BMP Masterclass

###Learning goals:

rebuild an understanding of electrolyte balance from the clinical application to the scientific / physiology (as opposed vice versa)
generate a better understanding of the gaps of our routine labs in assessment of the body's ability to maintain homeostasis

You're a physician in the early days of medicine and you need to come up with 7 tests to interrogate renal function... what do you choose? How did medicine arrive at the tests we did?

Sodium

surrogate for osmolality / tonicity of the serum.

When is this misleading?

of course this goes wrong if there is another major source of osmolality, such as alcohol / glucose / contrast

Potassium

important in the functioning of nerve cells (particularly the resting membrane potential)

Chloride

allows for calculation of the anion gap (characterize what anions on present in the blood, which is especially important to differentiate the different types of causes of metabolic acidosis)
Post-SMART trials, now understood to additionally be inherently renal-toxicity (vasoconstriction, predisposes to vasoconstriction)

Is Saline Nephrotoxic? Curious Clinicians

Bicarbonate

Does a high or low bicarbonate indicate that there must be a metabolic alkalosis or acidosis present?

Yes: under Stewart conception of acid base, the serum bicarbonate allows you to assess whether there is a metabolic acidosis or alkalosis present (though, it does not tell you if it is primary or compensatory - this requires a blood gas)

Keep in mind: Acid removal...

30 - 60 mg of fixed acid is removed in kidney
14,000 mg of volatile acid (CO2 via bicarbonate buffer system) is removed by the lungs

BUN

What information does the BUN give you that the creatinine doesn't?

it is reabsorbed in the tubules, so the BUN / creatinine ratio can tell you about how much the kidneys are trying to hold on to volume.
nitrogen balance (e.g. in a catabolic state such as with high dose steroids, BUN will go up. Also, in a GI bleed where

sCr

Allows for estimation of glomerular filtration rate, as it is not reabsorbed (it is somewhat actively secreted). What are the major roles of kidney's work to maintain hemostasis that are not interrogated by sCr?

tubule function (e.g. ability to reabsorb electrolytes)
function of filtration unit (GFR = amount filtered, not type of things filtered... e.g. is albumin getting through?)

Glucose

allows us to interrogate the insulin-glucagon axis functioning, as well as additional information on osmolality (e.g. in HHS where your sodium is likely low but overal osmolality is high due to all the glucose)

Calcium

role in clotting
role in nerve functioning

Albumin

surrogate for oncotic pressure in the vessels.

Other Acid Base

Metabolic Alkalosis

Chloride depletion alkalosis formerly known as contraction alkalosis - JASN

Key point: volume depletion is not required to maintain the alkalosis (just chloride depletion). So, metabolic alkalosis after diuretics should not be used as sole indication of adequate diuresis. Keep going (add acetazolamide if problematic)

Urine chloride measurement = surrogate for if chloride responsive or no.

Metabolic Acidosis

Anion gap - GOLDMARK

Non-anion gap

Urine anion gap

Surrogate for NH4+ excretion, which is the way that the urine gets rid of excess H+