Hyperkalemia. Potassium is mainly an intracellular ion. High
turnover of tumor cells leads to spill of potassium into the blood.
Symptoms usually do not manifest until levels are high and they
include * cardiac conduction abnormalities (can be fatal) * severe
muscle weakness or paralysis Hyperphosphatemia. Like potassium,
phosphates are also predominantly intracellular. Hyperphosphatemia
causes acute renal failure in tumor lysis syndrome, because of
deposition of calcium phosphate crystals in the renal parenchyma.
Hypocalcemia. Because of the hyperphosphatemia, calcium is
precipitated to form calcium phosphate, leading to hypocalcemia.
Symptoms of hypocalcemia include (but are not limited to): * tetany
* seizures * mental retardation / dementia * parkinsonian
(extrapyramidal) movement disorders * papilledema * emotional
instability / agitation / anxiety * myopathy Hyperuricemia[2] and
Hyperuricosuria. Acute uric acid nephropathy (AUAN) due to
hyperuricosuria has been a dominant cause of acute renal failure
but with the advent of effective treatments for hyperuricosuria,
AUAN has become a less common cause than hyperphosphatemia. Two
common conditions related to excess uric acid, gout and uric acid
nephrolithiasis, are not features of tumor lysis syndrome.
Pretreatment spontaneous tumor lysis syndrome. This entity is
associated with acute renal failure due to uric acid nephropathy
prior to the institution of chemotherapy and is largely associated
with lymphomas and leukemias. The important distinction between
this syndrome and the post-chemotherapy syndrome is that
spontaneous TLS is not associated with hyperphosphatemia. One
suggestion for the reason of this is that the high cell turnover
rate leads to high uric acid levels through nucleobase turnover but
the tumor reuses the released phosphate for growth of new tumor
cells. In post-chemotherapy TLS, tumor cells are destroyed and no
new tumor cells are being synthesized.
