Acute Tubular Necrosis

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Acute tubular necrosis is a common and important cause of reversible acute renal failure

In acute tubular necrosis (ATN), metabolic or toxic disturbances cause necrosis of renal tubular epithelial cells.
Although the tubular epithelial cells die and are shed, regeneration is possible if the damaging stimulus is corrected, since residual viable tubular epithelial cells can proliferate to re-populate the tubules.
It is this regenerative capacity of the tubular epithelial cells that permits adequate tubular functioning after renal transplantation following a prolonged period of hypoxia of the graft.

There are three phases to ATN:

1 Oliguric phase. A damaging stimulus causes necrosis of renal tubular epithelium. There is blockage of renal tubules by necrotic cells, and a secondary reduction in glomerular blood flow (caused by arteriolar constriction) reduces glomerular filtration. Macroscopically, kidneys are diffusely swollen and oedematous. Patients develop acute renal failure and oliguria. Supportive measures are required to prevent hyperkalaemia and fluid overload.

2 Polyuric phase. Over 1-3 weeks, regeneration of renal tubular epithelium takes place, with removal of dead material by phagocytic cells, as well as in the form of casts in urine. As tubules open up and glomerular blood flow increases, patients develop polyuria. This is because the regenerated tubular cells are undifferentiated and have not developed the specializations necessary for resorption of electrolytes and water. Replacement of fluid and electrolytes is needed to compensate for excessive loss from urine.

3 Recovery phase. Tubular cells re-establish differentiation and there is restoration of renal function.

Rare functional disturbances of tubules

Metabolic abnormalities may cause secondary tubular damage

Urate nephropathy is seen in a small proportion of patients with hyperuricaemia. Precipitation of urate crystals occurs in the renal collecting ducts, causing tubular damage, inflammation and later scarring.

Other crystal nephropathies are rare, the most important being associated with the inherited matabolic disorder, primary hyperoxaluria, in which oxalate crystals are precipitated in tubules and lead to extensive tubular and interstitial damage. This eventually leads to chronic renal failure.

Nephrocalcinosis is caused by persistent hypercalcaemia. Calcification occurs in the renal parenchyma, particularly tubular basement membrane, with tubular damage and later fibrosis. During development of this condition there is failure of tubular function, with development of polyuria.

Myeloma causes casts of secreted Bence-Jones protein to precipitate out in renal tubules, causing physical obstruction of tubules. Amyloid may develop in glomeruli (see amyloid) and, if the myeloma is associated with hypercalcaemia from bone destruction, there may be superimposed nephrocalcinosis. Urography with certain contrast agents may precipitate acute tubular blockage and acute renal failure.

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