Hypomagnesemia as a Risk Factor for the Non-recovery of the Renal Function in Critically Ill Patients With Acute Kidney Injury

Sarah Cascaes Alves; Cristiane Damiani Tomasi; Larissa Constantino; Vinícius Giombelli; Roberta Candal; Maria de Lourdes Bristot; Maria Fernanda Topanotti; Emmanuel A. Burdmann; Felipe Dal-Pizzol; Cassiana Mazon Fraga; Cristiane Ritter


Nephrol Dial Transplant. 2013;28(4):910-916. 

In This Article

Abstract and Introduction


Background The aim of this study was to evaluate the role of hypomagnesemia as a risk factor for the development of acute kidney injury (AKI) and non-recovery of renal function in critically ill patients.

Methods A cohort study was conducted by collecting data from March to June 2011 in 232 patients who were admitted into an intensive care unit (ICU). Magnesium serum levels were measured daily during ICU stay. Hypomagnesemia was defined as an episode of serum magnesium concentration of <0.70 mmol/L during ICU stay. The Risk, Injury, Failure, Loss and End-stage kidney disease (RIFLE) criteria were used to define AKI. Renal function recovery was defined as an absence of AKI by the RIFLE criteria over a 48-h period, or at ICU discharge, in the patients who developed AKI during ICU stay.

Results The presence of hypomagnesemia was similar in patients with or without AKI (47 and 62%, respectively, P = 0.36). The presence of hypomagnesemia was higher in patients who did not recover renal function when compared with patients who recovered renal function (70 versus 31%, P = 0.003). A multivariate analysis identified hypomagnesemia as an independent risk factor for non-recovery of renal function (P = 0.005). Patients with and without hypomagnesemia had similar mortality rates (P = 0.63).

Conclusions Hypomagnesemia was an independent risk factor for non-recovery of renal function in a cohort of critically ill AKI patients.


Acute kidney injury (AKI) is a common and serious complication in hospitalized patients, particularly in patients in the intensive care unit (ICU). The mortality rate in patients with AKI remains very high, despite significant advances in the care of critically ill patients. Hypomagnesemia, which is defined as a total serum magnesium concentration <0.70 mmol/L, is a frequent electrolyte abnormality, which occurs in >12% of hospitalized patients. This frequency rises from 60 to 65% in ICU patients due to inadequate nutrition, hypoalbuminemia, hypotension, sepsis and the use of drugs, such as diuretics and aminoglycosides.[1]

In animal experiments, hypomagnesemia decreases the glomerular filtration rate (GFR) and the renal blood flow (RBF), and enhances post-ischemic renal injury.[2] Conversely, administration of magnesium in an animal model of ischemic renal injury results in GFR and RBF increases.[3] However, there is only one report in the literature disclosing that hypomagnesemia was a risk factor for the non-recovery of renal function after an AKI episode in hospitalized patients with acquired immunodeficiency syndrome (AIDS).[4]

Thus, the aim of the current study was to assess the role of hypomagnesemia in the development of AKI and the recovery of renal function after an AKI episode in critically ill patients.