1. A beautiful explanation of the delta-delta ratio. 
- In brief:
- Delta gap/delta bicarb = absolute value (12 - measured gap) / absolute value (24 - bicarb)
- Firstoff: only some acids cause a gap-- the organic unmeasured anions. Acidemia caused by HCl (generated by diarrhea perhaps 2/2 Cl-/HCO3- transporters?) will not give you a gap because Cl is in the equation to calculate the gap.
- If you buffer every molecule of an organic acid with bicarb, you would expect to gain 1 organic acid for the loss of every bicarb (in reality because you buffer from bone and cells, you gain more organic acid than you lose bicarb... its like 1.6 acid for 1 bicarb. With ketoacidosis, you excrete the ketones pretty efficiently, while in lactic acidosis you often get a pre-renal azotemia 2/2 shock etc)
- But if you're losing way more bicarb than you would expect given the gap (caused by organic anions), that means there's another acid, that is not causing a gap, that is buffering away your bicarb-- i.e. HCl from diarrhea or renal failure. In this case, your measured bicarb is LOW. So if your measured bicarb is low, the denominator in your equation is HIGH, so your delta-delta will be LOW - <1.
- If you're losing way less bicarb than you would expect given the gap, that means something is giving you bicarb-- i.e. there's a concurrent metabolic alkalosis. In this case, you expect your bicarb to be high, which means your denominator will be LOW, which means you'll have an increased delta-delta (>2).
TL; DR: delta-delta <1 = concurrent non-gap acidosis, delta-delta > 2 = concurrent metabolic alkalosis.
2. Non-gap acidosis - is it renal or extrarenal? 
- If you're acidotic because your kidneys are retaining acid, you will expect low ammonium in your urine (ammonium is one way kidneys get rid of H+)
- If you're acidotic because an extrarenal process (say, you're losing bicarb through diarrhea) you expect your kidneys to compensate by increasing excretion of H+, ie. more ammonium in your pee.
- You can't generally measure urine NH4, but you can count it as an unmeasured cation and calculate the urine gap.
- Urine gap = Urine cations - Urine anions.
- Urine gap = Urine Na+K - Urine Cl.
- If there's tons of NH4 in your pee, there's tons of unmeasured cations, and you expect the Cl to be way high relative to Na and K, and you'll get a big, negative urine gap
- If there's little NH4 in your pee, the unmeasured cation is low, and you expect Na and K to be higher relative to Cl.
- Normal UG = 30-50
TL; DR: Urine gap high = renal, urine gap negative = extrarenal
3. Anion gap acidosis - is it alcohol or ethylene glycol? Calculate the osmolal gap.
- Osm gap = abs value (calculated osm - measured osm)
- Calculated osm= 2*Na + Glucose/18 + BUN/2.8
- Elevated osm gap = umeasured osmole in the blood, could be ethanol or ethylene glycol.
- Ethylene glycol: will see renal injury and calcium oxalate crystals in the urine.
4. Hyponatremia: 
- Can occur with decreased arterial perfusion ie. dehydration (blood vessel baroreceptors will stimulate ADH, even if Na is low-- your brain will sacrifice Na balance for perfusion volume) or CHF/cirrhosis/nephrotic syndrome-- i.e. decreased effective renal perfusion.
- Can occur with increased plasma solutes-- i.e. hyperglycemia will cause increased plasma osmolality, will cause water to leave cells and dilute plasma. {correction calculator} {data source - NEJM 1999}
- Pseudohypernatremia can occur when you have a significant amount of protein (hyperglobulinemia) or triglycerides in the blood, which will take up space and decrease the amount of plasma, leading to a falsely low measured Na.
5. Acetazolamide: blocks carbonic anhydrase IV, increases loss of urine bicarb and K => hypokalemic metabolic acidosis. Alkalinizes urine, thus increases secretion of weakly acidic drugs like salicylates and barbituates. (To acidify urine, give NH4Cl, helps excrete weak bases/tertiary amines like cocaine and amphetamines)
6. Kidneys and K: 
- Generally you don't get hypokalemic from renal disease until your GFR < 15, without the addition of aggravating factors like NSAID use.
- Thiazide diuretics are ineffective once your GFR < 30
- In the setting of hypokalemia, urine K < 20mEq/L suggests that the kidneys are adequately recovering K, implying extrarenal losses. Urine K > 20 mEq/L suggests renal losses.
7. Management of hyperkalemia: consideration of time: 
- Calcium gluconate for membrane stability - onset in 2-3 minutes
- Sodium bicarb for intracellular shift of K - onset in 10 minutes
- Albuterol - onset in 15-30 minutes
- Insulin/Glucose - onset in 30 minutes
8. Central vs nephrogenic DI: give desmopressin (selective AVP V2 receptor agonist) 1 to 2 ug subQ or IV, or give vasopressin (nonselective) 5U subQ
9. Sarcoid & Calcium
- Activated mcrophages in sarcoid granulomas secrete 1a-hydroxylase, which is the renal enzyme that converts 25-OH vitamin D to 1,25-OH vitamin D.
- Treat with steroids.
10. Phosphate
- Hypophosphatemia can develop in chronic alcoholics (decreased PO intake, vomiting, also ethanol directly stimulates kidney tubules to secrete phos)
- Often occurs 12-24 hours after admission; worsened by administration of IV glucose (stimulates insulin production, which pushes phos into cells-- also seen with refeeding syndrome)
- Sx: confusion, rhabdo, hemolysis, weakness - including weakness of respiratory muscles.
- You need phos to make ATP; without it, your ion pumps fail.