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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

4 pages



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USMLE® Step 1 style questions USMLE

of complete

A 32-year-old G1P2 female is undergoing therapy for induction of labor in the setting of severe pre-eclampsia. On rounds, the patient is noted to be somnolent. Past medical history is notable for hypothyroidism and gestational diabetes. Temperature is 37.0°C (98.6°F), pulse is 52/min, respirations are 7/min, blood pressure is 95/74 mmHg, and O2 saturation is 93% on room air. The patient’s physical examination is notable for absent deep tendon reflexes. Laboratory findings are demonstrated below:  
 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 
Which of the following is the most likely etiology of this patient's clinical presentation?


Content Reviewers

Rishi Desai, MD, MPH


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.


  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 Professional (2019)
  5. "Physiology and pathophysiology of the calcium-sensing receptor in the kidney" American Journal of Physiology-Renal Physiology (2010)
  6. "Cellular magnesium homeostasis" Archives of Biochemistry and Biophysics (2011)

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