vasoconstriction
*Increase in filtration fraction leads to an increase in oncotic pressure in post-glomerular capillaries with increase in salt and water absorption in pt.
NSAIDs
Block PG (block afferent arteriolar dilation) and ACE inhibitors/ARBs (block efferent>afferent arteriolar constriction) prevent proper homeostasis
CHF and cirrhosis
Can lead to decrease in effective arterial blood volume
**Cardinal feature of Pre-renal azotemia
Decrease in effective arterial blood volume (EABV)
Pre-renal azotemia may be a cause of acute or chronic kidney disease
Can vasoconstriction b/c activation of at II and sympathetics.
Pre-renal azotemia and AKI are NOT same thing
Pre-renal azotemia: Urine NaCl low, FENa 40, Uosm >500
AKI: >20 for urine NaCl and FENa >1% losing it all, U/P creatinine and urea <20 and isomolar Uosm.
Most common cause of pre-renal failure is extracellular fluid volume depletion from GI losses
Severe vomiting develops volume contraction.
Do NOT give ACE-Inhibitors or ARBs to patients with
Renal Artery Stenosis
NSAIDs cause
inhibition of PG synthesis which will lead to unopposed activity of these hormonal systems, resulting in exaggerated renal vasoconstriction and magnified antinatriuretic and anti-diuretic effects.
In pre-renal acute kidney injury
The same mechanism that ra’s Na is also responsible for ra of BUN.
Creatinine is NOT reabsorbed avidly by the proximal tubule and is secreted into the pt lumen from the blood.
In pre-renal case
BUN and Cr elevated b/c of DECREASE in GFR.
Urea high b/c avid proximal reabsorption.
URINE urea and creatinine concentrations are ELEVATED b/c of high concentration of urine due to ADH mediated water ra.
Pre-renal see HYPOkalemia
-renal K+ losses, aldosterone high
Na+ ra, K+ out.
Bicarb acts as a non-reabsorbable anion and also increases distal Na delivery.
Little K+ lost from vomiting b/c not much in gastric secretions.
Pre-renal see HYPOchloremia
1) loss b/c HCl in vomiting
2) Dilution with water, same reason why see hyponatremia
Pre-renal see total CO2 elevated b/c of loss of HCl
CO2 is about equal to plasma bicarb concentration
Summary pre-renal failure
Decrease in EABV triggers kidney to conserve sodium and water at expense of retaining excesses of nitrogenous wastes, creatine.
Kidney is working fine.
Reversible with restoration of effective circulatory volume.
Restore EABV allows kidney to regulate volume and electrolytes at normal levels once again.
Oliguric ATN flow less than 400 ml/day
Progressive rise in phosphorus, BUN, creatinine, and potassium as muscle breakdown due to hypercatabolism takes place in absence of renal excretory function.
Serum Ca2+ falls in consequence to the rise of serum phosphorus (due to solubility effect) and a sharp fall in 1,25 (OH)2 vitamin D levels and skeletal resistance to PTH levels.
Life threatening acidosis and hyperkalemia may develop.
ATN
most common form of intrinsic renal failure. Occurs after period of sustained period of ischemia or exposure to nephrotoxic agents.
Typically reversible form of renal failure.
Common causes nephrotoxic injury:
Aminoglycoside antibiotics
Radiocontrast agents
Myoglobin (rhabdomyolysis)
ATN associated with 4-6 fold increase in mortality.
Risk factors:
- Volume depletion
- Underlying chronic kidney disease
- Use of NSAIDs
- Diabetes mellitus
In ATN, tubular cells are damaged and cannot reabsorb Na+ and Cl- causing an
increase in Cl- delivery to MD and cause renal afferent arteriolar vasoconstriction to reduce intraglomerular hydraulic pressure and filtration. (good)
ATN patients are predisposed to
Development of volume overload since salt and water intake now easily exceeds the kidneys excretory capacity.
Low Na, Ca, higher K and P.
Ischemia
Low BP or prolonged volume depletion, sepsis
