2. What does this field of nephrology include?
- 1.
Electrolyte disorders of malignancy
- 2.
Secondary glomerular diseases of malignancy
- 3.
Chemotherapy-related kidney complications
- 4.
Targeted therapies and the kidney
- 5.
Paraproteinemia (see Chapter 39 )
- 6.
Thrombotic microangiopathy (TMA) and all its causes and treatment strategie (see Chapter 41 )
- 7.
Bone marrow transplant–related kidney diseases
- 8.
Radiation nephropathy
- 9.
Tumor lysis syndrome (TLS (see Chapter 38 )
- 10.
Acute kidney injury (AKI) in the hospitalized patient with malignancy
- 11.
The ethics of dialysis during end of life in malignanc (see Chapter 80 )
- 12.
Dosing of chemotherapy in chronic kidney disease (CKD) and end-stage kidney disease ESKD)
- 13.
Malignancy-associated obstructive kidney disease
- 14.
Renal cell carcinoma and related complications post-nephrectom (see Chapter 40 )
3. What are the major causes of AKI in the patients with malignancy?
AKI may occur by at least two mechanisms:
- 1.
A complication of a particular cancer treatment:
- a.
TLS
- b.
Drug-induced nephropathy
- c.
Post-transplant-related kidney diseases
- d.
Surgical procedures
- a.
- 2.
Related to the neoplasm itself
- a.
Renal cell cancer
- b.
Anatomic obstruction due to a metastatic lesion or obstructing mass
- c.
Myeloma/amyloid affecting the kidney
- a.
Patients with AKI and malignancy have a worse prognosis than AKI without malignancy.
4. How common is AKI in the patients with 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:
- 1.
The incidence of AKI among hospitalized patients with malignancy is higher than that of patients without cancer
- 2.
Acutely ill patients with cancer admitted to the ICU have an even higher risk of AKI
- 3.
Some cancers are associated with a higher risk of AKI than others:
- a.
Kidney
- b.
Gall bladder
- c.
Liver
- d.
Myeloma
- e.
Pancreas
- a.
- 4.
Treatment with a hematopoetic stem cell transplant (HSCT), especially myeloablative allogenic HSCT, further raises the risk of AKI associated with malignancies
5. What are the common causes of AKI in the cancer patient?
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 Acute interstitial nephritis Tumor lysis syndrome Cast nephropathy Thrombotic microangiopathy Calcineurin inhibitor toxicity | Obstruction due to
|
6. What is lymphomatous kidney infiltration (LKI)?
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.
7. What is the most common kidney-related oncologic emergency?
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 .
8. What are the risk factors for chemotherapy-induced AKI?
Patient risk factors for chemotherapy-induced nephrotoxicity include: older age, underlying AKI or CKD, and pharmacogenetics favoring drug toxicity. Volume depletion can enhance innate drug toxicity due to increased drug or metabolite concentration in the kidney and may involve formation of intra-tubular crystals by insoluble drug or metabolites. Kidney hypoperfusion can be due to decreased oral intake, over-diuresis, chemotherapy-induced cardiomyopathy, malignant ascites, or pleural effusion. Tumor-related factors predisposing to chemotherapy-induced nephrotoxicity include the presence of toxic tumor proteins, as with myeloma-related kidney injury, kidney infiltration by lymphoma, and cancer-associated glomerulopathies.
9. What is the connection between cancer and CKD?
CKD and cancer are connected in several ways. Cancer can lead not only to the development of CKD and ESRD—often indirectly, from multiple causes (chemotherapy, HSCT)—but also to the presence of CKD can be associated with cancer. Although the overall incidence and prevalence of CKD among patients with cancer is still uncertain, there is growing evidence to suggest that the risk is high and still increasing. The risk for developing CKD varies depending on whether the cancer is solid or hematologic in nature, whether the patient underwent nephrectomy or HSCT, or whether nephrotoxic chemotherapy was administered.
10. Which cancers are common as the glomerular filtration rate declines?
Men with CKD are more at risk for lung and urinary tract cancers. In one analysis, the estimated glomerular filtration rate (eGFR) < 60 mL/min per 1.73 m 2 appears to be a significant risk factor for death from cancer. The excess cancer mortality in those with reduced kidney function varied with site, with the greatest risk in those with breast and urinary tract cancer. Each decrease in eGFR by 10 mL/min per 1.73 m 2 increased the risk of cancer by 29% in men. Lung and urinary tract cancers comprised most of the excess cancer risk. No increased cancer risk in women with CKD was seen in the same study.
11. What is the most common paraneoplastic glomerular disease seen with solid tumors and hematologic malignances?
Membranous nephropathy (MN) remains the most common glomerular pathology reported in patients with solid tumors. The true prevalence of malignancy with MN is unknown. Minimal change disease (MCD) is the most common glomerular disease associated with hematologic malignancies. Table 37.2 summarizes the published list of paraneoplastic glomerular diseases seen with various types of cancer.
| TYPE OF CANCER | ASSOCIATED PARANEOPLASTIC GLOMERULAR DISEASE |
|---|---|
| Lung cancer (includes small cell, non-small-cell, squamous cell, and bronchogenic cancers) | MN, MCD, MPGN, IgAN, FSGS, CGN, HSP, TMA |
| Renal cell cancer | AAA, CGN, IgAN, MCD, FSGS, MPGN, HSP |
| Colon cancer | MN, MCD, CGN |
| Gastric cancer | MN, MPGN, CGN, HSP, TMA |
| Prostate cancer | MN, CGN, HSP |
| Pancreatic cancer | MN, MCD, IgAN |
| Breast cancer | MN, FSGS, MPGN, HSP, TMA |
| Esophageal cancer | MPGN, FSGS |
| Head and neck cancer | MN, IgAN |
| Ovarian cancer | MN, MCD |
| Cervical cancer | MN |
| Endometrial cancer | MN |
| Melanoma | MN, MPGN, MN |
| Hodgkin’s lymphoma | MCD, MN, MPGN, IgAN, FSGS, CGN, AAA, Anti-GBM disease, HSP |
| Non-Hodgkin’s lymphoma | MN, MCD, MPGN, IgAN, FSGS, HSP |
| Chronic lymphocytic leukemia | MPGN, MN, MCD, FSGS, CGN |
| Acute myelogenous leukemia | MN, FSGS |
| Chronic myelogenous leukemia | FSGS, MN, MCD, MPGN |
| MGUS | MPGN, TMA, C3GN |
| T-cell leukemia | FSGS |
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