AS WITH SPACE FLIGHT A MAGNESIUM DEFICIT MAY BE RESPONSIBLE FOR BOTH PERIPHERAL VASCULAR DYSFUNCTION AND KIDNEY DISEASE

                                                                                                                                                                                                                                                                              American Journal of Cardiology 2010; 105:1203-04.


Regarding the paper by Baber et al. (1) it was stressed that the pathophysiologic mechanisms responsible for the increased risk of both peripheral vascular disease and chronic kidney disease remains poorly understood.  Lessons learned from space flight (SF) can be applicable to studies on earth as well.  Oxidative stress, inflammation and endothelial dysfunction triggered by a magnesium (Mg.) deficit can be one underlying link responsible for both    (SF) - peripheral vascular dysfunction as well as renal dysfunction (2).  I have emphasized that both Irwin and Scott might have had underlying endothelial dysfunction – even prior to dust inhalation in the lunar  habitat – to account for the severe finger tip pain both experienced while on their first lunar excursion.

This is supported by the development of nail bed - cyanosis Irwin showed by the 18th minute during a stress test on the day of return from his 12 day mission, supporting my hypothesis that the pain was secondary to peripheral vasospasm of both the arterial and venous vessels.  I postulated that a Mg. deficit secondary to invariable SF- malabsorption and loss of skeletal muscle -storage sites for Mg. even with this brief 12 day mission could be responsible (3).  In support of my hypothesis is the decrease of calf blood flow of 40 % with SF, relative to supine conditions. Pre-flight measurements taken between 4-12 SF-days showed that calf vascular resistance doubled but returned to pre-flight levels after SF (4).  Furthermore SF- proteinuria (more pronounced after prolonged missions with disappearance after SF), elevations of serum creatinine, and impairment of kidney concentrating ability have been shown.

It is noteworthy that studies in rats after SF of < 3 weeks  invariably demonstrated elevated activity of the juxtaglomerular apparatus  (2).  Seelig  (5)  has emphasized  that experimental Mg. deficiency has been shown to cause hypertrophy of the juxtaglomerular  apparatus, resulting in aldosterone secretion which in turn  increases  Mg. loss and vicious cycles.  Also vicious cycles can develop from Mg. ion deficits with in turn catecholamine elevations and increased angiotensin effect. The latter can contribute to an upregulated Intrarenal renin-angiotensin system with hypertension (2)

REFERENCES

1.Baber U, Mann D, Schimbo D, Woodward M, Olin JW, Muntner P.  Combined role of reduced estimated glomerular filtration rate and microalbuminuria on the prevalence of peripheral arterial  disease. Am J C ardiol 2009; 104:1446-1451.
2. Rowe WJ.  Potential renovascular hypertension, space missions, and the role of magnesium . Internat  J  Nephrol  and Renovasc  Dis 2009; 2: 1-7.
3. Rowe WJ. Extraordinary hypertension after a lunar mission.  Am  J  Med  2009; 122: E1.
4. Watenpaugh DE, Buckey JC, Lane LD, Gaffney A, Levine BD, Moore WE, Wright SJ, Blomqvist  CG. Effects of spaceflight on human calf hemodynamics  J Appl Physiol  2001; 90 : 1552-1558.
5. Seelig M. Cardiovascular consequences of magnesium deficiency and loss; pathogenesis prevalence and manifestations – magnesium and chloride loss in refractory potassium repletion. Am J Cardiol 1989; 63: 4G-21G.

 

William J. Rowe M.D.  FBIS