Increased delivery of bicarbonate to the distal nephron obligates a cation. In the setting of increased aldosterone levels, sodium is retained and potassium excreted.
Potassium loss is most prominent early.
Actual losses in gastric juice are relatively small.
Diarrheal losses are usually accompanied by metabolic acidosis
Sweat losses- 5 – 10 mEq/L
The kidney and potassium
Nearly all potassium filtered at the glomerulus is reabsorbed in the proximal nephron. Urinary potassium is the result of distal potassium secretion.
To excrete potassium, the kidney requires an adequate number of nephrons, aldosterone, and a circulation adequate to provide adequate distal delivery of sodium for sodium/potassium exchange.
Renal losses of potassium
Diuretics- activate the renin-angiotensin-aldosterone cascade.
Primary aldosteronism/increased steroids.
Presentation of a non-resorbable anion distally, obligating a cation, which will lead to increased potassium excretion in the presence of aldosterone.
Renal losses of potassium
Renal tubular acidosis
Proximal, especially with therapy
Some distal types
Type IV RTA patients are typically hyperkalemic
What data do we want to diagnose the cause of hypokalemia in this pt?
Urinary potassium: 24 hour values better than spot specimens.
Aldosterone and renin levels.
Blood pressure measurements.
Potassium is being lost in the urine.
Primary aldosteronism is r/o by normal blood pressures.
ABG r/o renal tubular acidosis.
Diuretic abuse R/o history
Bartter’s and Gitelman’s syndromes
Bartter’s syndrome is usually diagnosed in childhood, sometimes associated with growth and mental retardation. The defect is impaired NaCl reabsorption in the loop of Henle. Findings are similar to administration of a loop acting diuretic:
Salt loss leading to volume depletion and activation of the renin-angiotensin system
Increased urinary calcium
Bartter’s and Gitelman’s Syndromes
3 or 4 types of Bartter’s have been identified:
Defects in the luminal Na-K-Cl transporter
Defects in the luminal potassium channel
Defects in the basolateral chloride channel
Like Bartter’s an autosomal recessive disorder, but not usually diagnosed early in life.
Findings mimic administration of a thiazide diuretic: the defect is in the Na-Cl transporter.
Patients may complain of polyuria, cramps.
They do not have hypercalciuria, but typically have low serum magnesium levels.
Diagnosis is made by history as well as lab findings. Lab findings are indistinguishable from thiazide use:
Hypokalemia, hypomagnesemia, increased renin and aldosterone levels, decreased urinary calcium.
1: Clin Nephrol. 2001 Mar;55(3):233-7. Related Articles, Links
Mimicry of surreptitious diuretic ingestion and the ability to make a genetic diagnosis. Schepkens H , Hoeben H , Vanholder R , Lameire N . Department of Internal Medicine, University Hospital Gent, Belgium. firstname.lastname@example.org Gitelman's syndrome, also known as "hypocalciuric variant of Bartter's syndrome", is a cause of chronic hypokalemia and hypomagnesemia in adults. A specific gene has been found responsible for this disorder, encoding the thiazide-sensitive NaCl coporter (TSC) in the distal convoluted tubule. We describe a psychiatric patient with chronic symptomatic hypokalemia and hypomagnesemia whose electrolyte disturbances were subsequently misdiagnosed as an acute alcohol and benzodiazepine withdrawal syndrome, as chronic diuretic abuse and as a classical Bartter's syndrome. Finally, genetic investigation revealed the presence of mutations in the SLC12A3 gene leading to the proper diagnosis of Gitelman's syndrome. We emphasize that Gitelman's syndrome should be suspected in every hypokalemic patient with biochemical resemblance of diuretic ingestion, especially when repeated toxic screens for diuretics are negative. The ability to make a molecular-genetic diagnosis can be of practical benefit in confusing clinical settings.
Gitelman’s syndrome: treatment
Aldactone or amiloride
NSAIDS of no benefit
General comments about the treatment of hypokalemia
Think about the cause of the hypokalemia you are treating? A cellular shift, e.g. hypokalemic periodic paralysis, will require a lot less potassium to correct than hypokalemia from potassium loss.
Orally or i.v.? Orally is safer; limit i.v. repletion to 20 mEq./hour except in very unusual circumstances- then monitor.
Anticipate: has K+ loss stopped or will it be ongoing?
Are you giving other drugs that will influence K+ levels? E.g. NSAIDs, ACEIs, ARBs.
Generally, use KCl vs. other preparations.
Followup with repeat levels- consider using the replacement protocols.