Onconephrology


1. What is onconephrology?

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.

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

  • 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

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

  • 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.

Table 37.1.
Pre-renal, Intrinsic and Post-renal Causes of Acute Kidney Injury 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

  • Protracted ischemia

  • Nephrotoxic agents: for example, IV contrast,

  • Ifosfamide, cisplatin, aminoglycoside

Lymphomatous infiltration of the kidney
Acute interstitial nephritis
Tumor lysis syndrome
Cast nephropathy
Thrombotic microangiopathy
Calcineurin inhibitor toxicity

Obstruction due to

  • Primary or metastatic abdominal or pelvic malignancy

  • Retroperitoneal fibrosis

  • Crystals (Acyclovir, urate, methotrexate)

ACEi , Angiotensin converting enzyme inhibitor; ARB , angiotensin receptor blocker; CAR-T , chimeric antigen receptor–T-cell therapy; IL , interleukin; IV , intravenous; NSAIDS , non-steroidal anti-inflammatory drugs.

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 .

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here