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Paroxysmal nocturnal hemoglobinuria is a rare clonal hematopoietic stem cell disorder characterized by intravascular hemolysis, hemoglobinuria, and inflammatory thrombotic state. Intravascular hemolysis in paroxysmal nocturnal hemoglobinuria (PNH) can lead to acute and chronic renal injury through hemoglobin-mediated toxicity. A 32-year-old pregnant woman with myelodysplastic syndrome was admitted to our hospital with severe preeclampsia. Shortly after an urgent caesarean section, she became obtunded and showed signs of acute kidney injury (AKI) with anuria, severe intravascular hemolysis, and hypermagnesemia. She was diagnosed with PNH with a positive Ham test and flow cytometry analysis. Renal magnetic resonance imaging revealed decreased signal intensity in the renal cortex due to hemosiderin deposition. Hemodialysis, plasma exchange, and administration of corticosteroids ameliorated her clinical condition and renal function. This case illustrates that careful management is required to prevent postpartum AKI in pregnant women with PNH.

As maintenance hemodialysis patients are exposed to large quantities of dialysis water, any contamination of it might be reflected in plasma levels. We present a series of cases due to such a contamination. Six maintenance hemodialysis patients dialyzing at the same peripheral hemodialysis facility presented to us over a short period of time with symptoms mimicking inadequate dialysis. Their blood urea and creatinine levels were not very high, but all the patients had hypermagnesemia [serum Mg levels = 1.8 (±0.3) mmol/L]. Except for one patient who had cardiac arrest at presentation, all patients improved after undergoing hemodialysis at our center [serum Mg at discharge = 0.86 (±0.01) mmol/L]. The origin of hypermagnesemia was traced to dialysis water contamination with magnesium due to inadequate maintenance of the water treatment system. Corrective measures improved the quality of water, and no further cases were reported from that center. Proper maintenance and periodic checks of the quality of water are central to the outcomes of maintenance hemodialysis patients.

Calcium, phosphorus, and magnesium homeostasis is altered in chronic kidney disease (CKD). Hypocalcemia, hyperphosphatemia, and hypermagnesemia are not seen until advanced CKD because adaptations develop. Increased parathyroid hormone (PTH) secretion maintains serum calcium normal by increasing calcium efflux from bone, renal calcium reabsorption, and phosphate excretion. Similarly, renal phosphate excretion in CKD is maintained by increased secretion of fibroblast growth factor 23 (FGF23) and PTH. However, the phosphaturic effect of FGF23 is reduced by downregulation of its cofactor Klotho necessary for binding FGF23 to FGF receptors. Intestinal phosphate absorption is diminished in CKD due in part to reduced levels of 1,25 dihydroxyvitamin D. Unlike calcium and phosphorus, magnesium is not regulated by a hormone, but fractional excretion of magnesium increases as CKD progresses. As 60-70% of magnesium is reabsorbed in the thick ascending limb of Henle, activation of the calcium-sensing receptor by magnesium may facilitate magnesium excretion in CKD. Modification of the TRPM6 channel in the distal tubule may also have a role. Besides abnormal bone morphology and vascular calcification, abnormalities in mineral homeostasis are associated with increased cardiovascular risk, increased mortality and progression of CKD.

Aims We investigated the relationship between renal function and serum magnesium concentration in elderly patients treated with magnesium oxide (MgO) in an outpatient setting of an urban hospital in Japan. Methods In the present study, 44 elderly outpatients (23 patients with constipation treated with daily oral MgO and 21 untreated patients in the control group) who visited Kameyama municipal medical center were enrolled. Variables were age, sex, weight, height, serum magnesium concentration, serum blood urea nitrogen level, serum creatinine level, use of other magnesium-containing supplements and symptoms associated with hypermagnesemia. We calculated the estimated glomerular filtration rate (eGFR) and classified patients based on eGFR category. Results Compared with the control group, the MgO group showed a significantly higher concentration of serum magnesium (median 2.2 mg/dL [interquartile range 2.1–2.3] vs 2.4 mg/dL [2.2–2.6], P 2.6 mg/dL) was noted only in the MgO group. However, symptoms associated with hypermagnesemia occurred in patients from both groups, with no significant difference between groups. In the MgO group, significant difference was seen in the median serum magnesium concentration between eGFR categories (P

Objective To review magnesium physiology including absorption, excretion, and function within the body, causes of magnesium abnormalities, and the current applications of magnesium monitoring and therapy in people and animals. Etiology Magnesium plays a pivotal role in energy production and specific functions in every cell in the body. Disorders of magnesium can be correlated with severity of disease, length of hospital stay, and recovery of the septic patient. Hypermagnesemia is seen infrequently in people and animals with significant consequences reported. Hypomagnesemia is more common in critically ill people and animals, and can be associated with platelet, immune system, neurological, and cardiovascular dysfunction as well as alterations in insulin responsiveness and electrolyte imbalance. Diagnosis Measurement of serum ionized magnesium in critically or chronically ill veterinary patients is practical and provides information necessary for stabilization and treatment. Tissue magnesium concentrations may be assessed using nuclear magnetic resonance spectroscopy as well as through the application of fluorescent dye techniques. Therapy Magnesium infusions may play a therapeutic role in reperfusion injury, myocardial ischemia, cerebral infarcts, systemic inflammatory response syndromes, tetanus, digitalis toxicity, bronchospasms, hypercoagulable states, and as an adjunct to specific anesthetic or analgesic protocols. Further veterinary studies are needed to establish the frequency and importance of magnesium disorders in animals and the potential benefit of magnesium infusions as a therapeutic adjunct to specific diseases. Prognosis The prognosis for most patients with magnesium disorders is variable and largely dependent on the underlying cause of the disorder.

Muscle water and electrolytes were determined in percutaneous muscle biopsy material from m. quadriceps femoris in 33 uremic patients undergoing continuous ambulatory peritoneal dialysis (CAPD) for 1–38 months, and in 34 normal subjects. The patients showed increased muscle contents of water, sodium, and chloride relative to fat-free solids (FFS); both intra- and extracellular water contents were increased. The total water content was inversely correlated with the duration of CAPD. The muscle potassium content was increased, both relative to FFS and to magnesium, whereas the intracellular potassium concentration was normal. Despite hypermagnesemia, the muscle content of magnesium was normal and the intracellular concentration was even slightly decreased due to the increase in intracellular water. We conclude that muscle water and electrolyte status is abnormal in CAPD patients, but the alterations appear to be less marked than in uremic patients undergoing other forms of therapy.

Magnesium (Mg) is the fourth most abundant cation in the body, mainly located within bone and skeletal muscle. The normal total plasma Mg concentration varies in a narrow range, with approximately 60% present as free Mg ions, the biologically active form. The kidney plays a principal role in Mg balance. Approximately 70-80% of plasma Mg is ultrafilterable, and under normal circumstances, 95% of the filtered load of Mg is reabsorbed. As chronic renal failure (CRF) progresses, urinary Mg excretion may be insufficient to balance intestinal Mg absorption and dietary Mg intake becomes a major determinant of serum and total body Mg levels. Until severe reductions in glomerular filtration rate (

Objective: To demonstrate whether ECG changes induced by hyperkalemia correspond with previously described changes. Design: Prospective Animals: Eighteen dogs and 22 cats with serum potassium levels >5.5 mEq/L as the result of various disease processes. Procedure: Once hyperkalemia was documented, the following data were collected: ECG (n=40), total magnesium (mg/dl) (n=18), total calcium (mg/dl) (n=31), and venous blood gas (n=20). Animals were divided into 5 groups based on expected ECG's changes associated with hyperkalemia (mEq/L): Group 1- 5.5–6.5; Group 2- 6.6–7.0; Group 3- 7.1–8.5; Group 4- 8.6–10.0; Group 5- >10.0. ECG's were interpreted to determine if the rate, rhythm and changes in the P-QRS-T complex were similar to those previously reported. Results: Twelve ECGs demonstrated changes previously described, while 28 did not: Group 1 (n=7)- 1/7; Group 2 (n=2)- 0/2; Group 3 (n=14)- 4/14; Group 4 (n=6)- 3/6; Group 5 (n=11)- 4/11. Many ECG abnormalities not previously described were also identified such as atrioventricular dissociation and ventricular tachyarrhythmias. Blood gas analysis revealed acidemia (19/20) with severe acidemia (pH

UNLABELLED The effects of maternal magnesium sulphate treatment on neonatal mineral status and parathyroid hormone secretory response were studied in 8 exposed and 27 control preterm infants during the first 2 wk of life. Antenatal magnesium sulphate resulted in hypermagnesaemia during the first 3-7 d of life without affecting other serum mineral concentrations. CONCLUSION Early hypermagnesaemia was associated with hypercalciuria during the first 3 d and parathyroid hormone suppression up to the age of 2 wk in the exposed infants.

Studies evaluating pericardial fluid analysis in dogs to determine the etiology of pericardial effusions have yielded conflicting results. The purpose of this prospective study was to compare acid-base status, electrolyte concentrations, glucose, and lactate of pericardial fluid to peripheral blood from dogs with pericardial effusion and to compare these variables between dogs with neoplastic and nonneoplastic pericardial effusion. Acid-base status, electrolyte concentrations, glucose, hematocrit, urea nitrogen, and lactate concentrations were evaluated in peripheral blood samples and in pericardial effusion samples of 41 client-owned dogs with pericardial effusion. Common abnormal findings in the peripheral blood of dogs with pericardial effusion included hyperlactatemia (n = 38 [of 41]; 93%), hyponatremia (n = 25/41; 61%), hyperglycemia (n = 13/41; 32%), and hypermagnesemia (n = 13/41; 32%). Bicarbonate, sodium, ionized calcium, glucose, and hematocrit were all significantly lower in the pericardial fluid compared with peripheral blood, whereas lactate, chloride, and PCO2 were significantly higher in the pericardial fluid. When comparing the concentrations of variables in the pericardial fluid of dogs with neoplasia (n = 28) to those without neoplasia (n = 13), pH, bicarbonate, and chloride were significantly lower in dogs with neoplasia, whereas lactate, hematocrit, and urea nitrogen were significantly higher in the pericardial fluid of dogs with neoplasia. The difference between peripheral and pericardial glucose concentrations was significantly larger in dogs with neoplasia than in dogs without neoplasia. Although differences between variables in dogs with neoplastic and nonneoplastic pericardial effusion were documented, clinical relevance is likely limited by the degree of overlap between the 2 groups.

We report a fatal case of hypermagnesemia caused by oral ingestion of milk containing magnesium chloride as a folk remedy. The autopsy of the 75-year-old woman showed no injury or illness as the cause of death. Neither alcohol nor controlled drugs were found by the toxicological analysis. Her posthumous serum magnesium concentration was 10.2 mg/dL. The concentration of magnesium in serum was higher than that of the previous reports. Therefore, the cause of death was considered to be hypermagnesemia. Recently, the prescription drugs, over-the-counter drugs, and health foods containing magnesium are consumed as supplements in the world, and their potential toxicity should be recognized.

Objective: To describe the clinical manifestations and treatment of hypermagnesemia and the potential drug errors that can lead to iatrogenic electrolyte toxicities. Summary: We report 2 cases of iatrogenic intravenous (IV) magnesium (Mg) overdose. Both cases developed extreme cardiovascular and neurologic symptoms consisting of vomiting, hypotension, bradycardia, flaccid paralysis, and severe mental depression. Diagnosis was made based upon serum ionized Mg levels (3.47 mmol/L; reference range: 0.43–0.58 mmol/L for Case #1; and 4.64 mmol/L; reference range: 0.42–0.55 mmol/L for Case #2). Each animal was treated with 0.9% NaCl for diuresis and IV calcium gluconate. Within 24 hours, the cardiovascular and neurologic status of both animals, as well as the serum Mg concentration, had normalized. Each animal was discharged with no complications. Both animals had been hospitalized for critical illness and had developed hypomagnesemia that was being treated with Mg sulfate infusions. The cause for the hypermagnesemia was due to miscalculations in treatment orders that led to erroneously administered Mg-containing solutions. Confusing drug labels and varying units of measurement can lead to erroneous miscalculations, especially in critically ill patients that receive multiple IV infusions. New information provided: This is the first case report of iatrogenic Mg overdose in veterinary medicine. These 2 cases had a good clinical outcome with prompt recognition and supportive care.

We carried out this retrospective study to examine the magnesium status of our chronic ambulatory peritoneal dialysis (CAPD) patients dialyzed with 0.75 mmol/L (group I) or 0.50 mmol/L (group II) magnesium peritoneal dialysis solution. A total of 34 anuric patients on CAPD (age:31-72 years; duration of CAPD:7-74 months) were studied. None of them received magnesium-containing phosphate binders or vitamin D. Biochemical parameters including magnesium, calcium, phosphate, parathormone, and albumin were measured in all patients. The corrected for hypoalbuminemia serum magnesium concentration in group I was significantly higher compared to that found in group II. However, there were no significant differences in the other measured parameters between the two groups of CAPD patients, though iPTH levels were somewhat increased in group II patients. Serum magnesium levels were weakly correlated with serum prealbumin levels in both groups of CAPD patients (r=0.16, P=0.08 and r=0.17, P=0.07). The incidence of hypermagnesemia was significantly higher in group I patients versus those in group II (13/19 68.4%] vs. 2/15 13.3%], P

Total serum magnesium concentration ([Mg 2 + ] s ) was prospectively determined for 57 cats admitted to the intensive care unit (ICU) of the Cornell University Hospital for Animals. Data were collected and analyzed to determine the following: prevalence and incidence of [Mg 2 + ] s abnormalities, medical disorders associated with altered [Mg 2 + ] s , association of altered [Mg 2 + ] s with other electrolyte abnormalities, length of hospitalization for cats with abnormalities of [Mg 2 + ] s versus those with normal [Mg 2 + ] s , and survival of cats with abnormal [Mg 2 + ] s versus those with normal [Mg 2 + ] s . The point prevalence of magnesium abnormalities was 26%, the period prevalence was 46%, and the cumulative incidence was 23%. Hypermagnesemia was associated with abnormalities of serum potassium (P = .04) and phosphate (P = .01) concentrations. Abnormalities of [Mg 2 + ] s were not associated with abnormal serum concentrations of Na + , Ca 2 + , or Cl - . On admission, hypomagnesemia was detected in cats with gastrointestinal, endocrine, and other disorders; hypermagnesemia was detected only in cats with renal disease, obstructive uropathy, or neoplastic disease. The median hospital stay for cats that developed abnormal [Mg 2 + ] s after admission was longer than for cats that remained normomagnesemic (5 versus 4 days, respectively; P = .03). Despite the longer hospital stay, the survival of these cats was lower than that of normomagnesemic cats (54 versus 77%; P = .05). When all cats were considered, the survival of cats with abnormal [Mg 2 + ], also was decreased compared with normomagnesemic cats (62 versus 81%; P = .05). We conclude that abnormalities of [Mg 2 + ] s may affect morbidity and mortality of affected cats.

Summary Serum magnesium (Mg) is an infrequnetly measured electrolyte in small animal patients. Currently, little is known about the prevalence and significance of abnormalities in serum Mg in animals. Therefore, a prospective study was performed to examine the incidence and clinical implications of abnormalities in serum Mg levels in critically ill dogs. Serum Mg and other electrolytes were measured in 93 normal dogs housed at the Purina Pet Care Center and in 48 ill dogs admitted to a small animal critical care unit. The normal reference range for canine serum Mg was determined to be 1.89 – 2.51 mg/dl. Based on this range, 54% of the critically ill dogs were hypomagnesemic ( 2.51 mg/dl). Of the electrolytes measured in these patients, serum Mg had the highest prevalence of abnormal values. Hypomagnesemic patients had a significantly higher incidence of concurrent hypokalemia and hyponatremia (p < 0.05), as well as a longer length of hospitalization (p < 0.05) than their normomagnesemic counterparts. Hypermagnesemic patients were 2.6 times more likely not to survive their illness when compared to patients with normal serum Mg levels. Abnormalities in serum Mg appear to be common in critically ill dogs. These patients commonly have other concurrent electrolyte abnormalities. Since serum Mg is not routinely measured, the presence of hypokalemia or hyponatremia should alert the clinician to the possibility of coexisting hypomagnesemia. The clinical implications of hypomagnesemia and hypermagnesemia in ill dogs appear to involve prolonged hospitalization and increased mortality, respectively: however, the exact etiology remains undetermined.

Present evidence suggests that the renal handling of magnesium is normally a filtration-reabsorption process as evidence for secretion is unsubstantiated. Magnesium reabsorption has distinctive features when compared with that of sodium and calcium. The proximal tubule concentration of magnesium rises to levels about 1.5 times greater than the glomerular filtrate and only 20–30% of the filtered magnesium is reabsorbed in this segment. Although the fractional reabsorption of magnesium is only half that of sodium, it changes in parallel with that of sodium in response to changes in extracellular fluid volume. The major portion of filtered magnesium (some 65%) is reabsorbed in the loop of Henle and evidence indicates that the thick ascending limb is the principal segment involved in magnesium absorption. Recent observations suggests that magnesium reabsorption in the ascending limb may be voltage dependent and secondary to active sodium chloride reabsorption. The loop of Henle appears to be the major nephron site where magnesium reabsorption is regulated possibly by cAMP-mediated hormones including parathyroid hormones, calcitonin, glucagon and antidiuretic hormone. About 10% of the filtered magnesium is delivered into the distal nephron. The distal tubule reabsorbs only a small fraction of the filtered magnesium which may be regulated by the same cAMP-mediated hormones involved in control of magnesium in the loop.

1. The regulation of c.s.f. Mg concentration was studied using the cat choroid plexus isolated in a chamber in situ. 2. An increase in plasma Mg concentration was accompanied by the usual reciprocal decrease in plasma Ca concentration. Chamber fluid Ca concentration was unaffected. 3. Hypermagnesemia (plasma Mg concentration greater than 6 m-equiv/1.) caused relatively small increases in c.s.f. Mg concentration (delta plasma [Mg]/ delta c.s.f. [Mg] = 4). 4. Various chamber fluid Mg concentrations (0, 2.4 or 4.8 m-equiv/1.) were rapidly (within 30--60 min) returned to near the control value of 1.83 m-equiv/1. 5. When plasma and chamber fluid Mg concentrations were altered simultaneously, the final chamber fluid Mg concentration was returned towards normal with or against a concentration gradient. 6. The data indicate that the choroid plexus is involved in maintaining the constancy of the c.s.f. Mg concentration by sensing changes in the normal c.s.f. Mg concentration and altering approximately its rate of active secretion of Mg.

The case history of a patient with severe muscular weakness resulting from magnesium intoxication following oral and rectal administration of magnesium citrate cathartics is reported. The findings of the electrophysiologic studies were characteristic of the neuromuscular blockade seen in this disorder, including marked reduction in evoked muscle action potential amplitude which progressively declined on nerve stimulation at low rates, and a striking degree of facilitation of evoked muscle action potential after exercise or on high-frequency stimulation. When the hypermagnesemia was corrected, strength returned to normal.