magnesium sulfate has been used for a long time in the obstetric population for management of premature labor , preeclampsia and eclampsia . high levels of serum magnesium ( 4.88.4  mg / dl ) 1 are targeted to exert its therapeutic effect in preeclampsia and eclampsia . while generally safe , a review of literature reveals infrequent occurrences of hypocalcemia or hyperkalemia secondary to high magnesium levels 2 . we report a patient who developed both electrolyte abnormalities due to hypermagnesemia and discuss potential mechanisms explaining the same . a 21-year - old african american female , g2p1 was hospitalized to the intensive care unit for the management of severe preeclampsia during her 17th week of gestation . however , she lacked a diagnosis of chronic hypertension , chronic renal disease or proteinuria . she presented with symptoms of headache , palpitations , abdominal pain , nausea and vomiting of 1  week duration . upon initial evaluation , rest of the vital signs were : pulse 98  bpm , temperature 36.5c and oxygen saturation of 99% in room air . physical examination revealed mild , diffuse abdominal tenderness to palpation and mild , symmetric peripheral edema . laboratory investigations were significant for marked proteinuria , bland urine sediment examination , slight elevation of hepatic enzymes , elevated serum uric acid and a normal renal function , as depicted in table1 . her admission blood gas showed a nonanion gap metabolic acidosis with mild respiratory alkalosis ( ph : 7.37 , hco3 : 15  meq / l , pco2 : 27  mm / hg and pao2 : 106  mm / hg , anion gap : 8) . an obstetric ultrasound was done revealing holoprosencephaly , enlarged anterior placenta with extremely elevated hcg levels ( 2285500  miu / ml ) , suggesting partial molar pregnancy . a diagnosis of early severe preeclampsia was made and the patient was managed with antihypertensive therapy , she was given three doses of intravenous ( iv ) hydralazine ( total 25  mg ) , one dose of iv labetalol 20  mg and then was started on nicardipine infusion with a mean arterial pressure goal of 120  mm / hg . she was also given multiple doses of furosemide as shown in table2 to manage her volume status . one dose of sodium polystyrene sulfonate ( kayexalate ) suspension ( 15  g ) to manage her mild hyperkalemia . infusion of magnesium sulfate in lactate ringer ( 40  g/500  ml ) was started at a rate of 25  ml / h for seizure prophylaxis , the infusion was continued for the first 3  days of hospitalization with close neurologic and electrolytes monitoring . an urgent delivery of the fetus was indicated due to severe preeclampsia and fetal ultrasound findings incompatible with life , so a cesarean section was performed as per patient 's preference . changes during magnesium infusion after delivery , the patient 's blood pressure started to improve gradually over the following few days . however , she was noted to have significant changes in serum calcium and potassium levels during that period , corresponding to high serum magnesium levels , as depicted in figure1 and table2 . work up for etiology of hyperkalemia included plasma aldosterone concentration ( pac ) ( 19.2  ng / dl ) , plasma renin activity ( pra ) ( 9.6  ng / ml / h ) and a trans - tubular potassium gradient ( ttkg ) of 4.6 . there was no evidence of hemolysis , acute decline in renal function or administration of medications known to affect serum potassium levels such as nsaids , beta blockers , heparin , etc . additionally , the patient was tested negative for hiv , hepatitis serologies , and serum ana . after excluding other causes of hyperkalemia , a diagnosis of hypermagnesemia - induced hyperkalemia was made . the serum potassium level started to decline after the discontinuation of magnesium infusion on day 3 of hospitalization . patient was noted to have slight hypokalemia after normalization of serum magnesium levels , which was attributed to administration of iv furosemide ( utilized for management of volume overload and hypertension ) . as also depicted in figure1 and table2 ; the calcium level started to decline , corresponding to increasing magnesium levels . serum parathyroid hormone ( pth ) was obtained and was 86  pg / ml ( normal ) . a number of reports in the medical literature describe the association between magnesium and other electrolytes mainly calcium and potassium . while it is well known that hypomagnesemia can cause resistant hypokalemia if not corrected 3 , there is little information that explains the relationship between hypermagnesemia and hyperkalemia . in the literature , we found three case reports describing persistent hyperkalemia during magnesium infusion in the setting of preeclampsia treatment 4,5 . our patient had persistent hyperkalemia despite medical therapy , and the fact that her urine potassium excretion was low ( ttkg 4.6 ) indicates that a renal defect plays a major role in her sustained hyperkalemia . it has been previously postulated that a hyporeninemic hypoaldosteronic state in the setting of hypermagnesemia in preeclamptic patients could be contributory to impaired renal potassium excretion 5 . this is derived from the observation of effects of magnesium infusion on pra and pac in two pregnant women with preeclampsia 6 . in this report , pra was inappropriately low for the pregnant state and pac was low despite the presence of hyperkalemia . however , as described above , in our patient the renin levels were actually high with normal aldosterone levels , suggesting that an alternative mechanism might explain this relationship . 7 studied the effect of magnesium infusion in normal subjects and similar to our observation , showed that magnesium infusion ( postinfusion serum magnesium level 2.32  meq / l ) increased renin levels and paradoxically suppressed aldosterone levels . the effect on pra was mitigated by administration of indomethacin and that on pac was abolished by administration of diltiazem . the authors thus concluded that the increase in pra resulted from increased renal prostaglandins and the suppression of pac was a result of intracellular calcium mobilization 7 . at the level of serum magnesium achieved and in normal healthy volunteers , serum potassium levels did not change , indicating that hyperkalemia likely occurs at much higher serum magnesium levels , this observation potentially explains the mild increase in serum potassium in our case , which might be potentially ameliorated further by the use of furosemide and sodium polystyrene sulfonate . conversely , some other changes in renal potassium excretion inherent to preeclamptic population could be contributory to the occurrence of hyperkalemia . other hypothesis includes the direct effect of magnesium infusion in suppressing the potassium excretion by the kidneys 810 . it has been reported that intracellular magnesium modulates the romk channel by direct inhibition , playing a major role in potassium wasting under conditions of low magnesium and potassium levels 1113 . the opposite could be postulated to be the cause for reduced potassium excretion in face of hypermagnesemia . it has been described that magnesium infusion increases sodium and chloride excretion but decreases potassium excretion via an unknown mechanism 8,9 . it has been suggested that in the presence of increased intracellular magnesium , an increase in atp : adp ratio could occur and this may exert an inhibitory effect on atp sensitive , romk channels , which play an important role in renal potassium secretion 6 . it is also important to mention here that significant hyperkalemia in the setting of magnesium infusion hasn't been reported in nonpregnant women with normal renal function 14,15 ; despite the fact that the effect on sodium and chloride was evident in one of the two cases reported by cheryl et  al . therefore , some of the factors contributing to the effect of magnesium on the renal potassium handling might be related to pregnancy . few reports of hypocalcemia associated with magnesium infusion in pregnancy document the relationship between magnesium and calcium 2,1618 . furthermore , magnesium can suppress pth secretion at the parathyroid gland level 18 . in our patient the pth levels were appropriately high and that may support that hypermagnesemia blunts the peripheral effect of pth as described by cholst et  al . noted a biphasic relationship between magnesium infusion and pth levels ; the beginning of the infusion was associated with a marked decline in pth levels without any change in calcium , followed by an increase in pth levels and decrease calcium levels later on . the high pth and low calcium levels in our patient might be representative of the later phase described above . other potential mechanisms contributing to the drop in calcium level is that magnesium might compete at the calcium sensing receptor on the basolateral surface of loop of henle 17,22 . molecular studies have shown that the calcium - sensing receptor is also sensitive to magnesium , although a much higher threshold is required at a ratio of 10:3 2325 . this might explain the effect of magnesium on calcium at high doses when utilized for the treatment of preeclampsia . urinary calcium excretion was not measured to support our hypothesis and vitamin d deficiency was not excluded as a cause of hypocalcemia in our patient , but the fact that calcium levels normalized once magnesium levels returned to normal supports the association , though . we report the development of hypocalcemia and hyperkalemia attributable to magnesium infusion in a preeclamptic patient . iatrogenic hypermagnesemia should be considered in the differential diagnoses of hypocalcemia and hyperkalemia whenever magnesium infusions are used , especially for obstetric indications . stopping the magnesium infusion will likely reverse the electrolytes changes , if the renal function is intact , but sometimes temporary stabilizing measures for management of hypocalcemia and hyperkalemia may be required .
key clinical messagewe present a case of prominent hypocalcemia and hyperkalemia attributed to magnesium infusion in a preeclamptic patient . 
 iatrogenic hypermagnesemia is an underrecognized cause of hypocalcemia and hyperkalemia . 
 our report illustrates the effects of magnesium therapy on serum calcium and potassium , necessitating close electrolytes monitoring when used .