Chapter 44 - Renal complications Flashcards
Nephrons in a kidney
1 million
Two types of nephrons
1) short loops of Henle 2) long loops of Henle
Renal artery course
1) Renal artery 2) Interlobar arteries (enter cortex) 3) arcuate arteries (junction of cortex and medulla) 4) cortical radial arteries (ascend through cortex) 5) afferent arterioles 6) glomeruli 7) efferent arteriole 8) vasa recta 9) medullary plexus 10) capillary plexus of outer stripes 11) ascending vasa recta 12) arcuate veins
Kidney’s basic processes
1) glomerular filtration 2) selective tubular secretion 3) selective tubular reabsorption
Cardiac output that goes to normal kidney
25% around 900L/d
Percentage of serum filtered by glomeruli and amount reabsorped
20% filtered 99% reabsorbed
Descending loop of Henle movements
Permeable to water minimally permeable to sodium and chloride
Ascending loop of Henle movement
Not permeable to water active transport to chloride and passive transport of sodium
Aldosterone effect
increases reabsorption of sodium from distal tubule and proximal collecting duct
Potassium absorption in the loop
Proximal convoluted tubule Thick ascending limb
Potassium secretion in the loop
Connecting cells in late distal tubule cortical collecting duct
Neuroendocrine modulators of renal function
1) baroreceptors in atrium 2) renal sympathetic nerve stimulation
How does sympathetic nerve reduce renal sodium excretion
1) constriction of afferent and efferent arteriole 2) reabsoption of sodium in proximal tubule and thick ascending loop of henle 3) stimulate renin secretion
Angiotensin II effects
1) arteriole construction 2) stimulate renal sodium reabsorption in proximal tubule 3) increase secretion of aldosterone
Aldosterone release from
zona glomerulosa of adrenal cortex
Aldosterone effect
sodium reabsorption in distal tubule and collecting duct
Major renal eicosanoids and their effect
PGE2, PGI2 vasodilator inhibit sodium reabsorption from thick ascending loop
Effect of COX-2 inhibition on renal function
1) decrease release of renin 2) reduce medullary blood flow 3) cause apoptosis of medullary intestitial cells therefore NSAID bad for kidney
Paracrine and endocrine modulators of renal function
1) eicosanoids 2) NO (medulla and cortex) 3) endothelin (efferent and afferent arterioles) 4) purines
Most common cause of post-op prerenal AKI
1) contracted intravascular volume due to inadequate fluid replacement 2) secondary to primary reduction in cardiac performance –> neurohormonal reflex to enhance intravascular volume by increasing tubular reabsorption of sodium and water
Ischemic nephropathy
Renal artery stenosis
Post-renal causes of AKI
1) hematuria traumatic catheter insertion obstruction 2) iatrogenic injury 3) epidural effect (should wait 6-12 hours) 4) prostatitis
Parenchymal cause of AKI
Acute tubular necrosis decrease ATP –> loss of actin cytoskeleton –> loss of renal tubular cell membrane polarity –> loss of intercellular tight junction
Causes of ATN
1) ischemic injury (shock, renal artery occlusion, multiorgan failure, atheroemboli) 2) toxic injury (myoglobinuria, antibiotics, contrast)
Two fold pathophysiology of acute ischemic renal injury
1) Tubular cell swelling after reperfusion –> tubular obstruction 2) interstitial edema –> tubular cell death and loss of basement membrane –> slough into tubule
Abciximab
Platelet glycoprotein IIb/IIIa inhibitor
Lab finding that is suggestive of atheroembolism
Eosinophilia 71%
5 year survival in patient with bilateral chronic ischemic nephropathy starting HD
12%
Aminoglycoside effecdt on kidney
1) tubular cell mitochondrial damage 2) cell membrane destruction 3) phospholipase activation 4) lysosome alteration
Treatment of myoglobinuria
1) IV fluid 2) diuretic (mannitol) 3) alkalinizing urine
Algorithm to prevent contrast-induced nephropathy
FIGURE 44.4
Fluid shifts in surgery
1) inflammatory mediators cause increased membrane permeability to albumin 2) flux of albumin into interstitium 3) decrease water reabsorption into intravascular space
Rate of AKI after TAAA and AAA repair
TAAA 18% infrarenal AAA 1-13%
Factors that predict renal dysfunction post-op
1) Cr > 133 2) cross time > 100 min
