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 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.