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In case of prerenal azotemia there is decreased urine sodium and decreased fractional excretion of sodium, however, urine osmolality is increased. How is this possible that urine sodium gets lower wherease osmolality increases? If this is true what are the solutes that result in increased urine osmolality in such a case?
 

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Good question

Am not sure about this but here's how I think of this issue.

The kidney in prerenal failure is essentially functioning (or over functioning) it's just it does not have enough perfusion. So it tries to conserve as much Sodium and Water as it can which leads to low urinary sodium and high urine osmolality. However, it does so on the expense of secreting creatinine and other solutes (that's why you have high BUN/creatinine ratio in prerenal failure).

This issue is the main reason they created the fractional excretion of Sodium. We want to know if the kidney is conserving Sodium or not (without having to look at water loss or re absorption) so we compare urine sodium to plasma sodium in the context of creatinine secretion not water excretion.
 

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This is how I think about it.

Concentration=mass/volume (c=m/v)

In pre-renal azothemia the final mass of urine Na is decreased (due to increased Na reabsorption in the proximal tubules from the low flow of urine, as well as to increased aldosterone due to systemic volume depletion) as well as the volume of urine (due to decreased GFR from the systemic volume loss).

However the urine volume reduction is much greater than the mass reduction, which result in increasing concentration of Na in the urine aka increased osmolarity :).

In renal azothemia, or else dysfunctioning kidney, Na cannot be retained and the mass is increasing, and the same is for volume thus reducing the concentration of the urine and the osmolarity.
 

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in pre-renal azotemia, the kidney gets more time to reabsorb things that it normally does reabsorb because the renal perfusion is low and GFR is decreased and capillary hydrostatic pressure (filtration pressure) is decreased. Also, the fluid in the peritubular capillaries and interstitium is decreased. This along with aldosterone and ADH try to reabsorb as much sodium and water as possible; but the points at which water (collecting ducts for ADH stimulated water absorption-no sodium) and the stimuli (aldosterone for Na and water, ADH for water only) can be absorbed are relatively increased. This leads to relative excess of sodium in the urine while originally total urine sodium and water are decreased. This relative gain of sodium in urine leads to it's increased osmolality.

Hope this helps!

(source: goljan audio)
 
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