Case of a drunk with hypokalemia, hypomagnesemia, refeeding syndrome and beer drinkers potomania. (Keynote, PDF)
FERE: Fractional excretion of random electrolytes
Magnesium:
- 142 controls: 1.8% (range 0.5-4%)
- 74 hypomagnesemic
- Extra-Renal origin 1.4% (range 0.5-2.7%)
- Renal origin 15% (range 4-48%)
- Authors conclusion: >4% per cent is indicative of inappropriate renal magnesium loss
Potassium
- 312 normal subjects: 8% (range 4-16%)
- 84 hypokalaemic patients
- Extra-renal origin: 2.8% (range 1.5-6.4%)
- Renal origin: 15% (range 9.5-24%)
- Authors conclusion: >6.5% per cent is indicative of inappropriate renal potassium loss
Gitelman syndrome and Pregnancy
One of my Gitelman patients (whom I kidding, “one of my Gitelman patients”, how about “my only Gitelman patient”) finally got pregnant. We had been managing her with amiloride and a truck load of oral potassium and magnesium supplements. I was shocked to find that amiloride is acceptable in pregnancy with a track record of successful births. Prior to starting amiloride the patient was taking twenty-eight 20 mEq pills of KCl a day. She abandoned her prior nephrologists when she was told to further increase her potassium pills.
 |
| from UpToDate |
We are now using magnesium sulfate infusions 4 grams twice a week to keep her magnesium north of zero. She was able to keep her magnesium around 1.4 with oral supplements and amiloride prior to being pregnant but now, despite 8 grams of weekly IV magnesium her magnesium is sitting around 1.1. This probably represents one of downsides of the up-regulated GFR of pregnancy.
Interestingly, she saw her labs and saw that her sodium was 132. Modest hyponatremia is a normal finding in pregnancy, so she decided to increase her dietary sodium intake. Bad move, increased renal sodium loads increases renal magnesium losses. Her serum mag fell 30% to 0.8.
The highest aldosterone I have ever seen
Patient came to me with hypokalemia and hypomagnesemia. She had been asymptomatic when she underwent routine pre-op labs for an elective procedure. Her potassium was 2.0 and the magnesium was later discovered to be 0.9 mmol/L.
She had been treated for 5 months with supplemental potassium and magnesium before she found her way into my office.
During her initial work-up we found:
- Aldosterone: 61.2
- Renin: 12.4
- Trans-tubular potassium gradient: 15.98
- Diuretic screen: negative
- 24-hour urine calcium: 57 mmol
Her blood pressure was 120s over 80s on 5 mg of amiloride daily. Her volume status appeared essentially normal.
No renal vascualr disease by MRA, normal CT scan of the abdomen (no renin producing tumor). She was not on aldactone.
Diagnosis: Gitelman’s syndrome.
The principle characteristics of Gitelman’s are: low potassium, low magnesium, initially presenting in adolescence or adulthood. Patients have normal growth. Blood pressure is low. When I first learned about Bartter’s and Gitelman’s I imagined them as congentital diuretics:
- Bartter’s is congenital Lasix
- Gitelman’s is congenital HCTZ
The conditions can be understood nearly completely with this crude model. They both have low blood pressure as can be expected from a diuretic-like action. The low blood pressure triggers the renin-angiotensin-aldosterone system resulting in high plasma levels of renin and aldosteronism. In primary hyperaldosteronism, renin is suppressed.
Increased distal delivery of sodium along with increased aldosterone levels leads to increased potassium and hydrogen wasting leading to metabolic alkalosis and hypokalemia.
The two diseases differ in a few areas. Bartter’s results in decreased concentrating ability while concentrating ability is generally intact in Gitelman’s. This is predictable as the Loop of Henle is the engine which drives urinary concentrating and diluting ability. Gitelman’s has a low urinary calcium just as found with thiazides.
What was remarkable to me, was how high the aldosterone level was. This is in a patient without adrenal disease, the aldosterone is released in response to normal stimuli, volume depletion in this case. In primary aldosteronism, where there is autonomous secretion of aldosterone by a tumor, the aldosterone level typically rises to 20-30. But in this patient, where the adrenal gland is intact, the aldo level goes bonkers to almost 70.
Incredible.
Fluid and Electrolyte lecture at Providence from Friday
Third in the series of interesting fluid and electrolyte cases.
I would add a slide on where I was going in potassium before the anorexia section.
SlideSpace botches the torn paper frames I used through out the lecture so if you have Keynote, download and look at the native file.
Here is a link to the Keynote file.