Renal Blood Flow & Autoregulation

Renal Blood Flow (RBF)

• measures the amount of blood AND plasma passing through kidneys

• RBF can be estimated via RPF and hematocrit

Renal Plasma Flow (RPF)

• measures the amount of PLASMA that passes through the glomerulus

  • Plasma contains NO CELLS

• RPF can be measured using creatinine or PAH

Renal plasma clearance

• the volume of plasma that is completely removed of a substance

• the rate at which the kidneys can clear a substance from the blood reflects total renal plasma flow.

• albumin & glucose 0% bc cant cross glomerulus

Renal clearance of Creatinine

• volume of plasma that is completely removed of creatinine

• should be 100%

  • creatinine filtered across the glomerulus but not reabsorbed by the nephrons

Constriction of afferent arteriole

• RPF: dec

• GFR: dec

• FF: no change

• dec glomerular hydrostatic pressure

Constriction of efferent arteriole

• RPF: dec

• GFR: inc

• FF: inc

• inc glomerular hydrostatic pressure

inc proteins in plasma

• RPF: no change

• GFR: dec

• FF: dec

• inc oncotic pressure

Constriction of ureter

• RPF: no change

• GFR: dec

• FF: dec

• due to inc Bowmans capsule hydrostatic pressure

GFR = creatinine clearance

• GFR = Creatinine in urine x urine vol / creatinine in blood

• filtered across the glomerulus but not reabsorbed by the nephrons

• Production of creatinine is in steady state in healthy person.

• Production, filtration, and ultrafiltrate excretion measurements are matched if GFR is normal

• An INCREASE in plasma creatinine ₌ inability to filter and excrete it

  • often caused by low GFR

Blood Urea Nitrogen (BUN)

• Urea is byproduct of protein catabolism

• partially reabsorbed along the nephron

• Reabsorption increases as water reabsorption increases

• Used to increases osmotic gradient

• Determinant of kidney function

• Typically excreted from the body

RAAS and ADH activated in the setting of perfusion problem ADH reabsorbes water and urea, which is why BUN is High in perfusion problems

Autoregulation

• Kidney can control its own blood flow in response to change in perfusion pressure

• v wide range

• hormones, sns, angiotension II, and ANP all effect autoregulation

Mechanisms of autoregulation

• Myogenic response

  • ­At the level of the smooth muscle

  • Reacts to blood flow/pressure changes, mechanical

• Tubuglomelur feedback

  • ­The nephron senses its own perfusion blood flow and adjusts

  • ­Reacts to ultrafiltrate flow changes/Intraglomerular pressure

• RAAS

  • Renin released from kidney, causes release of others

Myogenic response

• Response of smooth muscles to stretch

• Increase transmural pressure of vessel and decreases diameter of vessel

• Maintains constant flow by changing resistance

• Prevents high pressure from damaging the glomerulus

• increased Na = constrict afferet = dec hydrostatic= dec GFR

Tubuglomelur feedback

• Links tubular sodium concentration to GFR and blood pressure

  • High Na = high BP → High GFR → High Tubular Na

• Occurs at the Juxtaglomerular Apparatus

  • Macula Densa (right next to DCT)

  • Sodium sensor in DCT

  • high pressure/Na = inc adenosine (ADO)

    • ­Adenosine bind to A1 receptors to constrict afferent arteriole

    • inhibits renin release

      • to dilatate efferent arterioles

    

RAAS

• Renin released by the JGA when

  • Arterial pressure is low

  • ­Tubular Sodium decreases

  • ­Effective circulating volume (ECV) decreases

• Ang II and aldosterone inc pressure

  • Ang II : constricts EFFERENTS arteriole and stimulates release of ADH

  • ­Aldosterone increases Na reabsorption

• ADH released in setting of hypoperfusion

  • ­Reabsorbs free water and urea

• ALL INCREASE VOL AND PRESSURE

PRERENAL = PERFUSION PROBLEM

Vasoactive compounds

•  Norepinephrine and Epinephrine

  • Constrict AFFERENT and EFFERENT

  • dec GFR and RBF

• Endothelin

  • vasoconstrictor

  • dec GFR and RBF

• Nitric Oxide

  • Vasodilators

  • inc GFR and RBF

•  ANP/BNP

  • ­Inhibits renin, which causes naturesis (excretion of Na)

• Prostaglandins

  • Vasodilators of AFFERENTS

Nonperfusion AKI

• Kidney uses lots of ATP, thus produces lots of CO2

• BUN is not elevated

• Renal Ischemia can lead to loss of autoregulation due to death of cells in JGA

• Most damage will occur in the sites of greatest active transport

  • Proximal tubule

  • Thick ascending limb of JG nephron

  • ­Macula Densa

• Produces “Skip Lesions” where part of the nephron is damaged, but the rest is fine.