Renal Tubular Acidosis

Exam Cram

• Type 1:  hypokalaemia, distal tubule inability to excrete H+

• Type 2:  hypokalaemia, proximal tubule inability to re-absorb bicarbonate

• Type 3: very rare, carbonic anhydrase genetic abnormality

• Type 4:  hyperkalaemia, lack of renin & aldosterone from diabetic destruction of renin producing cells

Outline

Background 

There are four types of renal tubular acidosis. 

Type 1

Pathophysiology: Inability to excrete H+ (acid)

Location: Sistal convoluted tubule

Electrolytes: Hypokalaemia

Associations: (PANSS) PBC, amphotericin, nsaids, SLE, Sjogens

Type 2

Pathophysiology: Inability to absorb bicarbonate (HCO3-)

Location: Proximal convoluted tubule

Electrolytes: Hypokalaemia

Associations: (FAMP) Fanconi syndrome, acetazolamide, multiple myeloma, parathyroid (hyper)

Wilson's Disease & cisplatin

Type 3

Pathophysiology: Carbonic anhydrase II deficiency (mutation)

Location: Mixed proximal and distal tubules

Associations: Very rare

Type 4

Pathophysiology: Hyporeninemic hypoaldosteronism

Location: Distal convoluted tubule

Electrolytes: Hyperkalaemia

Associations: Diabetic nephropathy,  (destruction of juxtaglomerular cells who produce renin)

Presentation: 'unable to tolerate ACE inhibitor due to rise in creatine / hyperkalaemia', ddx renal artery stenosis

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Diagnosis

Diagnostic screening: 

• Acidosis

• Hypercholaemia

• Normal anion gap

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Management

1. Sodium bicarbonate

2. K+ replacement in those with low K+

References

1. BMJ Renal tubular acidosis, Renal tubular acidosis - Symptoms, diagnosis and treatment | BMJ Best Practice US. Available at: https://bestpractice.bmj.com/topics/en-gb/239 (Accessed: 27 September 2024).

Created in 2024. Produced off FOAM basis: free, open access, medical education. This is not clinical advice, education for multiple choice questions only! Produced to the best of the author's ability. Any issues please contact contact: MunroMedics@gmail.com