11 RTA

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• many times asymptomatic, discovered on routine blood work

• changes bicarb level: non-anion gap

Type 1

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• H channel defect, can't secrete H

• K held in lumen, no absorption

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• in metabolic acidosis, urine should be low to excrete H

• if high pH, there's defect excreting H

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• bilateral stones: think distal RTA

Calcium binds to negative albumin, competing with hydrogen ions

• Alkalosis: less H+ competing, more Ca binding, which decreases free calcium levels.

• Acidosis, increase H+ competing, less Ca binding, resulting in increased free calcium levels

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• very very high yield: sjogren or RA

• 1 shaped acid tube: renal tubular acidosis (RTA) type 1 is cumulative toxicity of amphotericin

• Depleted potassium banana peel: RTA type 1 is associated with hypokalemia

Urine Anion Gap

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• urinary anion gap equation different from plasma anion gap

• urine Cl goes up, UAG becomes negative

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Type 2

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• Fan cone: Fanconi syndrome (type 2 RTA) associated with use of expired tetracyclines

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Type 4

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• aldosterone doesn't work > hyperkalemia

• hyperkalemia > increased K into cell, increased H out of cell> high pH in PCT cells

• high pH > unable to excrete H and NH3

• Inadequate amount of NH3 available for buffering of protons. Even if only a few protons are secreted distally, urinary pH will fall in the absence of buffers.

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• diabetic renal: less renin production from renal insufficiency

• ace/ARB: less aldosterone

• bactrim: disrupt K excretion

• Hyperkalemic RTA is commonly seen in elderly patients who have poorly controlled diabetes with damage to the juxtaglomerular apparatus, which causes a state of hyporeninemic hypoaldosteronism.

• ACE I: high potassium cup

• Depleted mineral mine: NSAIDs can cause hypoaldosteronism (decreased mineralocorticoids)

• Big K: NSAID induced hypoaldosteronism can cause hyperkalemia. Type 4 RTA

• Mad scientist with 4 tubes of acid: Type IV renal tubular acidosis (RTA)

• K shape: Type IV RTA leads to hyperkalemia

• Elevated bananas: K+ sparing diuretics can cause hyperkalemia

• Acid spill into intracellular space: K+ sparing diuretics cause a normal anion gap metabolic acidosis (by decreasing the function of the H+ATPase)

• 4 acid tubes: K+ sparing diuretics inhibit the effects of aldosterone in the collecting duct causing a type 4 renal tubular acidosis (RTA)

• Big K: type 4 RTA is associated with hyperkalemia

• Depleted mineral mine: heparin can cause hypoaldosteronism (a mineralocorticoid)

• Big K: heparin induced hypoaldosteronism (Type 4 RTA) causes hyperkalemia

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• fludrocortisone: synthetic aldosterone

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