[Na+] = 140 mEq/L

[Na+] = TB Na^₊ content/TBW

4 mEq/L

 >98% of total body K+ is intracellular*

Insulin promotes uptake of K+ into cells (Insulin brings K+ In), Epi and high plasma levels of K+ also promote uptake.

Aldosterone and high plasma levels of K+ promote K+ excretion in the kidneys.

P_K+ is inversely proportional to HCO₃- reabsorption and to NH₄⁺ excretion*

GFR = LpS (ΔP - Δtau)

Where Lp =Capillary wall pressure, S = Glomular capillary SA avail for filtration, ΔP = hydrostatic P gradient between the capillary and Bowman's space, and Δtau = oncotic P gradient between capillary and Bowman's space.

GFR = U_in x V / P_in

C_x (ml/min) = (U_x x V)/P_x

Represents the volume of plasma cleared of substance x via elimination into the urine per unit time.

Clearence of Water

If C_H2O >0 urine is hypotonic (you are clearing water so the osmolarity of urine must be more than the osmolarity of plasma).

If C_H2O = 0 urine is isotonic.

If C_H2O < 0 urine is hypertonic because the osm of plasma is less than the osm of urine.

Clearance Ratio of x = C_x / GFR

The clearence ratio of a substance tells you what the kidneys are doing with it!
If CR > 1 the substance is being actively secreted.

If CR < 1 it suggests that resorption is occuring.

If CR = 0 the substance is either too large to be filtered or is completely resorbed (like Glc or amino acids)

An estimate of renal plasma flow (RPF)

C_PAH = RPF = U_PAH x V / P_PAH

Normal RPF = 600 mL/min

FF = GFR/RPF

Normal FF (based on NL GFR of 120 and NL RPF of 600) = 0.2

About 20% of RPF becomes GFR

[H+] = 24 (PaCO₂/[HCO₃-])

NL (@pH 7.4) = 24 nanoEq/L

Remember theat the kidneys control HCO₃- and the lungs control CO₂*

Short Cut:

[H+] ~ 80 - decimal digits of the pH

Ex: @pH 7.33, [H+]~ 80 - 33 = 47

pH = 6.1 + log ([HCO₃-] / (.031 x PCO₂))

pH = pKa + log ( [A-] / [HA])

CO₂ + H₂O >< H₂CO₃ >< H⁺ + HCO₃-

In acute respiratory conditions, for every change (↑ or ↓) in pCO2 by 10, there is a concurrent/compensatory ↑ or ↓ of HCO3- by 2 (if the change in HCO3- is much greater than 2 this it is a chronic condition!) Remember that for respiratory Acid Base disturbances you must specify Acute or Chronic.

*Remember that in Acid Base disturbances that pCO2 and HCO3- always move in the same direction.

NL HCO₃- = 24 mEq/L

P_AG = (P_Na+) - (P_Cl- + P_HCO3-) = Unmeasured anions (lactic acid, ketones, ethylene glycol, albumin) - Unmeasured cations (Ca2+, Mg2+)

NL P_AG = 10-12

Calculate in any case of metabolic acidosis.

If gap exists (greater than 12) the cause of the acidosis is due to a ↓ in unmeasured cations (K+, Mg, Ca), an ↑ in unmeasured anions (phosphates, ketones, lactic acid) which may be due to renal failure keto or lactic acidosis or ingestion of asprin, ethylene glycol, or methanol.

A measure of the number as well as the weight of solute particles present (the weight of a solution comapared to the weight of an equal volume of distilled water).

Ranges between 1.002 (when urine is its most dilute) to 1.040 (very concentrated urine)

Total body content of Na+ = TBW (L) x P_Na+

For a 70 kg man with normal sodium levels (140 mEq/L) total body content of sodium = (70 x 0.6) x 140 mEq/L = 42 L x 140 mEq/L = 5,880 mEq Na+ total

Trans-Tubular Potassium Gradient

TTKG=(U_K+/P_K+)/(U_osm/P_osm)=

(U_K+ x P_osm)/(U_osmx P_K+)

In the face of Hypo or Hyperkalemia, this ratio tells you whether or not K+ is being appropriately excreted (whther or not the mineralocorticoids are working correctly).

If pt is hypokalemic TTKG should be < 2

If they are hyperkalemic, TTKG should be > 8

Note that these measures are only accurate if the plasma sodium is > 20 mEq/L and the Uosm < 300

FWD = TBW x [(Current P_Na+/Desired P_Na+) - 1]

Desired P_Na+ = 140 mEq/L

Remember that water lost is from TBW so to find the change in ECFV multiply by .33 (1/3 of TBW is extracellular) and of ECFV 1/4 is plasma and 3/4 is interstitial volume.

TBW = 0.6 x weight

ICFV = 0.4 x weight

ECFV = 0.2 x weight

2/3 of TBW is intracellular.

1/3 of TBW is therefore extracellular.

Within the ECFV 3/4 is interstitial and 1/4 is plasma volume.

~ 2 [Na+] (solid estimate)

but to be complete = 2[Na+] + (BUN/2.8) + (Glc/18)

Remember that P_Osm always = Intracellular Osm

NL range = 275 - 299 Osm/kg

Mnemonic: KUSMAL

Ketones (in DKA),

Uremia (in renal failure),

Salicates (in aspirin OD),

Methanol (wood alcohol, desperate alcoholics),

Alcohols (rubbing or other),

Lactic Acid (in ischemia/shock)

If there is metabolic acidosis without a P_AG the next step is to calculate the urine anion gap:

U_AG = (U_Na+ + U_K+) - (U_Cl-)

Note that K+ must be included here and that bicarbonate is not considered*

The presence of a negative urine anion gap tells you that the kidneys are functioning as they should and excreting excess chloride (the anion to NH4+) in response to the acidosis and therefore that the problem lies outside the kidney (usually GI as in diarrhea).

If there is no urine anion gap the kidneys are malfunctioning and are likely the source of the acidosis (as in RTA).

Check Urine [Cl-]

If the kidneys are losing Cl- (U_Cl- > 10) the problem is renal. If U_Cl- < 10 the problem is more likely to be GI.

Acidosis:

Carbonic Anhydrase Inhibitors (decrease HCO3- reabsorption) and K+ Sparing diuretics (blockade of aldosterone causes retention of H+ and K+. Increased [K]+ also drives K+ into cells in exchange for H+.

 Side Note: Laxatives cause acidosis*

Alkalosis:

Loop Diuretics and Thiazide Diuretics (volume contraction triggers AT II release which increases Na+/K+ exchange at the PCT which promotes HCO3- retention. Loss of K+ drives K+ out of cells in exchange for H+)

Fractional Excretion of Na+ = (U_Na+ x P_Cr) / (U_Cr x P_Na+)

Gives you information on the nature of renal failure.

If  FE_Na+ is....

MCC of Acute Renal Failure;

Muddy Brown Casts, skip lesions in the tubules, and a FE_Na+ >2% suggest ATN;

Causes are either Ischemic (RAS, hypovolemia, shock) or Toxic (Abx like methicillin, ethylene glycol, Hb/Mb as in rhabdomyolysis)

Dysfunctional Proximal Tubule (MCC by cystinosis, a lysosomal storage disease that damages the kidneys but can also be caused by other GSDs, metals, and Wilson's disease);

Urinary loss of aa, Glc, phosphate, uric acid, and bicarbonate;

Presents as Hyperchloremic, Hypokalemic, metabolic acidosis often w/ muslce cramps, polyuia, fatigue, rickets and elevated ALP;

RTA II and hypophosphatemic rickets can be present

Autosomal Recessive disorder of the Distal tubule;

Defect in the Na/K/2Cl pump and the K+ back transporter;

Mimics the effects of a loop diuretic;
Causes hypochlremic metabolic alkalosis (huge loss of volume activates RAAS which causes Na+ retention with wasting of K and H. As bicarb up, Cl- down);

Hypokalemic, hypercalcuria, hyperaldostronism, hyperplasia of the JG cells;

Clinically there is polyuria/polydipsia, hypercalcuria and possible nephrocalcinosis.

Disorder of the Distal tubule (milder form of Bartter's);

Mutation in the Thiazide-sensitive transporter in the DCT (the Na+/Cl- symporter) which has thiazide-like effects;

Produces hypochloremic metabolic alkalosis like Bartter's but also has significant hypomagnesemia (loss of Mg in urine) but overall is less sympotmatic since less sodium is conserved in the DCT than in TAL.

Normal Anion Gap, Positive Urinary Anion Gap Metabolic Acidosis conditions*

Type I: Distal - failure to secrete ammonia (NH₄Cl). Hypokalemic, hyperchloremic, metabolic acidosis. U_HCO3-/P_HCO3- < 8%. High urinary pH (acid can't get into urine) > 5.5, Increased urine Calcium.

Type II: Proximal - failure to reabsorb bicarbonate (bicarb wasting in the urine). Hypokalemic metabolic acidosis. Urine pH is still < 5.5

U_HCO3-/P_HCO3- > 8% (often up near 15%)

Type IV: Aldosterone Deficiency (Hypoaldosteronism) causing a physiological reduction in ammonium secretion. Hyperkalemic metabolic acidosis (milder).

U_HCO3-/P_HCO3- < 8%

GFR = ([140 - pt age] / Serum Cr) x 0.85

0.85 is the correction factor for women, for men it is (?)

Plasma Osm Gap = Measured Osm - Calculated Osm

Useful for screening for the presence of unmeasured low MW osmotically active particles (alcohols, glycine, mannitol etc...)

Drugs,

Pyelonephritis,

SLE,

Sjoren's Syndrome,

Ca/urate/oxylate crystal deposition,

heavy metal poisoning,

lymphoma/myeloma,

adult polycystic kidney dz.

Beta lactams,

Cephalosporins,

Rifampin,

Aminoglycosides (Gentamicin),

Furosamine and Metolazone (sulfonamides),

Cimitidine (H2 antag),

Allopurinol.