Renal Physiology and Anesthesia by sammyc2007

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									Renal Physiology and Anesthesia
Clinical Anesthesiology Chapter 31 Morgan and Mikhail

Major Functions of the Kidney
Regulation of volume Regulation of composition of body fluids Elimination of toxins Elaboration of hormones

Anatomic and Functional Divisions of the Kidney
1. Glomerular capillaries
2. Proximal convoluted tubules 3. Loop of Henle

4. Distal renal tubule
5. Collecting tubule 6. Juxtaglomerular apparatus

Glomerular Capillaries
1. Blood flow from single afferent

arteriole to single efferent arteriole 2. Endothelial/epithelial basement membrane forms barrier 3. Filtration pressure is 60% MAP 4. 20% of plasma normally filtered

Proximal tubule
60–75% of ultrafiltrate from Bowman’s capsule is isotonically absorbed in the Proximal tubule 2. Major function is sodium reabsorption 3. Na reabsorption is coupled with the reabsorption of other solutes and secretion of H+ 4. Norepinephrine and angiotensin II enhance, dopamine decreases Na+ reabsorption

Proximal tubule
1. Na+-K+ ATPase at basolateral side

creates gradient 2. Na+ reabsorption coupled with secretion of H+ 3. Secretion of H+ responsible for reabsorption of 90% of HCO3-

Loop of Henle
1. Solute and water reabsorption is

passive—follows osmotic and concentration gradient 2. Thick ascending limb impermeable to water 3. Countercurrent multiplier mechanism increases hypertonicity with increasing depth into medulla

Distal Tubule
Relatively impermeable to water and sodium 2. Accounts for 5% of reabsorption of Na+ 3. Major site of PTH and Vit D mediated Ca+ reabsorption 4. Late distal tubule involved in aldosterone mediated Na+ reabsorption

Collecting tubule
1. Differential permeability for urea

between cortical and medullary collecting tubules accounts for up to half of hypertonicity of the renal medulla 2. Medullary portion is site of ADH action - luminal membrane becomes permeable to water under ADH effect

Juxtaglomerular apparatus
Afferent arteriole contains juxtaglomerular cells which contain renin 2. Macula densa located at end of thick ascending cortical segment of the loop of Henle 3. Release of renin : change in Cl flow past macula densa, change in afferent arteriolar wall pressure, ß1 adrenergic stimulation

Renal Circulation
Blood flow through kidney is 20-25% of total C.O. 2. Single renal artery > interlobar > arcuate (jxn cortex and medulla)> interlobular > afferent arteriole supplying each nephron 3. Efferent arteriole branches into 2nd system of capillaries (peritubular) which are primarily reabsorptive

Renal Blood Flow
1. Renal clearance: volume of blood

completely cleared of a substance per unit of time 2. Renal Plasma Flow: clearance of PAH which is completely cleared by filtration and secretion in one passage through the kidneys

RPF = (PAHurine/PAHplasma) x urine flow Normal = 660 ml/min RBF = RPF/(1-hematocrit) Normal = 1200 ml/min GFR normally 20% of RPF Creatinine clearance overestimates because Cr secreted by renal tubules GFR dependent on relative tone of afferent and efferent arterioles

Regulation of RBF
Autoregulation between MAP 80 and 180 mmHg Thought to be myogenic response of afferent arterioles to change in BP RBF is pressure dependent outside of autoregulatory range. GF ceases when MAP<40-40mmHg

Hormonal regulation
Increased afferent arteriolar pressure > release of renin and angiotensin II Angiotensin II increases afferent and efferent tone > GFR preserved Epi and norepi increase afferent arteriolar tone. Decreased GFR minimized through activation of renin and angiotensin II release

Neuronal Regulation
T4-L1 sympathetic outflow via celiac and renal plexuses Juxtaglomerular apparatus – ß1 and Renal vasculature - 1 results in stress induced reduction in RBF 1 receptors enhance sodium reabsorption in proximal tubules and promote water retention

Tubuloglomerular feedback
Increases in renal tubular flow decrease GFR, and visa versa Macula densa probably plays role by inducing reflex changes in afferent arteriolar tone and glomerular capillary permeability

Effects of Anesthesia
General and regional anesthesia result in reversible decreases in RBF, GFR, urinary flow, and sodium excretion Most changes are indirect, mediated by hormonal and autonomic influences Maintainance of normal BP and adequate intravascular volume can partially counteract these effects

Direct Effects
Volatile Agents: halothane, isoflurane, desflurane, sevoflurane—decrease renal vascular resistance Methoxyflurane>polyuric renal failure – dose related, secondary to fluoride ion release following metabolic degradation Plasma fluoride conc>50mol/L

Sevoflurane – nephrotoxin Compound A forms when sevo flows through CO2 absorbent containing sodium hydroxide and potassium hydroxide Exposure should be limited to 2 MAC hrs at flows of 1-2 L/min Amsorb- new CO2 absorbent without NaOH or KOH > no formation of Compound A in excess of that normally present in sevoflurane

IV Agents
Opioids and barbiturates in combination with nitrous oxide have effect similar to inhalation agents Antidopaminergic agents – phenothiazines, metoclopramide, droperidol – may impair renal response to dopamine

NSAIDS including ketorolac prevent the renal production of vasodilatory prostaglandins. Attenuation of vasodilation in patient with high level of norepi or angiotensin II may promote renal dysfunction ACE inhibitors may also potentiate detrimental effect of anesthetic agents on renal perfusion

Indirect Effects
Cardiovascular: cardiac depression and vasodilatation from anesthetic drugs can decrease MAP. Sympathetic blocks also cause vasodilatation. If MAP falls below autoregulatory range, RBF, GFR, UO will be decreased Neural: sympathetic activation increases renal vascular resistance and results in release of renin, angiotensin II, ADH, etc

All decrease reabsorption of Na and water All are highly protein bound and must be secreted by the proximal tubule to exert an effect Resistance to diuretics in pt with renal impairment due to impaired delivery of agent into the renal tubule

Osmotic Diuretics
Mannitol – 6 carbon sugar filtered at the glomerulus, not reabsorbed in proximal tubule. Passive water reabsorption that usually follows Na reabsorption consequently limited Impairs water and solute reabsorption in the loop of Henle

Used in patients with major hemolytic reaction, rhabdomyolysis, severe jaundice, cardiac, aortic surgery Efficacy related to dilution of nephrotoxic substances within renal tubules, prevention of sludging / obstruction, maintainance of renal blood flow Used for eval of acute oliguria –will augment UOP due to hypovolemia

Rapid intra to extra- cellular shift of water can result in transient intravascular volume increase - can precipitate pulmonary edema and cardiac failure in patients with limited reserve Watch for hypovolemia, hypokalemia, hypernatremia following diuresis

Loop Diuretics
Action- inhibition of Na+ and Cl- reabsorption in the thick ascending limb Na+ K+ 2Cl – carrier protein functions only when all 4 sites occupied. Loop diuretics compete for Cl- site on protein Increased delivery of Na+ to distal and collecting tubules increases K+ and H+ secretion – can result in hypokalemia and metabolic acidosis

Furosemide, ethacrynic acid (nonsulfonamide), bumetanide, torsemide Uses include: sodium overload states— CHF, cirrhosis, renal insufficiency, nephrotic syndrome ; hypertension ; eval of acute oliguria ; Rx of hypercalcemia

Thiazide diuretics
Act in distal tubule by competing for Cl site on NaCl carrier protein. Also have some carbonic anhydrase inhibiting action in prox tubule Only in oral form Often see hypokalemia as side effect

Potassium sparing diuretics
Aldosterone antagonists – inhibit aldosterone mediated Na reabsorption and K secretion; only effective in patients with hyperaldosteronism Triamterene and amiloride – K sparing, non competative; often used in conjunction with other diuretic to prevent hypokalemia

Carbonic Anhydrase Inhibitors
Acetazolamide – interferes with Na reabsorption and H secretion in proximal tubule > impair bicarb reabsorption Side effect – hyperchloremic metabolic acidosis

Board Q’s

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