Recently Diagnosed or Relapsed? Stop Looking For a Miracle Cure, and Use Evidence-Based Therapies To Enhance Your Treatment and Prolong Your Remission
Multiple Myeloma an incurable disease, but I have spent the last 25 years in remission using a blend of conventional oncology and evidence-based nutrition, supplementation, and lifestyle therapies from peer-reviewed studies that your oncologist probably hasn't told you about.
Click the orange button to the right to learn more about what you can start doing today.
- You are here:
- Home »
- Blog »
- Multiple Myeloma »
- Does ASCT Cause Kidney Damage in Myeloma?
Does ASCT Cause Kidney Damage in Myeloma?
Does autologous stem cell transplantation (ASCT) cause kidney damage? Do you want/need aggressive therapy for your newly diagnosed MM?
According to the article linked below, melphalan causes kidney damage. And melphalan is a key component of autologous stem cell transplants (ASCT). And ASCT is part of the FDA approved standard-of-care therapy plan for all newly diagnosed myeloma patients.
- According to research, almost 50% of NDMM patients are diagnosed with kidney involvement.
- Further, according to research, kidney failure is one of the top causes of death for MM patients.
- Lastly, according to research, ASCT can lead to a longer average PFS (first remission) but not a longer OS aka overall survival.
Faced with the above facts, I think the average NDMM patient must ask themselves two important questions.
- What does my diagnostic testing say about my kidney health (creatinine, BUN, eGFR)?
- How advanced is my MM upon diagnosis? In other words, is aggressive therapy worth it? Yes, an ASCT is aggressive therapy.
- Does an autologous stem cell transplantation cause kidney damage?
If you are a NDMM patient wondering about your kidney health and you’d like to learn more about non-conventional kidney health therapies email me at David.PeopleBeatingCancer@gmail.com
Thank you,
David Emerson
- MM Survivor
- MM Cancer Coach
- Director PeopleBeatingCancer
Chemotherapy-induced acute kidney injury: epidemiology, pathophysiology, and therapeutic approaches
“Despite significant advancements in oncology, conventional chemotherapy remains the primary treatment for diverse malignancies. Acute kidney injury (AKI) stands out as one of the most prevalent and severe adverse effects associated with these cytotoxic agents.
While platinum compounds are well-known for their nephrotoxic potential, other drugs including:
- antimetabolites,
- alkylating agents,
- and antitumor antibiotics
are also associated. The onset of AKI poses substantial risks, including heightened morbidity and mortality rates, prolonged hospital stays, treatment interruptions, and the need for renal replacement therapy, all of which impede optimal patient care. Various proactive measures, such as aggressive hydration and diuresis, have been identified as potential strategies to mitigate AKI; however, preventing its occurrence during chemotherapy remains challenging.
Additionally, several factors, including intravascular volume depletion, sepsis, exposure to other nephrotoxic agents, tumor lysis syndrome, and direct damage from cancer’s pathophysiology, frequently contribute to or exacerbate kidney injury. This article aims to comprehensively review the epidemiology, mechanisms of injury, diagnosis, treatment options, and prevention strategies for AKI induced by conventional chemotherapy…
Melphalan
Melphalan is a chemotherapeutic agent commonly used in the treatment of multiple myeloma. Its renal excretion is minimal, ranging from 5.8% to 21.3%, contributing to the idea that this drug could be non-nephrotoxic. However, evidence suggests that certain patients may experience kidney injury, albeit rarely (21).
A study involving patients with AL amyloidosis and pre-existing tubular injury who received high-dose melphalan revealed the development of ATI. The study indicates that pre-existing tubular dysfunction might be a prerequisite for renal injury. Additionally, oval fat bodies were detected in 60% of patients who developed AKI after high-dose melphalan, compared to only 25% of those without AKI, leading to the conclusion that it could serve as a predictor of AKI following high-dose melphalan administration (21).
The incidence of AKI in patients receiving melphalan ranges from 1.6% to 18.8% and its occurrence has been linked with poorer survival rates (21, 253). Several risk factors contribute to the development of AKI, including advanced age, high urine sediment score, hypoalbuminemia, nephrotic-range proteinuria, and diuretic usage.
Among these factors, age and urine sediment score emerged as the most significant predictors. Patients aged 50 years or older with high urine sediment were found to be 10 times more likely to develop AKI compared to those lacking these risk factors (with an incidence of 73% versus 7%) (21).
While a study conducted on rats suggested a potential protective effect of quercetin against melphalan-associated AKI, there is currently no available data regarding its efficacy in humans (254).
The literature presents varying recommendations for dose adjustment of melphalan. According to the FDA, in the palliative setting, patients with pre-existing renal insufficiency with BUN levels ≥ 30 mg/dl could undergo a 50% dose reduction due to the heightened risk of myelosuppression.
However, in the conditioning treatment, all patients should receive the full dose (253). In contrast, the International Myeloma Working Group offers different recommendations based on the patient’s CrCl.
For patients with normal renal function, the oral melphalan dose should range from 0.15 to 0.25 mg/kg/day. If CrCl is between 15 and 59 mL/min, the melphalan dosage must be reduced by 25%. In cases where CrCl falls below 15 mL/min or if the patient is on dialysis, the oral melphalan dose should be reduced by 50%.
For the high-dose IV melphalan protocol, the recommended dose is 200 mg/m2 for patients with normal renal function. However, if CrCl is less than 60 or if the patient is on dialysis, the dose should be reduced to 100-140 mg/m2 (255).
4 Conclusion
Chemotherapy-induced AKI presents a significant challenge at the intersection of oncology and nephrology, complicating cancer treatment, particularly with platinum compounds. The overarching objective remains the optimization of renal health in oncologic patients while preserving the antitumor efficacy of their treatment. Understanding the diverse mechanisms of AKI is essential and requires further elucidation, as they vary among the different classes of chemotherapeutic agents. Tailoring precise protective measures, in addition to general strategies such as hydration protocols, is crucial in mitigating this limiting side effect.
Further clarification of risk factors is needed, and early diagnosis is essential for initiating therapeutic interventions, including dose adjustments and drug discontinuation. Addressing knowledge gaps, overcoming challenges, and incorporating emerging trends in prevention and management are essential to reduce the burden associated with AKI induced by conventional chemotherapy.