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Type 2 Renal Tubular Acidosis

Title               

Ñ    Type 2 Renal Tubular Acidosis

Pathogenesis

Causes

Ñ    Genetic:

Autosomal dominant

Ñ    Carbonic anhydrase II deficiency

Ñ    Drugs:

Acetazolamide

Ñ    Post-renal transplant

Ñ    Hyperparathyroidism

Ñ    Fanconi syndrome:

The Fanconi syndrome refers to a:

·          Disturbance of proximal tubular function

That results in:

·          Generalised aminoaciduria

·          Phosphate wasting

·          Metabolic bone disease

·          Renal tubular acidosis

·          Renal glycosuria.

Fanconi syndrome may be:

·          Primary Idiopathic

Or:

Secondary to:

·          Systemic Factors

E&M

Cystinosis, tyrosinaemia, Wilson’s disease, Lowe’s syndrome, galactosaemia, hereditary fructose intolerance

Hyperparathyroidism either primary or secondary

KUS

Acute tubular necrosis, hypokalaemic nephropathy, transplant rejection

HS

Myeloma

LMS

Sjögren’s syndrome

Toxins

Heavy metals

Drugs

6-mercaptopurine

Pathophysiology

Ñ    Failure of sodium bicarbonate reabsorption in the proximal tubule

This gives rise to:

Ñ    Acidosis

Ñ    Hypokalaemia

Ñ    Inability to lower urinary pH < 5.5 despite systemic acidosis

Ñ    Bicarbonate in urine despite low plasma bicarbonate

Clinical Features

KUS

Ñ    Metabolic acidosis

Ñ    Polyuria

Ñ    Polydypsia

CNS

Ñ    Proximal myopathy

LMS

Ñ    Rickets and osteomalacia

Investigations

Fluids

Blood

Biochemistry

Ñ    Acidosis

Ñ    Hypokalaemia

Ñ    Hyperchloraemia

Urine

Ñ    pH > 5.5

Ñ    Aminoaciduria

Ñ    Glycosuria

Management

Control

Drugs

Ñ    Bicarbonate supplements

Ñ    Potassium supplements

Ñ    Thiazide diuretics:

Decreases filtered load of bicarbonate

May necessitate increased potassium supplementation

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