Help with renal questions...

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ihatescience

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Input on these questions would be truly appreciated 🙂 Thanks so much!

1. In what portion of, or at what point on, the glucose titration curve, is the renal vein glucose concentration equal to renal artery glucose concentration?

2. what is the effect of dilation of the efferent arteriole on filtration fraction?

3. how does spironolactone cause hyperkalemia?

Answers:

1. at all plasma glucose concentrations below threshold

2. decreased

3. my own puzzlement leading me to ask this 😳

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1. The renal artery represents plasma that the kidney is seeing and filtering, while the renal vein represents what didn't get filtered (large proteins that can't penetrate the glomerular basement membrane) or things that are filtered and actively re-absorbed (like glucose). If the plasma glucose reaches a certain level (I believe > 200), the capacity for re-absorption is exceeded and some of the glucose will be lost in the urine. So the renal artery glucose will be > 200 and the renal vein's maximum saturation is determined by the ability for re-absorption of glucose (~200). Up until that level, the renal artery and vein glucose levels should be equal.

2. Filtration fraction is the fraction of solute that's filtered at the glomerulus. That's determined by the hydrostatic pressure and oncotic pressure favoring filtration across the glomerular basement membrane. Dilating the efferent arteriole while holding the afferent arteriole steady decreases the hydrostatic pressure and thus the driving force to filter solute, leading to a reduction in filtration fraction.

3. Spironolactone antagonizes the mineralcorticoid receptor, leading to decreased aldosterone activity, which serves to make it more difficult to re-absorb sodium and secrete potassium.
 
Input on these questions would be truly appreciated 🙂 Thanks so much!

1. In what portion of, or at what point on, the glucose titration curve, is the renal vein glucose concentration equal to renal artery glucose concentration?

2. what is the effect of dilation of the efferent arteriole on filtration fraction?

3. how does spironolactone cause hyperkalemia?

Answers:

1. at all plasma glucose concentrations below threshold

2. decreased

3. my own puzzlement leading me to ask this 😳

1) Everything below threshold (varies with age) all the glucose will be reabsorbed. So it will go in through the artery, get filtered through the glomerulus and then all of it will get reabsorbed. The reabsorbed material will eventually make it's way back to the renal vein.

2) BRS phys (or maybe it is big costanzo phys) has a good chart for this.

3) Spironolactone antagonizes aldosterone. Aldo causes Na reabsorption, K and H secretion. So stopping this would causes K and H retention.
 
2. Filtration fraction is the fraction of solute that's filtered at the glomerulus. That's determined by the hydrostatic pressure and oncotic pressure favoring filtration across the glomerular basement membrane. Dilating the efferent arteriole while holding the afferent arteriole steady decreases the hydrostatic pressure and thus the driving force to filter solute, leading to a reduction in filtration fraction.

Thought I'd add the equation

FF = GFR/RPF

as mortal lessons explained, GFR decreases due to starling forces (decreased hydrostatic pressure). The excess blood goes into the peritubular capillaries and increases RPF.

GFR decreases, RPF increases --> FF decreases
 
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