* Hyperkalemia. Potassium is mainly an intracellular ion. High turnover of<unk>  cells leads to spill of potassium into the blood. Symptoms usually do not manifest until levels are high (> 6.5 mmol/L) normal 3.5–5.0 mmol/L and they include * palpitations, cardiac conduction abnormalities, and arrhythmias (can be fatal) * muscle weakness or paralysis * Hyperphosphatemia. Like potassium, phosphates are also predominantly intracellular. Hyperphosphatemia causes acute kidney injury in<unk> , because of deposition of calcium phosphate crystals in the kidney 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 * paresthesias * muscle cramps * muscle weakness * sudden changes in mental status, including emotional lability * Parkinsonian (extrapyramidal) movement disorders * papilledema * Hyperuricemia and hyperuricosuria. Massive cell death and nuclear breakdown generates large quantities of nucleic acids. Of these, the purines (adenine and guanine) are converted to uric acid via the purine degradation pathway and excreted in the urine. However, at the high concentrations of uric acid generated by<unk><unk> , uric acid is apt to precipitate as monosodium urate crystals. Acute uric acid nephropathy (AUAN) due to hyperuricosuria has been a dominant cause of acute kidney 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<unk> . * Lactic acidosis. * Pretreatment spontaneous<unk> . This entity is associated with acute kidney failure due to uric acid nephropathy prior to the institution of chemotherapy and is largely associated with lymphoma and leukemia. The important distinction between this syndrome and the post-chemotherapy syndrome is that spontaneous<unk>  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<unk>  reuses the released phosphate for growth of new<unk>  cells. In post-chemotherapy<unk> ,<unk>  cells are destroyed and no new<unk>  cells are being synthesized.<unk>  is most common during cytotoxic treatment of hematologic neoplasms.
Tumor lysis syndrome
Distributive shock
Sepsis
Multiple organ dysfunction syndrome
Cryptic shock
Septic shock
Vasodilatory shock
Hypovolemic shock