1. HYPONATREMIA

2. What is the Osmolality? Osmolality Normal High Low Hypertonic HypoNa+ Causes an osmotic shift of water out of cells ↑ glucose Mannitol use Isotonic HypoNa+ (pseudohypoNa+) Lab error – sodium is miscalculated ↑ proteins ↑ lipids The real deal!

3. Hypotonic Hyponatremia Assess Volume Status HypovolemicEuvolemicHypervolemic √ Urine Sodium√ Urine Osm√ Urine Sodium Renal loss U Na > 20 Extra Renal U Na < 10 U osm >100 SIADH HypThy ↓ cortisol U osm var Reset Osmmostat U Na < 10 CHF Cirrhosis Nephrosis U Na > 20 Renal failure U osm <100 1° polydyp Low solute

4. Treatment If hypovolemic – give fluids If severe symptomatic hyponatremia –Give 3% saline –Rate of correction not to exceed 0.5mEq/L/h –2mEq/L/h for the first 2-3 hours for life threatening symptoms –Not more than 10-12mEq/L/d –Central pontine myelinolysis!

5. SIADH Find out the underlying cause Fluid restriction AVP receptor antagonists –Conivaptan (IV) –Tolvaptan (oral) Demeclocycline & Lithium – inhibits ADH What will happen to the Na + level if you give Normal Saline?

6. Hypernatremia

7. Basics Water deficit relative to Sodium All patients are hypertonic Check Volume Status

8. Hypernatremia Assess Volume Status HypovolemicEuvolemicHypervolemic √ Urine Sodium √ Urine Osm Renal loss U Na > 20 U osm 300-600 Extra Renal U Na < 20 U osm > 600 U osm <300 Complete DI U osm > 600 Intracell osmole generation U osm 300-600 Partial DI Exogenous hypertonic saline Minerelocorticoid excess

9. Treatment - hypovolemic Calculate free water deficit –Male patient = [Na] serum – 140 x 0.6 140 –Male patient = [Na] serum – 140 x 0.5 140 Infusate: 1/2NS to D 5 W (free H 2 0-orally) Correction should not exceed 0.5mEq/L/h Cerebral edema!

10. Treatment - DI Central: desmopressin Nephrogenic: –Treat underlying cause if possible –Na restriction + thiazide diuretics

11. Treatment - hypervolemic D 5 W with loop diuretics

12. Potassium Homeostasis

13. Overview Renal – K + excretion regulated by collecting tubule –Increased distal Na+ delivery and urine flow – increased Na+ absorption – lumen electronegative – K+ excretion –Aldosterone: Na+ absorption & K+ excretion Transcellular shifts: most common mechanism in ΔK+ –Acid-base disturbance –Insulin – stimulates Na-K ATPase –Catecholamines – stimulate Na-K ATPase –Digoxin – blocks Na-K ATPase –Tissue breakdown –Hypo or hyperkalemic periodic paralysis - rare

14. Transtubular Potassium Gradient Ratio – tubular K : plasma K Normal 8 to 9 Assumptions –That the urine osmolality at the end of the cortical collecting tubule is similar to that of the plasma, since equilibration with the isosmotic interstitium will occur in the presence of antidiuretic hormone –That little or no potassium secretion or reabsorption takes place in the medullary collecting tubule

15. This formula is relatively accurate as long as –the urine osmolality exceeds that of the plasma (so that the potassium concentration at the end of the cortical collecting tubule can be estimated) –and the urine sodium concentration is above 25 meq/L (so that sodium delivery is not limiting)

16. Hyperkalemia – estimate the degree ro aldosterone activity –Kidneys should try to loose the K+ –TTKG should increase Hypokalemia – assess if kidneys are loosing the K+ –Kidneys should try and conserve K+ –TTKG should decrease