NP11 Nephrology

Electrolyte Disorders

Essential Med Notes 2015

DIABETES INSIPIDUS
collecting tubule is impermeable to water due to absence of ADH or impaired response to ADH
defect in central release of ADH (central DI) or renal response to ADH (nephrogenic DI)
Etiology
central DI: neurosurgery, granulomatous diseases, trauma, vascular events, and malignancy
nephrogenic DI: lithium (most common), hypokalemia, hypercalcemia, and congenital
Diagnosis
urine osmolality inappropriately low in patient with hypernatremia (Uosm <300 mOsm/kg)
serum vasopressin concentration may be absent, low (central), or elevated (nephrogenic)
dehydration test: H2O deprivation until loss of 3% of body weight or until urine osmolality rises
above plasma osmolality; if urine osmolality remains <300 (fails to concentrate urine), most
likely DI
administer DDAVP (exogenous ADH) (10 g intranasally or 2 g SC or IV)
central DI: diagnosed if there is rise in urine osmolality, fall in urine volume
treat with DDAVP
nephrogenic DI: exogenous ADH fails to concentrate urine as kidneys do not respond
treat with water (IV D5W or PO water), thiazides may help as well (reduced ECF volume
stimulates proximal tubular reabsorption of sodium and water, leading to less delivery
of glomerular filtrate to ADH sensitive parts of renal tubule, and therefore lower urine
volume results)

Potassium Homeostasis
approximately 98% of total body K+ stores are intracellular
normal serum K+ ranges from 3.5-5.0 mEq/L
in response to K+ load, rapid removal from ECF is necessary to prevent life-threatening
hyperkalemia
insulin, catecholamines, and acid-base status influence K+ movement into cells
aldosterone has a minor effect
potassium excretion is regulated at the distal nephron
K+ excretion = urine flow rate x urine [K+]
Factors which Increase Renal K+ Loss
hyperkalemia
increased distal tubular urine flow rate and Na+ delivery (thiazides and loop diuretics)
increased aldosterone activates epithelial sodium channel in cortical collecting duct, causing
Na+ reabsorption and K+ excretion
metabolic alkalosis
hypomagnesemia
increased non-reabsorbable anions in tubule lumen: HCO3, penicillin, salicylate

Hypokalemia
serum [K+] <3.5 mEq/L

Normal

U wave

U wave progression

Figure 6. ECG changes in hypokalemia

Andrea Cormier

Signs and Symptoms

usually asymptomatic, particularly when mild (3.0-3.5 mEq/L)
N/V, fatigue, generalized weakness, myalgia, muscle cramps, and constipation
if severe: arrhythmias, muscle necrosis, and rarely paralysis with eventual respiratory
impairment
arrhythmias occur at variable levels of K+; more likely if digoxin use, hypomagnesemia, or CAD
ECG changes are more predictive of clinical picture than serum [K+]
U waves most important (low amplitude wave following a T wave)
flattened or inverted T waves
depressed ST segment
prolongation of Q-T interval
with severe hypokalemia: P-R prolongation, wide QRS, arrhythmias; increases risk of
digitalis toxicity

Na+ = predominating extracellular ion

K+ = predominating intracellular ion