HDCN Article Review/Hyperlink

Mehrotra R, Nolph KD, Kathuria P, Dotson L

Hypokalemic metabolic alkalosis with hypomagnesuric hypermagnesemia and severe hypocalciuria: a new syndrome?

Am J Kidney Dis (Jan) 29:106-114 1997

The authors report a 44-year-old man with hypokalemia who they believe may have a new tubular disease distinct from Bartter's and Gitelman's syndromes. This patient had hypokalemia (K 2.8-3.0 meq/L), metabolic alkalosis, mild azotemia (creat clearance 59 ml/min), hypocalciuria (FE Ca 0.08%) with normocalcemia, hypomagnesuria (FE Mg 3.2-5.2%) with hypermagnesemia (Mg 2.1-2.8 meq/L), normal PTH levels, and glucosuria. Secondary aldosteronism was also present. Clearance studies done during oral water loading revealed normal sodium and water handling in both the thick ascending limb of Henle (TALH) and distal tubule, but evidence for a defect in proximal tubule reabsorption (glucosuria, supranormal water clearance, and high distal delivery). After administration of furosemide, calcium and magnesium excretions increased 30- and 5-fold, respectively. The authors postulate a proximal tubular defect in NaCl reabsorption leading to hypocalciuria, hypomagnesuria, and potassium wasting. Increased calcium and magnesium reabsorption in the TALH (which are reversed by furosemide) may be passive processes secondary to chronic volume contraction.

Comment: This is an interesting study, and the details of the clearance studies will be of interest to those who enjoy classical clinical tubular physiology. It is clear that this patient does not have either Gitelman's or Bartter's syndromes becuase of the hypermagnesemia. Indeed, as the authors point out, hypermagnesemia is very unusual in the absence of severe renal failure (or exogenous magnesium administration). Serum magnesium levels were 2.1-2.8 mEq/L, and fractional excretion was 3.2-5.2%, which is remarkably low in the face of hypermagnesemia. In CRF, FE Mg should exceed 50% before hypermagnesemia occurs. Thus, these findings cannot be explained by the mild CRF seen in this patient. (David J. Leehey, M.D., Loyola University at Chicago)

The abstract to this paper is available from the NKF at this site.