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Sunday, 6 November 2016

Renal Tubular Acidosis – Essential Revision Notes

Type 1 (distal) RTA

It result in many diseases that mainly involve medullary part of the kidneys.

Causes include:

·        Primary Type 1 RTA : genetic or idiopathic
·        Tubulointerstitial disease: chronic interstitial nephritis
·        , chronic pyelonephritis, , obstructive uropathy, or renal transplant rejection
·        Nephrocalcinosis: chronic hypercalcaemia or, medullary sponge kidney
·        Autoimmune disease: systemic lupus erythematosus (SLE), chronic active hepatitis, Sjögren syndrome
·        Drugs and toxins: amphotericin , lithium

Type 2 (proximal) RTA


Causes include:

·        Primary: idiopathic
·        Tubulointerstitial disease: interstitial nephritis, amyloidosis , or  multiple myeloma

·        In association with other diseases : Wilson's disease, Sjögren syndrome, and fructose intolerance
·        Drugs and toxins: heavy metals (lead and mercury, acetazolamide, and sulfonamides

Consequences of RTA Type 1 and Type 2

Nephrocalcinosis and renal calculi
due increased urinary calcium excretion. This is more common in Type II because severe acidosis is more frequent.

Hypokalaemia (in Type 1 RTA)
Oteomalacia/rickets (in Type 2 RTA)

Treatment of RTA:
Oral potassium and bicarbonate replacement.
Treatment of underlying or associated disease.

Type 3 RTA : Both Type 1 and Type 2 combined

Type 4 RTA

Metabolic acidosis  plus hyperkalaemia in Chronic Kidney Disease
Cause :  commonly caused by mineralocorticoid deficiency
Less commonly
due to abnormal collecting duct function
or treatment with spironolactone or amiloride

In the common cases with mineralocorticoid deficiency it could be either:

1- Hyporeninaemic hypoaldosteronism:
Secondary to diabetes mellitus or treatment with NSAIDs
Characterized by Low renin, low aldosterone  


2- Hyperreninaemic hypoaldosteronism
Secondary to adrenal disease , congenital enzyme deficiencies , or treatment with ACE inhibitors
Characterized by High renin, low aldosterone

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