Mitomycin-Associated Renal Failure

Hamner, Ronald W.

doi:10.1001/archinte.1983.00350040193029

Cited by 39 publications

(5 citation statements)

References 11 publications

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“…Mitomycin C (MMC) is a potent alkylating agent which is often employed in the treat ment of solid tumors, mainly of gastrointesti nal, breast and prostatic origin [1], Adverse effects of this drug include rash, myelosuppression, alopecia, cardiotoxicity, pulmonary fibrosis and nephrotoxicity [2][3][4].…”

Section: Introductionmentioning

confidence: 99%

Pulmonary Hemorrhage as a Clinical Manifestation of Hemolytic-Uremic Syndrome Associated with Mitomycin C Therapy

Torrá

Poch²,

Torrás³

et al. 1993

Chemotherapy

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Mitomycin C (MMC) is an alkylating agent that has been recently associated with the hemolyticuremic syndrome (HUS). Pulmonary impairment in the HUS is rarely reported in the literature, and no reports of pulmonary hemorrhage, as a clinical feature of the HUS, have been documented. We describe two women who developed HUS after MMC therapy and presented massive pulmonary bleeding. Pulmonary hemorrhage is an uncommon feature in the HUS, and seems to appear especially in the HUS associated with MMC therapy. It is extremely resistant to standard treatment, and confers a poor prognosis for this disease.

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Section: Introductionmentioning

confidence: 99%

Pulmonary Hemorrhage as a Clinical Manifestation of Hemolytic-Uremic Syndrome Associated with Mitomycin C Therapy

Torrá

Poch²,

Torrás³

et al. 1993

Chemotherapy

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“…Specifically, metabolized DOX accumulates in the kidneys, and ~4 -8% of administered DOX is slowly excreted through urine over several days (72,113). Although the accretion of DOX within the kidneys is necessary for its elimination, renal failure has been demonstrated in patients undergoing Adriamycin chemotherapy (10,44,100). Indeed, the necessity to closely monitor kidney function in patients was first established in 1977 in a case study demonstrating that DOX therapy was associated with renal failure (10).…”

Section: Dox-induced Nephrotoxicitymentioning

confidence: 99%

“…DOX can cause nephropathy in cancer patients for a variety of reasons. For example, DOX-induced tumor lysis and collection within the kidneys can result in the increased deposition of potassium, phosphate, and uric acid into the renal tubules, as well as deposition of fibrin thrombi within the glomeruli and the need for maintenance dialysis (44,100).…”

Section: Dox-induced Nephrotoxicitymentioning

confidence: 99%

Exercise stimulates beneficial adaptations to diminish doxorubicin-induced cellular toxicity

Smuder

2019

American Journal of Physiology-Regulatory, Integrative and Comp

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Doxorubicin (DOX) is a highly effective antitumor agent used for the treatment of a wide range of cancers. Unfortunately, DOX treatment results in cytotoxic side effects due to its accumulation within off-target tissues. DOX-induced cellular toxicity occurs as a result of increased oxidative damage, resulting in apoptosis and cell death. While there is no standard-of-care practice to prevent DOX-induced toxicity to healthy organs, exercise has been shown to prevent cellular dysfunction when combined with DOX chemotherapy. Endurance exercise stimulates numerous biochemical adaptations that promote a healthy phenotype in several vulnerable tissues without affecting the antineoplastic properties of DOX. Therefore, for the development of an effective strategy to combat the pathological effects of DOX, it is important to determine the appropriate exercise regimen to prescribe to cancer patients receiving DOX therapy and to understand the mechanisms responsible for exercise-induced protection against DOX toxicity to noncancer cells. This review summarizes the cytotoxic effects of DOX on the heart, skeletal muscle, liver, and kidneys and discusses the current understanding of the clinical benefits of regular physical activity and the potential mechanisms mediating the positive effects of exercise on each organ system.

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“…Thrombotic microangiopathy, either in the form of thrombotic thrombocytopenic purpura (TTP) or hemolytic uremic syndrome (HUS), is a recently described complication of antineoplastic therapy [1][2][3][4][5][6][7][8][9][10][11][12]. Here, we describe a patient developing TTP subsequent to intense consolidation chemotherapy for acute myelogenous leukemia (AML).…”

Section: Introductionmentioning

confidence: 99%

Thrombotic thrombocytopenic purpura subsequent to acute myelogenous leukemia chemotherapy

et al. 1986

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A woman in complete remission from acute myeloblastic leukemia developed thrombotic thrombocytopenic purpura (TTP) subsequent to the third intensive consolidation cycle of cytosine arabinoside and daunorubicin chemotherapy. The constellation of clinical manifestations indicative of TTP were recognized only in retrospect, as they were initially attributed to more usual complications of bone marrow-ablative chemotherapy. The manifestations, probably fueled by numerous red cell and platelet transfusions, increased at the time of recovery of hematopoiesis. At postmortem examination, characteristic microvascular lesions were found in most organs. Similar thrombotic microangiopathy has been described with mitomycin-based chemotherapy regimens and with the combination of cisplatin, vinblastine, and bleomycin. Successful management of this serious complication of chemotherapy requires increased awareness and earlier recognition.

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Mitomycin-Associated Renal Failure

Cited by 39 publications

References 11 publications

Pulmonary Hemorrhage as a Clinical Manifestation of Hemolytic-Uremic Syndrome Associated with Mitomycin C Therapy

Pulmonary Hemorrhage as a Clinical Manifestation of Hemolytic-Uremic Syndrome Associated with Mitomycin C Therapy

Exercise stimulates beneficial adaptations to diminish doxorubicin-induced cellular toxicity

Thrombotic thrombocytopenic purpura subsequent to acute myelogenous leukemia chemotherapy

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