Tumor Lysis Syndrome

Chapter 171 Tumor Lysis Syndrome







PATHOGENESIS AND METABOLIC COMPLICATIONS


The pathogenesis of TLS is related to rapid tumor cell destruction, which may result in release of intracellular ions and metabolic byproducts into the extracellular environment and systemic circulation. The metabolic complications of TLS are therefore characterized by hyperphosphatemia, hyperkalemia, and metabolic acidosis with or without azotemia.1,5 The hyperphosphatemia can secondarily induce hypocalcemia.


Acute renal failure is a common sequela of TLS and the pathophysiology is likely multifactorial.9 Not only do hyperphosphatemia and hyperuricemia result from TLS, they also contribute to the oliguric acute renal failure in these patients. Causes may include tubular precipitation of calcium phosphate and nucleic acid metabolites (and secondary intraluminal tubular obstruction), intravascular volume depletion, and poorly understood malignancy-associated nephrotoxins. A diagram of the purine metabolism pathway is shown in Figure 171-1 and is discussed further in the Treatment section.


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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Tumor Lysis Syndrome

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