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Renal system

Renal and ureteral disorders

Renal agenesis

Horseshoe kidney

Potter sequence











Renal tubular acidosis

Minimal change disease

Diabetic nephropathy

Focal segmental glomerulosclerosis (NORD)


Membranous nephropathy

Lupus nephritis

Membranoproliferative glomerulonephritis

Poststreptococcal glomerulonephritis

Goodpasture syndrome

Rapidly progressive glomerulonephritis

IgA nephropathy (NORD)

Lupus nephritis

Alport syndrome

Kidney stones


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


Nephroblastoma (Wilms tumor)

WAGR syndrome

Beckwith-Wiedemann syndrome

Bladder and urethral disorders

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

Renal system pathology review

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




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USMLE® Step 1 questions

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High Yield Notes

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USMLE® Step 1 style questions USMLE

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A 72-year-old male is in the cardiac intensive care unit due to decompensated heart failure. He has been undergoing diuretic therapy with a bumetanide intravenous infusion for the past week. The patient’s hospital course has been complicated by Clostridium difficile colitis, and he has had multiple episodes of profuse diarrhea. During rounds, the patient becomes acutely altered. A telemetry monitoring rhythm strip is shown below.  

Reproduced from: Wikipedia  

Which of the following electrolyte disturbances is the most likely precipitant of these ECG findings?


Content Reviewers

Rishi Desai, MD, MPH


Tanner Marshall, MS

With hypomagnesemia, ‘hypo-’ means ‘lower’ and ‘-magnes-’ refers to magnesium, and -emia refers to the blood, so hypomagnesemia means lower than normal magnesium levels in the blood, and symptoms typically develop at a level below 1 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 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 vessels 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 inside the kidney, that magnesium gets filtered into the nephron, and 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. And that leaves only 5% to get excreted by the kidneys.

Magnesium levels can fall in a few situations. One scenario is when the nephron fails to reabsorb the magnesium that’s filtered out of the blood, which would mean more would be excreted in the urine instead of kept in the blood.

Magnesium reabsorption is mostly a passive process where the positively charged magnesium ion follows the electrochemical gradient and moves from the positively charged lumen into the cells lining the lumen which usually have a negative charge.

Now, loop and thiazide diuretics can disrupt that process, because they both make the lumen less positively charged, and this diminishes magnesium’s electrochemical gradient and causing more of the ions to stick around in the filtrate and get peed out.

Another sort of similar scenario is a genetic mutation affecting channels that regulate ion flow, which again could change the electrochemical gradient and cause more magnesium to stick around in the lumen and get peed out.

An example of this is Gitelman syndrome, where there’s a mutation in the gene coding for the Na-Cl cotransporters in the distal tubule.


  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  5. "Genetic causes of hypomagnesemia, a clinical overview" Pediatric Nephrology (2016)
  6. "Physiology and pathophysiology of the calcium-sensing receptor in the kidney" American Journal of Physiology-Renal Physiology (2010)
  7. "Cellular magnesium homeostasis" Archives of Biochemistry and Biophysics (2011)

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