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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

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USMLE® Step 1 style questions USMLE

of complete

A 27-year-old female is admitted to the hospital with suicidal ideation. Today is the fourth day of hospitalization, and the course has been uncomplicated. The patient has been participating in therapy, taking medications, and eating daily. During rounds, the patient is noted to have altered mental status. Temperature is 37.0°C (98.6°F), pulse is 76/min, respirations are 22/min, blood pressure is 102/74 mmHg, and BMI is 17 kg/m2. On physical exam, the patient appears thin and cachectic with several healing lacerations noted over the volar aspect of the wrists. Multiple calluses are present over the knuckles of the right hand. She has 2+ pitting edema in the lower extremities bilaterally and faint bibasilar rales on pulmonary auscultation. She is having intermittent convulsions in the upper and lower extremities bilaterally. Which of the following electrolyte abnormalities is most likely present?  

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Hypophosphatemia p. 615

aluminum hydroxide use p. 408

hyperparathyroidism p. 344


hypophosphatemia p. 615


Content Reviewers

Rishi Desai, MD, MPH


Charles Davis, MD

Sam Gillespie, BSc

Tanner Marshall, MS

Hypo- means under, phosphat- refers to phosphate, and -emia refers to the blood, so hypophosphatemia means having a low phosphate level in the blood, typically below 2.5mg/dL.

Phosphate is made up of one central phosphorus atom surrounded by four oxygen atoms in a tetrahedral arrangement, like a mini pyramid, and has a charge of minus 3 and is written PO43-.

In the body, about 85% of the phosphate is stored in the bones, where it combines with calcium to make a tough compound called hydroxyapatite which is the stuff that makes bones hard.

Of the remaining phosphate, a tiny amount is extracellular, or outside cells like in the blood, so this is the bit that gets measured, and the majority is intracellular, or inside cells, where it does all sorts of things.

It’s responsible for phosphorylation, where it binds to fats and proteins.

It forms the high energy bonds of adenosine triphosphate or ATP, which is the most common energy currency in the cell.

It’s part of the DNA and RNA backbone that links individual nucleotides together, and is also part of cellular signaling molecules like cyclic-adenosine monophosphate or cAMP.

Bottom line - phosphate is super important.

Because most of the phosphate is locked up with calcium in the bones, the levels of phosphate are heavily tied with the levels of ionized calcium in the body.

If calcium levels fall, the four parathyroid glands buried within the thyroid gland release parathyroid hormone which frees up both calcium and phosphate ions from the bones.

It does this by stimulating osteoclasts, the cells that break bone down, to release hydrogen ions which dissolves the hard, mineralized hydroxyapatite.

As soon as the positively-charged calcium and negatively-charged phosphate are released from the bones, they grab onto each other again like a pair of star-crossed lovers, meaning that the ionized calcium level doesn’t really go up very much at all.

Now, these two make their way to the nephron of the kidney, and at this point in the proximal convoluted tubule, phosphate usually gets reabsorbed back into the blood via sodium-phosphate cotransporters.


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