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Renal system
Renal agenesis
Horseshoe kidney
Potter sequence
Hyperphosphatemia
Hypophosphatemia
Hypernatremia
Hyponatremia
Hypermagnesemia
Hypomagnesemia
Hyperkalemia
Hypokalemia
Hypercalcemia
Hypocalcemia
Renal tubular acidosis
Minimal change disease
Diabetic nephropathy
Focal segmental glomerulosclerosis (NORD)
Amyloidosis
Membranous nephropathy
Lupus nephritis
Membranoproliferative glomerulonephritis
Poststreptococcal glomerulonephritis
Goodpasture syndrome
Rapidly progressive glomerulonephritis
IgA nephropathy (NORD)
Lupus nephritis
Alport syndrome
Kidney stones
Hydronephrosis
Acute pyelonephritis
Chronic pyelonephritis
Prerenal azotemia
Renal azotemia
Acute tubular necrosis
Postrenal azotemia
Renal papillary necrosis
Renal cortical necrosis
Chronic kidney disease
Polycystic kidney disease
Multicystic dysplastic kidney
Medullary cystic kidney disease
Medullary sponge kidney
Renal artery stenosis
Renal cell carcinoma
Angiomyolipoma
Nephroblastoma (Wilms tumor)
WAGR syndrome
Beckwith-Wiedemann syndrome
Posterior urethral valves
Hypospadias and epispadias
Vesicoureteral reflux
Bladder exstrophy
Urinary incontinence
Neurogenic bladder
Lower urinary tract infection
Transitional cell carcinoma
Non-urothelial bladder cancers
Congenital renal disorders: Pathology review
Renal tubular defects: Pathology review
Renal tubular acidosis: Pathology review
Acid-base disturbances: Pathology review
Electrolyte disturbances: Pathology review
Renal failure: Pathology review
Nephrotic syndromes: Pathology review
Nephritic syndromes: Pathology review
Urinary incontinence: Pathology review
Urinary tract infections: Pathology review
Kidney stones: Pathology review
Renal and urinary tract masses: Pathology review
Hypermagnesemia
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Laboratory value, serum | Result |
Sodium | 136 mEq/L |
Potassium | 4.2 mEq/L |
Chloride | 98 mEq/L |
HCO3- | 28 mEq/L |
Calcium | 7.2 mg/dL |
Creatinine | 1.2 mg/dL |
Albumin | 3.2 g/dL |
TSH | 4.0 mU/L |
T4 | 3 µg/dL |
Tanner Marshall, MS
Samantha McBundy, MFA, CMI
‘Hyper-’ means ‘over’ and ‘-magnes-’ refers to magnesium, and -emia refers to the blood, so hypermagnesemia means higher than normal magnesium levels in the blood, and symptoms typically develop at a level over 4 mEq/L.
An average adult has about 25 grams of magnesium in their body.
About half is stored in the bones, and most of the other half is found within cells.
In fact, magnesium is a really common positively charged ion found within the cell, second only to king potassium.
A very tiny fraction, roughly 1% of the total magnesium in the body, is in the extracellular space which includes both the intravascular space - the blood and lymphatic vessels, and the interstitial space - the space between cells.
About 20% of the magnesium in the extracellular space, which would be about 0.2% of the total magnesium, is bound to negatively charged proteins like albumin, but the other 80% or 0.8% of the total magnesium, can be filtered into the kidneys.
So in the kidney, that magnesium gets filtered into the nephron, andi about 30% gets reabsorbed at the proximal convoluted tubule, 60% gets reabsorbed in the ascending loop of Henle, and 5% get reabsorbed at the distal convoluted tubule.
That leaves only 5% to get excreted by the kidneys.
So, in order for there to be too much magnesium in the blood, this normal balance has to be disturbed.
The most common reason is when those nephrons in the kidneys can’t excrete magnesium properly - which can happen in renal failure, when the kidneys typically aren’t able to excrete anything properly.
Another cause of hypermagnesemia is ingesting more magnesium than the kidneys can excrete.
Sometimes this can be due to an intravenous infusion of magnesium that isn’t prepared correctly.
Other times it can be due to a magnesium containing medication like magnesium hydroxide which can be used to treat symptoms like constipation and heartburn.
If these medications are taken in excess over a long period of time, it can lead to hypermagnesemia.
There are some less common causes of hypermagnesemia.
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