Electrolyte disturbances: Pathology review


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Electrolyte disturbances: Pathology review


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


Electrolyte disturbances: Pathology review

USMLE® Step 1 questions

0 / 10 complete


USMLE® Step 1 style questions USMLE

of complete

A 67-year-old female presents to the emergency department with nausea, vomiting, and lethargy. The patient is currently undergoing treatment for diffuse large B-cell lymphoma and last received chemotherapy two days ago. The patient’s temperature is 37.0°C (98.6°F), pulse is 121/min, respirations are 18/min, blood pressure is 92/74 mmHg, and O2 saturation is 94% on room air. On physical exam, she is pale and ill-appearing, intermittently convulsing, and has tenderness to palpation over the left flank. Laboratory findings are demonstrated below:  
 Laboratory Value  Result 
 Erythrocytes  20/hpf 
 Leukocytes  30/hpf 
 Fractional excretion of sodium (FENa  >3%  
 Urine Microscopy  + uric acid crystals 
Which of the following metabolic derangements best explains this patient's clinical presentation?


Content Reviewers

Antonia Syrnioti, MD


Anca-Elena Stefan, MD

Sam Gillespie, BSc

Jennifer Montague, PhD

Kaia Chessen, MScBMC

Two people came to the Emergency Department during your shift. One of them is 75-year-old Karen who has palpitations and muscle weakness. Karen also has heart failure and one of the medications she’s currently on is digitalis. The other one is 25-year-old Carmen who has tetany. On the clinical examination, Carmen has a positive Chvostek sign. In both these individuals, an ECG was done and levels of electrolytes were taken. Karen’s ECG showed a wide QRS complex with peaked T waves and high levels of potassium, while Carmen’s ECG showed prolonged QT and low levels of calcium.

Okay, now let’s start talking about electrolytes and what happens when their levels are either too high or too low.

Let’s begin with potassium, which is a cation that’s mostly in the intracellular fluid, or ICF for short. It’s essential for the normal functioning of excitable tissues, such as nerves and muscles, including the cardiac muscle, and also maintains the resting membrane potential.

So, with hyperkalemia, there’s too much potassium in the extracellular fluid or ECF. And in order for there to be hyperkalemia, there are two possibilities. The first is an external balance shift, like when there’s decreased potassium excretion by the kidneys, leading to increased serum potassium. There’s also internal balance shift where potassium moves out of cells, and into the interstitium and blood. One potential cause is hyperosmolarity. Osmolarity reflects the number of solute particles per liter of solvent, and normally, the osmolarity of the ICF equals the osmolarity of the ECF, even though the exact composition of solutes differs. So when there’s hyperosmolarity, this means that there’s something in the ECF that creates an osmotic force capable of dragging water from inside the cells, like glucose, for example. As water leaves the cells, the intracellular potassium concentration increases and this creates a driving force for potassium to leave the cell, leading to a rise in extracellular potassium and hyperkalemia.

Next, acid-base disturbances also play a role in this. pH reflects the concentration of hydrogen ions and normal blood pH is about 7.4. To maintain pH balance, hydrogen moves in and out of the cells. In order for hydrogen to move across the cell membrane, it must be accompanied by an anion, meaning an ion with a negative charge, or it must be exchanged for another cation, like potassium. When there’s an increase in the hydrogen ion concentration in the blood, this is called metabolic acidosis. As a coping mechanism, hydrogen must enter the cells in exchange for potassium, which leaves the cells. And this leads to hyperkalemia.


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  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Practical Renal Pathology, A Diagnostic Approach E-Book" Elsevier Health Sciences (2012)
  4. "Physiology E-Book" Elsevier Health Sciences (2017)
  5. "Rosen's Emergency Medicine" Elsiever (2017)
  6. "Hyponatraemia in Hospitalized Adults: a Guide for the Junior Doctor" Ulster Med J. (2017)
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  8. "Electrolyte Disorders" Clinics in Perinatology (2014)
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