Correction from The New England Journal of Medicine — The Tumor Lysis Syndrome. Correspondence from The New England Journal of Medicine — The Tumor Lysis Syndrome. N Engl J Med. May 12;(19) doi: /NEJMra The tumor lysis syndrome. Howard SC(1), Jones DP, Pui CH. Author information.

Author: Kazracage Moogubar
Country: Vietnam
Language: English (Spanish)
Genre: Personal Growth
Published (Last): 8 December 2016
Pages: 453
PDF File Size: 15.85 Mb
ePub File Size: 10.27 Mb
ISBN: 968-9-16007-310-9
Downloads: 16262
Price: Free* [*Free Regsitration Required]
Uploader: Makinos

Thus, a thorough clinical history is of paramount importance when dealing with a cancer patient who has presented with an acute decline in kidney function. Furthermore, a secondary decrease in free calcium concentration due to phosphorus binding is manifested by indications of central nervous toxicity such as seizures and psychiatric complaints, prolongation of the QT interval on ECG, and muscle tetany[ 12 ]. The dosage of rasburicase is based on the underlying risk of Tuomr.

The most widely used diagnostic criteria are those proposed by Cairo et al[ 2 ] in N Engl J Med. Prophylaxis is the mainstay of management and should be routinely implemented in high and intermediate risk patients. A medication mimicking urate oxidase named rasburicase was approved by Food and Drug Association in for use in subjects at risk of TLS[ 21 ].

Furthermore, calcium products do not lower potassium sybdrome and they must be used in conjunction with modalities which lower the serum concentration of potassium.

It is likely that advanced age predisposes to TLS via a decrease in the renal reserve, and may complicate volume replacement therapy due to higher rates of cardiac dysfunction.

Clinicians should stratify every hospitalized cancer patient, especially those receiving chemotherapy, for the risk of TLS. Nephrotoxic effects often develop from overproduction of monoclonal immunoglobulins and free light chains, synrdome to cast nephropathy the most common cause of acute kidney injurylight-chain—related proximal tubular injury, and various glomerulopathies such as light-chain deposition disease and amyloid light-chain AL amyloidosis.

Nevertheless, despite the availability of allopurinol, there is a significant number of patients who still develop ssyndrome kidney damage due to uric acid toxicity. Read the new Review Article on this topic.

Also, an alkaline pH promotes calcium binding to albumin, which can be very dangerous in patients with TLS who tend to have lower calcium levels at baseline, leading to neuromuscular and cardiac toxicity.


Targeted agents, defined as drugs designed to target specific gene mutations in malignant tissue, inhibit oncogenic signaling cascades associated with tumor growth.


The tumor lysis syndrome.

Other general comorbid conditions such as cardiac disease, diabetes mellitus, and renal disease should be considered prior to hydration since patients with these medical problems might easily develop symptomatic volume overload. First, all patients at intermediate and high risk should be actively hydrated with IV fluids.

Hyperkalemia is one of the key laboratory manifestations of TLS. Typically, a carbonic anhydrase inhibitor acetazolamide or sodium bicarbonate are used to reach a urine pH of at least 6.

Acute Kidney Injury in Patients with Cancer | NEJM Resident

Rise in creatinine is not attributable to chemotherapeutic agent s. National Center for Biotechnology InformationU. Furthermore, it is likely that physicians will manage a greater number of cancer patients in future in the future, due to the improved survival rates of ,ysis with cancer, ageing and growing population.

Thus, in patients at high risk the recommended dose is 0. Another aspect of the risk stratification which we use is the type and burden of malignancy. The decision to start phosphate binders should be decided nejmm a case by case basis and always discussed with the patient prior to its initiation.

Tumor lysis syndrome: A clinical review

However, this approach has not been shown to be superior to the administration of normal saline alone[ 29 ]. Single-dose rasburicase nejmm tumour lysis syndrome in adults: Potassium and phosphorus should be eliminated from the diet and intravenous IV fluids. When in excess, phosphorus tends to bind to calcium, forming the so-called calcium phosphorus product or calcium phosphate[ 2 – 4 ].

Cardiac arrhythmias not attributable to chemotherapeutic agent s Life-threatening e. However, there are other mechanisms for uric acid mediated kidney impairment such as endothelial dysfunction and local ischemia, proinflammatory and proxidative states, and impairment of local renal repair mechanisms[ 1011 ].

First seizures in adults. Put simply, purines are metabolized initially to hypoxanthine and xanthine via enzyme xanthine oxidase to uric acid, which is a final byproduct in humans. Uric Acid – key ingredient in the recipe for cardiorenal metabolic syndrome.


Is tumor-cell infiltration of the kidneys a common cause of acute kidney injury in patients with leukemia and lymphoma? Certain parameters should be monitored in individuals at high tumo for TLS such as uric acid, phosphorus, potassium, and LDH 4 h after the initiation of chemotherapy or radiation therapy.

Seizure of any kind which are prolonged, repetitive or difficult to control e.

Rheumatology Oxford ; This article has been cited by other articles in PMC. Uric acid can crystalize and obstruct the flow in the renal tubules, leading to acute kidney injury[ 2 – 410 ]. However, some mammals have an additional enzyme called urate oxidase that converts uric acid to the much more water soluble allantoin, which is easily removed by renal system. Furthermore, cancer has been found by the Centers for Disease Control and Prevention to be the second leading cause of death among United States residents in [ 1 ].

Calcium containing phosphate binders should theoretically be the first choice given the frequent presence of hypocalcemia in patients with TLS. Individuals deemed to be at increased risk of fluid overload, such as patients with cardiac and baseline renal disease, we consider the administration of IV loop diuretics such as furosemide to decrease the risk of pulmonary edema and augment urine output. When assessing the risk of TLS in a particular patient, it is essential to bear in mind both the general and tumor-related predictors of risk.

TLS is an oncometabolic emergency resulting from rapid cell death.

It is important to note that calcium phosphate crystals facilitate the deposition of uric acid in renal tissue[ 2 ]. Certain patient factors such advanced age and the presence of preexistent renal and cardiac diseases warrant a closer follow up during preventive hydration.