Hypomagnesemia Following the Diuresis of Post-Renal Obstruction and Renal Transplant

Bb, Davis; Hg, Preuss; Hv, Murdaugh

doi:10.1159/000180457

Cited by 27 publications

(6 citation statements)

References 5 publications

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“…Our assessment in change in Mg(2+) levels without regard to renal function or fluid replacement, may have contributed to alterations in Mg(2+) regulation and serum levels. Impaired renal function can lead to retention(21) or wasting(22) of Mg(2+) which may lead to normal serum levels of serum Mg(2+) despite an underlying pathophysiologic state. Further, fluid replacement or diuresis during the first 24 hours of hospitalization may have artificially impacted our observed change in Mg(2+) homeostasis during the acute phase of stroke.…”

Section: Discussionmentioning

confidence: 99%

Acute Decrease in Serum Magnesium Level after Ischemic Stroke May Not Predict Decrease in Neurologic Function

Siegler

Boehme

Albright

et al. 2013

Journal of Stroke and Cerebrovascular Diseases

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Background Higher serum levels of magnesium (Mg(2+)) may contribute to improved outcome following ischemic stroke, and this may be related to vessel recanalization. Patients with low or normal serum magnesium levels during the acute phase of ischemic stroke may be more susceptible to neurologic deterioration and worse outcomes. Methods All patients who presented to our center within 48hrs of acute ischemic stroke (07/2008-12/2010) were retrospectively identified. Patient demographics, laboratory values, and multiple outcome measures, including neurologic deterioration (ND), were compared across admission serum Mg(2+) groups as well as change in Mg(2+) from baseline to 24hr groups. Results Three hundred thirteen patients met inclusion criteria (mean age 64.8 years, 42.2% female, 64.0% black). Mg(2+) groups at baseline were not predictive of poor functional outcome, death or discharge disposition. Patients whose serum Mg(2+) decreased during the first 24hrs of admission were also not at greater odds of ND or poor outcome measures compared to patients with unchanging or increasing Mg(2+) levels. Conclusions Our results suggest that patients who have low Mg(2+) at baseline or a reduction in Mg(2+) 24hrs after admission are not at a higher risk of experiencing ND or poor short-term outcome. Ongoing prospective interventional trials will determine if hyperacute aggressive magnesium replacement affords neuroprotection in stroke.

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Section: Discussionmentioning

confidence: 99%

Acute Decrease in Serum Magnesium Level after Ischemic Stroke May Not Predict Decrease in Neurologic Function

Siegler

Boehme

Albright

et al. 2013

Journal of Stroke and Cerebrovascular Diseases

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“…It has been proven that there is an increase in auricular natriuretic peptide, and this event can play an important role in the excretion of water and salt after obstruction relief; furthermore, potassium excretion increases considerably [45]. Hypercalciuria increases, as does magnesiuria, which can lead to alterations in the reabsorption of solutes in the loop of Henle [46] (Figure 4).…”

Section: Polyuria and Nephrogenic Diabetes Insipidus After Urinary Obmentioning

confidence: 99%

Acute Kidney Injury Caused by Obstructive Nephropathy

Chávez-Íñiguez

Navarro-Gallardo

Medina-González

et al. 2020

International Journal of Nephrology

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Acute kidney injury secondary to obstructive nephropathy is a frequent event that accounts for 5 to 10% of all acute kidney injury cases and has a great impact on the morbidity and mortality in those affected. The obstruction in the urinary tract has a profound impact on kidney function due to damage produced by ischemic and inflammatory factors that have been associated with intense fibrosis. This pathology is characterized by its effects on the management of fluids, electrolytes, and the acid-base mechanisms by the renal tubule; consequently, metabolic acidosis, hyperkalemia, uremia, and anuria are seen during acute kidney injury due to obstructive nephropathy, and after drainage, polyuria may occur. Acute urine retention is the typical presentation. The diagnosis consists of a complete medical history and should include changes in urinary voiding and urgency and enuresis, history of urinary tract infections, hematuria, renal lithiasis, prior urinary interventions, and constipation. Imaging studies included tomography or ultrasound in which hydronephrosis can be seen. Management includes, in addition to drainage of the obstructed urinary tract system, providing supportive treatment, correcting all the metabolic abnormalities, and initiating renal replacement therapy when required. Although its recovery is in most cases favorable, it seems to be an undervalued event in nephrology and urology. This is because it is mistakenly believed that the resolution and recovery of kidney function is complete once the urinary tract is unobstructed. It can have serious kidney sequelae. In this review, we report the epidemiology, incidence, pathophysiological mechanisms, diagnosis, and treatment of acute kidney injury due to obstructive nephropathy.

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“…Prominent among these are postobstructive nephropa thy, the resolving phase of acute tubular necrosis, chronic glomerulonephri -tis and pyelonephritis, and post renal transplantation (1,46). Renal tubular acidosis may also cause magnesium loss (1,39).…”

Section: Disorders Causing Magnesium Deficiencymentioning

confidence: 99%