Azotemia, Pre-renal failure, K+ levels

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metview

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In azotemia, I understand that K+ and H+ levels increase due to decreased GFR (is this correct?)

However, in pre-renal azotemia, I thought the RAAS system is activated because of the low kidney perfusion? Wouldn't this increase aldosterone levels --> hypokalemia and metabolic alkalosis?

Please help. Thank You!
 
In azotemia, I understand that K+ and H+ levels increase due to decreased GFR (is this correct?)

However, in pre-renal azotemia, I thought the RAAS system is activated because of the low kidney perfusion? Wouldn't this increase aldosterone levels --> hypokalemia and metabolic alkalosis?

Please help. Thank You!

The RAAS takes many hours to kick in and have an appreciable effect. And if you're not filtering because of decreased renal perfusion then K+ and H+ will be high no matter what aldosterone tries to do. The hallmark of renal failure is high H+ (low HCO3-, low pH), high K+ (due to decreased filtration and cellular exchange due to acidosis), variable Na+ (but often high), high phosphate, low calcium.

The USMLE likes heart failure as a cause of pre-renal failure. Sepsis and shock can cause renal hypoperfusion, but they can also lead to ATN (intra-renal failure).

So always always always, no matter what the clinical picture/aetiology appear to be, look at the BUN/Cr ratio in the question. Sometimes hypoperfusion in a vague question will have <20 and you know it's ATN, not pre-renal.

And HY for Step 2 is IV contrast causing renal failure can lead to ATN, but it also notably causes spasm of the afferent arterioles, leading to pre-renal failure. So if you get a question on IV contrast, the answer is fractional excretion of sodium <1%, urine osmolality >550 (both pre-renal findings).

Also, if the USMLE tells you a patient in distress with high Na+, high K+ and low HCO3- has his or her clinical picture improved with a drug, angiotensin might be the answer (that's right, not angiotensin I or angiotensin II, they might just say angiotensin). Angiotensin receptor agonism constricts efferent arterioles, thereby increasing GFR and mitigating a renal failure presentation.

The USMLE also likes uremic pericarditis as a sequela of renal failure.

The USMLE also likes uremic platelet dysfunction as a sequela of renal failure. This is a qualitative, not quantitative, effect. Platelet number is normal in isolated renal failure but function is impaired.
 
Just some thoughts..

Complete uremia sequelae(compiled from kaplan/FA/Uworld : 1)Pericarditis (probably fibrinous) 2)Reduced platelet function ( Increased bleeding time ) , 3)ARDS , 4) Paralytic Ileus , 5) Reduced peripheral conversion of T4 to T3--> Functional hypothyroidism 6)encephalopathy/asterixis(affects TCA cycle in neurons and accumulation of glutamine and some degree of cerebral edema)


also don't confuse azotemia with uremia … 1)Azotemia --> Increased NH3 in blood
2) Uremia --> Clinical syndrome attributed to increased NH3 in blood
 
Last edited:
Just some thoughts..

Complete uremia sequelae(compiled from kaplan/FA/Uworld : 1)Pericarditis (probably fibrinous) 2)Reduced platelet function ( Increased bleeding time ) , 3)ARDS , 4) Paralytic Ileus , 5) Reduced peripheral conversion of T4 to T3--> Functional hypothyroidism 6)encephalopathy/asterixis(affects TCA cycle in neurons and accumulation of glutamine and some degree of cerebral edema)


also don't confuse azotemia with uremia … 1)Azotemia --> Increased NH3 in blood
2) Uremia --> Clinical syndrome attributed to increased NH3 in blood

For the last part I thought you were going to say don't confuse uremia with hyperuricemia, which isn't uncommon.
 
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