From the Guidelines
Chronic myeloid leukemia (CML) patients on tyrosine kinase inhibitors (TKIs) like imatinib should be monitored for microalbuminuria every 6-12 months, as it may indicate early kidney damage, and treatment should involve optimizing blood pressure control and glycemic control, with potential dose adjustment or switching of TKI therapy if necessary. The connection between CML treatment and microalbuminuria stems from the potential nephrotoxicity of TKIs, which can affect podocyte function and glomerular filtration, as reported in a study published in Leukemia in 2016 1. Some key points to consider in the management of CML patients with microalbuminuria include:
- Regular screening for microalbuminuria using a spot urine albumin-to-creatinine ratio (UACR), with values of 30-300 mg/g indicating microalbuminuria
- Referral to a nephrologist for further evaluation and management if microalbuminuria is detected
- Optimizing blood pressure control with ACE inhibitors or ARBs, such as lisinopril 10-40 mg daily or losartan 50-100 mg daily, which have renoprotective effects beyond blood pressure reduction
- Optimizing glycemic control if the patient has diabetes
- Potential dose adjustment or switching of TKI therapy to a different TKI with less renal toxicity based on individual patient factors The importance of monitoring and managing microalbuminuria in CML patients is also highlighted by the association between renal impairment and increased cardiovascular disease (CVD) risk, as reported in a study published in the European Heart Journal in 2007 1. Early detection and management of microalbuminuria can help prevent progression to overt proteinuria and chronic kidney disease in CML patients, and ultimately reduce the risk of CVD and other complications.
From the Research
CML and Microalbuminuria
- There is no direct evidence in the provided studies that links Chronic Myeloid Leukemia (CML) to microalbuminuria.
- CML is a myeloproliferative neoplasm characterized by the presence of the Philadelphia chromosome, which is defined by the BCR::ABL1 oncogene 2, 3, 4, 5, 6.
- The treatment of CML typically involves tyrosine kinase inhibitors (TKIs) that target the BCR::ABL1 fusion oncogene, with options including imatinib, dasatinib, bosutinib, and nilotinib for first-line treatment 2, 4, 5, 6.
- Hematological adverse events are common with TKI therapy, including anemia, neutropenia, and thrombocytopenia, with varying prevalence depending on the specific TKI used 3.
- The management of CML also considers the phase of the disease, with chronic phase (CML-CP) being the most common presentation, and advanced phases such as accelerated phase and blast phase requiring more aggressive treatment approaches 2, 4, 5, 6.
- While microalbuminuria, which is a marker of early kidney damage, is not directly discussed in the context of CML in the provided studies, patients with CML may experience a range of systemic effects due to their disease or its treatment that could potentially impact kidney function. However, without specific evidence, it's not possible to draw conclusions about the relationship between CML and microalbuminuria based on these studies.