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Onconephrology focuses on all aspects of kidney disease in patients with malignancy, as well as areas where nephrology intersects with hematology. As the name implies, nephrologists and oncologists are well positioned to collaborate on this area of medicine.
Electrolyte disorders of malignancy
Secondary glomerular diseases of malignancy
Chemotherapy-related kidney complications
Targeted therapies and the kidney
Paraproteinemia (see Chapter 39 )
Thrombotic microangiopathy (TMA) and all its causes and treatment strategie (see Chapter 41 )
Bone marrow transplant–related kidney diseases
Radiation nephropathy
Tumor lysis syndrome (TLS (see Chapter 38 )
Acute kidney injury (AKI) in the hospitalized patient with malignancy
The ethics of dialysis during end of life in malignanc (see Chapter 80 )
Dosing of chemotherapy in chronic kidney disease (CKD) and end-stage kidney disease ESKD)
Malignancy-associated obstructive kidney disease
Renal cell carcinoma and related complications post-nephrectom (see Chapter 40 )
AKI may occur by at least two mechanisms:
A complication of a particular cancer treatment:
TLS
Drug-induced nephropathy
Post-transplant-related kidney diseases
Surgical procedures
Related to the neoplasm itself
Renal cell cancer
Anatomic obstruction due to a metastatic lesion or obstructing mass
Myeloma/amyloid affecting the kidney
Patients with AKI and malignancy have a worse prognosis than AKI without malignancy.
The answer depends on the sub-population of patients with a particular malignancy, as well as the clinical setting, for example, intensive care unit (ICU) versus general inpatient service versus outpatient. Four main points may be deduced from major studies:
The incidence of AKI among hospitalized patients with malignancy is higher than that of patients without cancer
Acutely ill patients with cancer admitted to the ICU have an even higher risk of AKI
Some cancers are associated with a higher risk of AKI than others:
Kidney
Gall bladder
Liver
Myeloma
Pancreas
Treatment with a hematopoetic stem cell transplant (HSCT), especially myeloablative allogenic HSCT, further raises the risk of AKI associated with malignancies
Table 37.1 summarizes the pre-renal, intrinsic, and post-renal causes of AKI in the cancer patient.
PRE-RENAL | INTRINSIC | POST-RENAL |
---|---|---|
Kidney hypo-perfusion due to sepsis, ascites, and effusions Volume depletion (↓ oral intake, diarrhea, over-diuresis) Impaired cardiac output Hepatic sinusoid obstructive syndrome Hypercalcemia Non-chemotherapeutic drugs (NSAIDS, ACEi/ARB, calcineurin inhibitors) Capillary leak syndrome (e.g., due to IL2, CAR-T therapy) |
Acute tubular necrosis due to
Lymphomatous infiltration of the kidney |
Obstruction due to
|
LKI is common, albeit underdiagnosed, among patients with cancer. In most studies, LKI was found to have a high incidence. While the incidence is high, the association with kidney failure is low. The mechanism of LKI-induced AKI is not completely established. The tubules and glomeruli usually appear morphologically normal on biopsy; it has been proposed that interstitial and intraglomerular pressure elevation due to lymphocytic infiltrations of these compartments is the underlying mechanism of the AKI. Diagnosis can be made via a kidney ultrasound and computed tomography scan imaging in some cases, but a kidney biopsy is required for a definite diagnosis. The management of LKI is focused on the treatment of the underlying malignancy.
TLS is the most common oncologic emergency with an incidence as high as 26% in high-grade B-cell acute lymphoblastic leukemia. TLS results from rapid release of intracellular contents of dying cancer cells into the bloodstream, either spontaneously or in response to cancer therapy. It is biochemically characterized by hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. Cardiac arrhythmias, seizures, and superimposed AKI are common clinical presentations. The pathophysiology of TLS-mediated AKI involves intratubular obstruction and inflammation by the precipitation of crystals of uric acid, calcium phosphate, and/or xanthine. Consensus recommendations for TLS prophylaxis include volume expansion for all risk groups, the use of allopurinol in medium- and high-risk groups, and the use of recombinant urate oxidase (rasburicase) in high-risk groups. See Chapter 13 .
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