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Non-urothelial bladder cancers
Transitional cell carcinoma
Hypospadias and epispadias
Posterior urethral valves
Lower urinary tract infection
Acute tubular necrosis
Renal cortical necrosis
Renal papillary necrosis
IgA nephropathy (NORD)
Rapidly progressive glomerulonephritis
Focal segmental glomerulosclerosis (NORD)
Minimal change disease
Medullary cystic kidney disease
Medullary sponge kidney
Multicystic dysplastic kidney
Polycystic kidney disease
Chronic kidney disease
Renal tubular acidosis
Nephroblastoma (Wilms tumor)
Renal cell carcinoma
Renal artery stenosis
Acid-base disturbances: Pathology review
Congenital renal disorders: Pathology review
Electrolyte disturbances: Pathology review
Kidney stones: Pathology review
Nephritic syndromes: Pathology review
Nephrotic syndromes: Pathology review
Renal and urinary tract masses: Pathology review
Renal failure: Pathology review
Renal tubular acidosis: Pathology review
Renal tubular defects: Pathology review
Urinary incontinence: Pathology review
Urinary tract infections: Pathology review
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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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