Nephrology

Written By Kate Worster

Nephrology/urology

Notes & Study aids

INNERVATION

  • Sympathetic

    • NE -> b-Adrenergic -> NOT empty bladder

    • Relaxes detrusor/bladder, contracts inner sphincter to store urine

    • Hypogastric nerve

  • Parasympathetic

    • ACh -> Muscarinic -> involuntarily empty bladder

    • Contracts detrusor/bladder, relaxes inner sphincter to release urine

  • Somatic

    • ACh -> Nicotinic (motor) -> voluntarily empty bladder

    • Pudenal nerve 

FILTRATION

Glomerular filtration is a passive process. No reabsorption into capillaries of glomerulus occurs!

  • Outward - Promote (increase) filtrate formation:

    • Glomerular capillaries hydrostatic pressure (HPgc) is main force pushes water/solutes out of blood. ~55mmHg

    • Colloid osmotic pressure in capsule is negligible ~0mmHg

  • Inward - Inhibit (decrease) filtrate formation

    • Hydrostatic pressure in capsular space (HPcs) ~15mmHg

    • Colloid osmotic pressure in capillaries (OPgc) is pull of proteins in blood, ~30mHg

AUTOREGULATION - RAAS MECHANISM

RAAS is one way the kidneys autoregulate and is an extrinsic control mechanism. If there is low systemic blood pressure, this means there is low GBR and decreased GFR. The RAAS mechanism acts in several ways to raise blood pressure. Starts with low BP triggering the juxtaglomerular cells on the afferent arterioles to release renin. Renin activates Angiotensinogen released from the Liver. Angiotensinogen becomes Angiotensin I. ACE released from the lungs converts Angiotensin I into Angiotensin II.

  • CNS: Angiotensin II stimulates the pituitary to release ADH (antidiuretic hormone). ADH acts on the DCT by stimulating aquaporin II to create water channels in the membrane. This increases water reabsorption and thus increases plasma [H2O], which then ­blood volume and finally ­BP.

  • Adrenal Cortex: Angiotensin II acts on the adrenal cortex’s cells in the Zona Glomerulosa to release aldosterone. Aldosterone acts on DCT cells to make them more permeable to water. This increases water reabsorption and thus increases plasma [H2O], which then ­blood volume and finally ­BP.

  • Kidneys: Angiotensin II acts on the efferent arteriole (a little on afferent) and causes vasoconstriction. More blood stays in the glomerulus so there is a longer transit time and thus ­GFR.

    • Also acts on PCT cells to reabsorb Na+ and H2O. Increase in plasma Na+ and H2O lead to ­blood volume and finally ­BP.

  • Systemically, Angiotensin II acts on arteries/veins by causing vasoconstriction. This leads to ­systemic resistance and then ­blood volume/­BP, ­perfusion to kidneys, and ­GFR.

EQUATIONS

  • Net Glomerular Filtration NGF = HPGCaps – (HPBow + OPGCaps)

    • HPGCaps = hydrostatic pressure in glomerular capillaries (~55mmHg)

    • OPGCaps = oncotic/osmotic pressure in glomerular capillaries (negligible)

    • HPBow = hydrostatic pressure in Bowman’s capsule (~15mmHg)

    • OPGCaps = oncotic/osmotic pressure in glomerular capillaries (~30mmHg)

  • Renal Clearance (Cs): Cs = (Ux * V)/Px

    • Cs is clearance rate of substance ‘X’ in mL/min

    • Ux is urine concentration of substance ‘X’ in mg/mL

    • V is urine flow rate in mL/min

    • Px is plasma concentration of substance ‘X’ in mg/mL

    • Note: A substance with a higher clearance than inulin, means more is secreted than reabsorbed.

  • Transport maximum (Tm): exists for almost every reabsorbed substance, reflects number of available carriers in renal tubules, when carriers for solute are saturate -> excess secreted in urine (e.g., hyperglycemia -> glucosuria)

Resources

Kate Worster
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