Contributions to nephrology
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Tumor lysis syndrome (TLS) is a constellation of metabolic disturbances that may be observed in patients with malignancies. Clinically significant TLS can occur spontaneously, but most often is seen 48-72 h after initiation of cancer treatment. The metabolic abnormalities observed in patients with TLS include hyperkalemia, hyperuricemia, and hyperphosphatemia, which leads to secondary hypocalcemia. ⋯ Hemodynamic changes reducing glomerular flow due to still undefined mediators are also involved in TLS pathophysiology. Pre-existing volume depletion or renal dysfunction may worsen metabolic derangements and ARF. A good comprehension of TLS pathophysiology has provided the basis for an effective and rational treatment of this complication, adversely affecting the outcome of cancer patients.
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Uric acid nephropathy is a potentially reversible cause of acute renal failure resulting from diffuse urate crystal depositions in the tubules in the setting of excessive uricosuria. Hyperuricemia is frequently encountered in ICU patients with acute renal failure of any etiology, but it is rarely a prominent feature or a major pathophysiological element in the renal failures of nonhematology/ oncology patients. ⋯ The most frequent clinical context is, nevertheless, hematological, when patients with large tumor burden and rapid cell turnover develop acute tumor lysis syndrome (ATLS). The purpose of this chapter is to review the pharmacological tools currently available and their optimal use in the treatment of patients admitted in intensive care unit with hyperuricemia and severe acute renal failure.