PreRenal Azotemia Question

[wanderluste]

Could someone please explain this? Thanks!
A 75-year-old man has had increasing shortness of breath with exertion during the
past 2 weeks. He has a 25-year history of hypertension well controlled with diuretics.
Two months ago, serum urea nitrogen and creatinine concentrations were within the
reference ranges. His pulse is 98/min, respirations are 19/min, and blood pressure is
180/11 mm Hg. The lungs are dull to percussion at the bases, and crackles are heard
one third of the way up bilaterally. Cardiac examination shows increased jugular
venous pressure, and S3 gallop, and no murmur. There is 3+ pitting edema of the
lower extremities. Serum studies show:
Na+126 mEq/L
K+ 5.4 mEq/L
Cl-108 mEq/L
HCO3- 16 mEq/L
Urea nitrogen 75 mg/dL
Creatinine 3 mg/dL
This patient most likely has which of the following types of acid-base disturbance?
(A) Metabolic acidosis
(B) Metabolic alkalosis
(C) Respiratory acidosis
(D) Respiratory alkalosis

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[Jamiu22]

Could someone please explain this? Thanks!
A 75-year-old man has had increasing shortness of breath with exertion during the
past 2 weeks. He has a 25-year history of hypertension well controlled with diuretics.
Two months ago, serum urea nitrogen and creatinine concentrations were within the
reference ranges. His pulse is 98/min, respirations are 19/min, and blood pressure is
180/11 mm Hg. The lungs are dull to percussion at the bases, and crackles are heard
one third of the way up bilaterally. Cardiac examination shows increased jugular
venous pressure, and S3 gallop, and no murmur. There is 3+ pitting edema of the
lower extremities. Serum studies show:
Na+126 mEq/L
K+ 5.4 mEq/L
Cl-108 mEq/L
HCO3- 16 mEq/L
Urea nitrogen 75 mg/dL
Creatinine 3 mg/dL
This patient most likely has which of the following types of acid-base disturbance?
(A) Metabolic acidosis
(B) Metabolic alkalosis
(C) Respiratory acidosis
(D) Respiratory alkalosis

I believe the answer is (A) Metabolic Acidosis - you can't get rid of potassium since the kidney is damaged... so you tend to retain a lot more H+, while getting rid of HCO3... over time though you would get (D) Respitatory Alkalosis as a compensatory mechanism... but it's still primarily (A).

 

[withrye]

I think the answer is actually metabolic alk. The tubules are working fine in cases of prerenal azotemia, so you actually end up wasting K+ and H+ in the collecting ducts, leading to a metabolic alk.

 

[Jamiu22]

I think the answer is actually metabolic alk. The tubules are working fine in cases of prerenal azotemia, so you actually end up wasting K+ and H+ in the collecting ducts, leading to a metabolic alk.

I was thinking that initially, but then I saw the hyperkalemia and hyponatremia in the patient. So even though the BUN/Cr is > 20 (as in pre-renal azotemia)... I don't see how that explains plasma K+ or Na+ levels...it seems like the kidney's been damaged to show those data - it said history of hypertension for a long time, but then again it's well controlled. So I thought high plasma K+ tends to always point to metabolic acidosis... but I see what you are saying and I'm a little stumped by the question too... on the other hand the dialated heart could release ANP causing loss of sodium

😕 😕 😕

 

[addo]

Could someone please explain this? Thanks!
A 75-year-old man has had increasing shortness of breath with exertion during the
past 2 weeks. He has a 25-year history of hypertension well controlled with diuretics.
Two months ago, serum urea nitrogen and creatinine concentrations were within the
reference ranges. His pulse is 98/min, respirations are 19/min, and blood pressure is
180/11 mm Hg. The lungs are dull to percussion at the bases, and crackles are heard
one third of the way up bilaterally. Cardiac examination shows increased jugular
venous pressure, and S3 gallop, and no murmur. There is 3+ pitting edema of the
lower extremities. Serum studies show:
Na+126 mEq/L
K+ 5.4 mEq/L
Cl-108 mEq/L
HCO3- 16 mEq/L
Urea nitrogen 75 mg/dL
Creatinine 3 mg/dL
This patient most likely has which of the following types of acid-base disturbance?
(A) Metabolic acidosis
(B) Metabolic alkalosis
(C) Respiratory acidosis
(D) Respiratory alkalosis

I would have put A too.
But I see how the right answer is metabolic alkalosis. You already said he has pre renal failure, which fits with BUN/Cr>20. It sounds like he has CHF which would produce a decrease in effective arterial blood volume--> ADH increase and retention of free water. I think this partially accounts for the finding of hyponatremia.
The other interesting finding is hyperkalemia. You would think that hyponatremia and hyperkalemia would result in high aldosterone levels and therefore metabolic alkalosis and hypokalemia, not hyperkalemia. Hes probably on a potassium sparing diuretic like spirionlactone, which will reverse the effects of aldosterone, worsening the hyponatremia, and causing hyperkalemia.... Im not sure what the effect of spirinolactone is on the handling of bicarbonate. If it also reverses the action of aldosterone on bicarbonate, then you wouldnt expect metabolic alkalosis.

 

[addo]

It makes sense that he would be on spironolactone especially given his long history of HTN and being on diuretics... also just read that the higher the aldosterone level, the greater the effect spironolactone has.
That question was tough... i have now seen a fifth degree of reasoning to get to the right answer question.

 

[USCTrojan11]

So uh what's the answer

 

[tiedyeddog]

I thought prerenal azotemia occured at the latter end of CHF once blood pressure started falling? I know the pulse pressure is huge here, but the systolic pressure is extremely elevated. How do we know by the question stem that prerenal azotemia is actually occurring?

Also, shouldn't the bicarb by elevated?

I was thinking this could be metabolic acidosis due to spironolactone use.

 

[CaptainSSO]

I thought prerenal azotemia occured at the latter end of CHF once blood pressure started falling? I know the pulse pressure is huge here, but the systolic pressure is extremely elevated. How do we know by the question stem that prerenal azotemia is actually occurring?

Also, shouldn't the bicarb by elevated?

I was thinking this could be metabolic acidosis due to spironolactone use.

Yea, metabolic alk. makes no sense with bicarbonate at 16. K+ sparing diuretic is enough to explain this question.

That explains the hypovolemia (BUN > 20x creatinine), the excess K+, hyponatremia, and the acidosis.

 

[tiedyeddog]

Yea, metabolic alk. makes no sense with bicarbonate at 16.

yeah, totally agree. I think with these questions where the pH and pCO2 aren't given you have to look at two things:

1. What is the bicarb?
2. What is the respiration rate?
3. What is the anion gap?

Bicarb is low (normal is 24). Respiratory rate is normal (under 24). Anion gap is normal.

Because of the low bicarb this could either be: metabolic acidosis(bicarb is eaten up trying to buffer the blood back to 7.4) or this could be respiratory alkalosis ( too much CO2 blown off, so bicarb over a long time period decreases reabsorption of bicarb).

Given that spironlactone use causes normal anion gap metabolic acidosis, (remember the HARDASS pnemonic) I would go with that. It doesn't seem like the patient is hyperpneic, meaning too much CO2 is blown off.

This is basically a type 4 renal tubular acidosis. See article on it here. Patient is hyperkalemic, which reinforces that diagnosis. http://www.turner-white.com/pdf/hp_nov01_renal.pdf

Now, watch OP come back and prove me totally wrong. 😉

 

[MLT2MT2DO]

I think the answer is actually metabolic alk. The tubules are working fine in cases of prerenal azotemia, so you actually end up wasting K+ and H+ in the collecting ducts, leading to a metabolic alk.

Pretty sure you can't call a metabolic alkalosis with a HCO3 of 16. Though I'm sure a urologist could probably come up with something.

Without over thinking the answer you can get rid of respiratory problems, if the BUN/Crea ratio is that high it most likely has nothing to do with respiratory. Another way to eliminate, if you have respiratory acidosis I would expect RR to be lower and HCO3 to compensate (if not acute) at very least be in normal limit. Respiratory alkalosis is almost always an acute issue and the kidneys/HCO3 usually don't have time to compensate for the decrease in CO2.

 

[addo]

So spironolactone does cause metabolic acidosis... in that case its hard to make a case for metabolic alkalosis.

 

[Jamiu22]

So spironolactone does cause metabolic acidosis... in that case its hard to make a case for metabolic alkalosis.

You are right....

Lessons learned is that, although...the question makes the case for pre renal azotemia....the labs say that the kidneys damaged...and you have metabolic acidosis. We shouldnt really overthink it.

 

[withrye]

I think the answer is actually metabolic alk. The tubules are working fine in cases of prerenal azotemia, so you actually end up wasting K+ and H+ in the collecting ducts, leading to a metabolic alk.

My bad, I basically answered the question about prerenal azotemia without looking at the actual question. Since it's asking for an acid-base disturbance and the bicarb is low, it's either metabolic acidosis or compensated respiratory alk, and based on his rate of breathing it can't be resp alk, so it must be met acidosis.

 

[USCTrojan11]

Can we get an official answer from the source - this just isn't cool

 

[natxbug]

two months later.. just in case anyone still cares:

USMLE website says the correct answer is Metabolic Acidosis (it's one of the practice questions)

 

[Dream-2-Reality]

I believe the answer is (A) Metabolic Acidosis - you can't get rid of potassium since the kidney is damaged... so you tend to retain a lot more H+, while getting rid of HCO3... over time though you would get (D) Respitatory Alkalosis as a compensatory mechanism... but it's still primarily (A).

This makes sense, is this correct explanation?

 

[thehundredthone]

This makes sense, is this correct explanation?

More or less. This is secondary hypoaldosteronism. The hyperkalemia due to spironolactone's effect on potassium is central to everything here. What the hyperkalemia does is create a relative intracellular alkalosis. This means that less HCO3- is reabsorbed, and also that NH4+ excretion is impaired, leading to H+ retention and acidosis. The secondary hypoaldosteronism also explains the hyponatremia, and hence the non gap acidosis.

If you want corroborative evidence, the respiratory rate of 19 isn't really enough to cause alveolar hyperventilation that would lead to metabolic alkalosis, which would be the only other explanation for an HCO3- of 16 mEq, which would also need a primary pCO2 of 20 mmHg (and he'd appear much worse off).

A pH would definitely have made the picture clearer. After looking at the pH and confirming that it's acidosis, there are only a few considerations when it comes to the overall picture.

1. If the HCO3- is down, it's metabolic acidosis.
2. If the pCO2 is up, it's respiratory acidosis.
3. If both of the above are present, it's a mixed respiratory and metabolic acidosis.

Beyond that, if they ask you about compensation, then you start to look at the relative change in each of the two values. If it's mixed, there is no question of compensation.