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Overview of Kidney Disease in Patients With Cancer - UpToDate
Overview of Kidney Disease in Patients With Cancer - UpToDate
All topics are updated as new evidence becomes available and our peer review process is complete.
INTRODUCTION
Cancer is the second leading cause of death in the United States and is associated with
significant morbidity [1]. As survival rates of patients with cancer have improved over the
past few decades, an increasing number of cancer survivors have or will develop kidney
disease associated with malignancy or its treatment. A variety of kidney complications can
occur among patients with cancer, including acute kidney injury (AKI), chronic kidney disease
(CKD), proteinuria and nephrotic syndrome, and electrolyte disorders.
This topic will provide an overview of the major kidney complications that affect patients with
cancer. Kidney disease in patients with multiple myeloma or other monoclonal
gammopathies, kidney disease among patients with cancer who have undergone
hematopoietic cell transplantation (HCT), and the nephrotoxicity of specific
chemotherapeutic agents are discussed elsewhere:
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AKI in patients with cancer — Acute kidney injury (AKI) is a common complication in
patients with cancer and is associated with reduced treatment dose intensity, lower
remission rates, shorter duration of disease control, and increased mortality, hospital length
of stay, and cost [2-6]. The incidence of AKI in patients with cancer is likely higher than the
incidence observed in patients without cancer.
● In a Danish population-based study that followed 37,267 patients with incident cancer
from 1999 to 2006, the one- and five-year risks of AKI, as defined by a >50 percent
increase in serum creatinine compared with a baseline serum creatinine measured
within one year of cancer diagnosis, were 17.5 and 27 percent, respectively [7]. The risk
of AKI was highest in patients with kidney cancer (44 percent), liver cancer (33 percent),
and multiple myeloma (32 percent). Kidney replacement therapy (KRT) was required in
5.1 percent of patients within one year of AKI onset.
● In a study of 9828 children in China hospitalized with cancer from 2013 to 2015, 17
percent experienced AKI, including 6 percent with community-acquired AKI and 11
percent with hospital-acquired AKI [6]. The cancers with the highest incidence of AKI
were urinary tract cancer (26 percent), liver cancer (19 percent), and retroperitoneal
malignancies (19 percent). In-hospital mortality was higher among children with AKI
compared with those without AKI (5.4 versus 0.9 percent, respectively).
● In other studies, the risk of AKI was higher in patients with cancer who were critically ill
[9,10], those receiving treatment for a high-risk myelodysplastic syndrome or acute
leukemia [11], recipients of hematopoietic cell transplantation (HCT), and those who
had undergone nephrectomy for renal cell carcinoma (RCC) [12,13]. (See "Kidney
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Most observational studies have shown that patients with cancer who develop AKI,
particularly those who require KRT, have a higher risk of mortality than those who do not
have AKI [4,6,9,11,14-17]. In one study of 288 patients with cancer admitted to a cancer
intensive care unit in Brazil, mortality among patients with RIFLE Risk, Injury, and Failure
stages of AKI was 49, 62, and 87 percent, respectively, compared with 14 percent among
those without AKI [9]. (See "Definition and staging criteria of acute kidney injury in adults".)
Overall severity of illness, age, and functional status are likely to contribute to the prognosis
in these patients, and the presence of cancer should not be considered an absolute exclusion
criterion for KRT.
CKD in patients with cancer — Chronic kidney disease (CKD) is also a common complication
of cancer and its therapy. This may be related in part to the high prevalence of preexisting
CKD in patients with various types of malignancy. Two large observational studies, each
involving nearly 5000 patients with cancer, found that approximately 50 percent of patients
with an active malignancy had an estimated glomerular filtration rate (eGFR) of <90
mL/min/1.73 m2 [18,19]. The prevalence of stage 3 and 4 CKD among these patients was 12
and less than 1 percent, respectively. In a prospective study of 4077 patients with various
cancers, 30 percent had an eGFR of 45 to 59 mL/min/1.73 m2, and 8.3 percent had an eGFR of
<45 mL/min/1.73 m2 [20]. Similar rates of CKD have been reported in other large
observational studies of patients with cancer [21,22]. (See "Definition and staging of chronic
kidney disease in adults".)
Having cancer appears to increase the risk of kidney failure needing kidney replacement
therapy (KRT; hemodialysis or peritoneal dialysis, or kidney transplantation). In a Korean
population-based cohort study that compared 824,365 patients newly diagnosed with cancer
with 1,648,730 patients without cancer who were matched for age, sex, eGFR, hypertension,
and diabetes, having cancer was associated with an increased risk of kidney failure requiring
KRT after adjusting for multiple variables (adjusted hazard ratio [HR] 2.29, 95% CI 2.20-2.39)
[23]. Multiple myeloma was associated with the highest risk of kidney failure requiring KRT
(adjusted HR 18.97, 95% CI 14.31-25.15) compared with other cancer types, followed by
leukemia, lymphoma, kidney cancer, ovarian cancer, and liver cancer. The contribution of
chemotherapy administration, and the specific cytotoxic agents used, was not addressed.
Adult survivors of childhood cancer are also at risk for long-term CKD and albuminuria. In a
Dutch nationwide cross-sectional cohort study of 1024 adult childhood cancer survivors who
had undergone nephrectomy, abdominal radiotherapy, total body irradiation (TBI), cisplatin,
carboplatin, ifosfamide, or hematopoietic cell transplantation five or more years prior to
study entry, at a median age of 32 (range 27 to 37) approximately 4 percent had an eGFR of
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<60 mL/min/1.73 m2, compared with none of age- and sex-matched controls [24].
Albuminuria (defined as a urine albumin-to-creatinine ratio >3 mg/mmol [26.6 mg/g]) was
present in 16 percent of survivors compared with 1 percent of controls. Risk factors for CKD
included nephrectomy (odds ratio [OR] 3.7), abdominal radiotherapy (OR 1.8), prior
ifosfamide (OR 2.9), and cumulative cisplatin dose >500 mg/m2 (OR 7.2); risk factors for
albuminuria included TBI (OR 2.3), abdominal radiotherapy dose >30 Gy (OR 2.6), and prior
ifosfamide (OR 1.6).
Patients with cancer and CKD may have an increased risk of death compared with those
without CKD. However, the risk may vary by cancer type, and some studies have found no
differences in mortality between patients with cancer with and without CKD [20-22,25].
The relationship between CKD and cancer appears to be reciprocal since both CKD and end-
stage kidney disease (ESKD) appear to be risk factors for the development of a number of
malignancies. A retrospective study of more than 1 million adults assessed the association
between severity of kidney disease and the risk of incident cancer [26]. Lower eGFR was
associated with an increased risk of kidney cancer (adjusted HR 2.3, 95% confidence interval
[CI] 1.8-2.9 for an eGFR of <30 mL/min/1.73 m2) and urothelial cancer but not other cancers.
Patients with ESKD on dialysis have an increased risk for kidney parenchymal cancer that is
related to the development of acquired kidney cystic disease, which increases with time on
dialysis [27,28]. (See "Cancer screening in patients on maintenance dialysis" and "Acquired
cystic disease of the kidney in adults", section on 'Renal cell carcinoma'.)
Patients with cancer require frequent assessment of kidney function to ensure proper dosing
of chemotherapeutic agents and to monitor ongoing therapies for evidence of
nephrotoxicity. There is no consensus on the optimal formula to estimate glomerular
filtration rate (GFR) in patients with cancer. The preferred formula is the 2021 Chronic Kidney
Disease Epidemiology Collaboration (CKD-EPI) formula, which is also the preferred formula
among patients without cancer. However, other measures of kidney function such as the
Cockcroft-Gault equation for creatinine clearance are still sometimes used in calculating dose
adjustments for chemotherapeutic agents. Measurement of GFR (real-time GFR assessment)
would be the optimal method to assess GFR in patients with cancer and would allow more
accurate drug dosing in this population, especially in those with kidney function impairment.
However, this method is complex, time consuming, and cumbersome to do in clinical
practice. (See "Assessment of kidney function".)
● Certain tyrosine kinase inhibitors (such as anaplastic lymphoma kinase [ALK] inhibitors,
BCR-ABL inhibitors, epidermal growth factor receptor [EGFR] inhibitors, and human
epidermal growth factor receptor 2 [HER2] inhibitors)
Acute kidney injury (AKI) is a common complication among patients with cancer [2,3,7]. The
etiologies of AKI in patients with cancer include all those that occur in the general population
as well as certain etiologies that are specific to this patient group ( table 1). These
etiologies can be categorized into prerenal, intrinsic renal, and postrenal causes based upon
the location of the lesion. However, in many cases, the cause of AKI in patients with cancer is
multifactorial.
The evaluation of the patient with AKI is presented elsewhere. (See "Evaluation of acute
kidney injury among hospitalized adult patients".)
Prerenal causes — The most frequent cause of AKI in patients with cancer is prerenal
disease, which often results from volume depletion (as a consequence of chemotherapy-
related nausea, vomiting, or diarrhea) and/or the use of medications such as diuretics
( table 1) [30-32]. Hypercalcemia or the use of medications that affect renal autoregulation,
such as angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, or
nonsteroidal antiinflammatory drugs, can further exacerbate the risk and severity of
prerenal AKI [30-32]. Given the risks of kidney dysfunction, the risk-to-benefit ratio of using
any of these agents should be carefully considered in patients with advanced malignancy as
well as those who are at high risk of volume depletion during chemotherapy.
● (See "Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute
kidney injury in adults", section on 'Causes of prerenal disease'.)
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Intrinsic renal causes — There are multiple intrinsic renal causes of AKI among patients
with cancer ( table 1). Etiologies that are specific to patients with cancer are discussed
below. (See "Evaluation of acute kidney injury among hospitalized adult patients", section on
'Major causes and classification of AKI'.)
Light chain cast nephropathy (formerly called myeloma kidney) — Light chain cast
nephropathy refers to acute or chronic kidney disease (CKD) that results from the
overproduction and filtration of toxic light chains, leading to both tubular injury and
intratubular cast formation and obstruction. Light chain cast nephropathy is a common
cause of AKI among patients with multiple myeloma and is the most common histologic
lesion in kidney biopsies of patients with monoclonal gammopathy. It has been rarely
reported in patients with other monoclonal gammopathies such as Waldenström
macroglobulinemia, lymphoma, and chronic lymphocytic leukemia (CLL).
Tumor lysis syndrome — Tumor lysis syndrome (TLS), considered an oncologic emergency,
is caused by massive tumor cell lysis, which releases large amounts of intracellular contents
into the systemic circulation, resulting in hyperkalemia, hyperuricemia, hyperphosphatemia,
and hypocalcemia. AKI due to TLS results from the formation of crystals composed of uric
acid, calcium phosphate, and/or xanthine, which can cause intratubular obstruction,
inflammation, and a reduction in glomerular filtration rate (GFR). TLS most often occurs after
initiation of chemotherapy in patients with high-grade lymphomas (such as Burkitt
lymphoma) or leukemias, although it may develop spontaneously or with treatment of other
cancers that have a high proliferative rate or large tumor burden.
Tumor infiltration — Metastases to the kidney are not uncommon. However, involvement
that is severe enough to impair kidney function requires that both kidneys are involved and
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occurs mainly with rapidly growing hematologic malignancies, such as lymphoma or acute
leukemia [33-35]. Among patients with lymphoma, kidney parenchymal infiltration has been
reported in up to 60 percent of cases [36-38]; however, most of these cases are undiagnosed
[37]. Parenchymal infiltration is usually subclinical, although patients may present with AKI,
proteinuria and/or hematuria, and bilaterally enlarged kidneys on imaging. The diagnosis is
established by kidney biopsy, although this is not always required. The mechanism by which
kidney parenchymal infiltration causes AKI is unclear but may involve compression of the
renal tubules and microvasculature, leading to tubular obstruction and ischemia. Successful
treatment of the primary malignancy with chemotherapy may result in an improvement in
kidney function.
Plasma cell infiltration of the kidney can occur in patients with multiple myeloma, but this
only rarely causes AKI [36,39,40]. (See "Kidney disease in multiple myeloma and other
monoclonal gammopathies: Etiology and evaluation", section on 'Less common causes of
AKI'.)
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Less common etiologies — Less common causes of intrinsic AKI among patients with
cancer include the following:
● Lysozymuria – This is a rare disorder that has been observed in patients with acute
promyelocytic, monocytic, or chronic myelomonocytic leukemia [51,52]. In these cases,
clonal proliferation of mononuclear cells produces large quantities of lysozyme, which
is reabsorbed by proximal tubular cells, a process that leads to toxic proximal tubular
injury. Elevated serum and urine lysozyme concentrations are suggestive of the
diagnosis. Kidney biopsy may show positive staining for lysozyme by
immunohistochemistry and accumulation of lysosomes in damaged proximal tubular
cells.
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● (See "Clinical manifestations and diagnosis of urinary tract obstruction (UTO) and
hydronephrosis".)
The clinical spectrum of malignant ureteral obstruction was illustrated by a case series of 102
patients [57]. Obstruction was bilateral in 68 percent of patients. Initial management with a
percutaneous nephrostomy or ureteral stent was successful in 95 percent of cases. Despite
successful decompression, 53 percent of patients developed complications (mostly, urinary
tract infection and obstruction of nephrostomy tubes or stents). Overall survival was poor
(median of seven months), reflecting the advanced stage of malignancy in such patients.
AKI after hematopoietic cell transplantation — Acute kidney injury (AKI) is a common
complication after HCT, occurring in 12 to 66 percent of patients [58]. The risk of AKI depends
upon the type of HCT performed (allogeneic versus autologous), the conditioning regimen
(myeloablative versus nonmyeloablative) used prior to transplantation, as well the use of
nephrotoxic medications and development of GVHD. A more detailed discussion of the
causes and management of AKI after HCT is presented elsewhere. (See "Kidney disease
following hematopoietic cell transplantation", section on 'Causes of AKI'.)
AKI after nephrectomy — A large percentage of patients with renal cell carcinoma (RCC)
have underlying CKD and are at higher risk for postoperative acute kidney injury (AKI)
following either radical or partial nephrectomy. Removal of a kidney in such patients is likely
to cause AKI because of patients' preexisting kidney disease and diminished kidney
functional reserve. Even among patients with an estimated glomerular filtration rate (eGFR)
of ≥60 mL/min per 1.73 m2, 33 percent develop AKI after a radical nephrectomy, and
postoperative AKI is associated with a 4.2-fold increase in the risk of new-onset CKD at one
year after surgery [12]. Among patients undergoing partial nephrectomy, nearly 20 percent
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develop AKI postoperatively [59]. (See "Definitive surgical management of renal cell
carcinoma".)
Patients with cancer may develop chronic kidney disease (CKD) from causes that are related
or unrelated to the malignancy and its treatment. Preexisting CKD among such patients has
important implications for issues such as proper drug dosing and avoidance of potential
nephrotoxins.
The management of the complications related to CKD (eg, hypertension, anemia, mineral
bone disorder) in patients with cancer is broadly similar to that in patients without cancer
and is discussed separately. However, erythropoiesis-stimulating agents should be
prescribed with caution because of concerns regarding their adverse effects (including
higher rates of thromboembolism and faster progression of the underlying disease) in
patients with cancer. (See "Overview of the management of chronic kidney disease in adults"
and "Role of erythropoiesis-stimulating agents in the treatment of anemia in patients with
cancer".)
Causes of CKD in patients with cancer — The causes of chronic kidney disease (CKD)
among patients with cancer include all of the causes that are seen in patients without cancer.
In addition, kidney insults directly related to cancer or its therapy can lead to progressive
CKD [60]. These include:
● Prior episodes of acute kidney injury (AKI) (see 'Acute kidney injury in patients with
cancer' above)
● Reduction in kidney mass following nephrectomy for renal cell (RCC) or urothelial
cancers or kidney cancers associated with von Hippel-Lindau disease (see 'Patients with
renal cell carcinoma' below and "Clinical features, diagnosis, and management of von
Hippel-Lindau disease")
● Kidney irradiation
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Patients with renal cell carcinoma — Chronic kidney disease (CKD) occurs commonly in
patients with RCC, either as a preexisting condition or as a consequence of treatment [13].
Patients who have localized RCC are typically treated with radical or partial nephrectomy
depending upon factors such as the size and location of the tumor as well as the baseline
kidney function of the patient. However, patients who undergo nephrectomy for RCC are at
risk for developing CKD as a consequence of the reduction in kidney mass and other factors,
such as the development of postoperative AKI. Observational studies have shown that the
risk of CKD is greater with radical nephrectomy than with partial nephrectomy [61-65]. A
clinical scoring system based upon readily available parameters has been developed to
identify patients at higher risk of developing significant CKD after nephrectomy [66].
● (See "Overview of the treatment of renal cell carcinoma", section on 'Localized renal cell
carcinoma'.)
Patients with cancer may present with proteinuria or the nephrotic syndrome, which can be
caused by the underlying malignancy (paraneoplastic) or its treatment. Chemotherapy-
associated glomerular diseases may present at various times during treatment, and
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therefore, patients receiving these drugs (especially therapies targeting the vascular
endothelial growth factor [VEGF] pathway as well as immune checkpoint inhibitors) should
be monitored for the development of proteinuria and/or kidney function impairment. In
addition, proteinuria and the nephrotic syndrome are common presenting features of
disorders associated with monoclonal gammopathies. (See "Non-cardiovascular toxicities of
molecularly targeted antiangiogenic agents", section on 'Kidney toxicity'.)
Treatment of the cancer is often associated with improvement of the kidney disease. Patients
diagnosed with MN of unclear etiology should undergo routine cancer screening. These
issues are discussed in detail separately. (See "Membranous nephropathy: Clinical
manifestations and diagnosis", section on 'Screening for malignancy'.)
Minimal change disease — MCD may occur in association with Hodgkin lymphoma and,
less commonly, other lymphoproliferative disorders as well as solid tumors. One putative
mechanism is secretion of a glomerular-toxic lymphokine by abnormal T cells. Lymphoma-
associated MCD is frequently resistant to treatment with glucocorticoids and cyclosporine
[83,84]; therefore, a poor response to the treatment of MCD with these agents should
prompt an investigation for an underlying malignancy. In some but not all patients with
lymphoma-associated MCD, the course of MCD correlates with that of the lymphoma. (See
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"Minimal change disease: Etiology, clinical features, and diagnosis in adults", section on
'Malignancies'.)
proteinuria and nephrotic syndrome as well as kidney function impairment. (See "Renal
amyloidosis" and "Clinical presentation, laboratory manifestations, and diagnosis of
immunoglobulin light chain (AL) amyloidosis".)
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Electrolyte disorders are commonly seen in patients with malignancies, and in many cases,
the etiologies of these disorders are the same as those seen in the general population. In
other circumstances, electrolyte disorders can be caused by the cancer (ie, paraneoplastic
syndromes) or its treatment.
● Hypovolemia due to gastrointestinal fluid losses, poor oral intake, and/or effective
circulating volume depletion (such as with third-spacing of fluids, heart failure, or
cirrhosis). (See "Causes of hypotonic hyponatremia in adults".)
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● Syndrome of inappropriate antidiuretic hormone (SIADH). SIADH may result from the
ectopic production of antidiuretic hormone (ADH) by malignancies such as small-cell
cancer of the lung, head and neck tumors, and primary or secondary brain tumors. In
addition, SIADH can be induced by high-dose intravenous cyclophosphamide and the
vinca alkaloids, vincristine or vinblastine.
In patients with SIADH, the aggressive hydration administered with certain chemotherapy
regimens may worsen hyponatremia, and the serum sodium must be closely monitored.
Water restriction can be problematic in patients with cancer, particularly for those with
stomatitis or other difficulties in maintaining oral hydration and nutrition, and should be
prescribed with caution.
The evaluation and treatment of hyponatremia are presented elsewhere. (See "Diagnostic
evaluation of adults with hyponatremia" and "Overview of the treatment of hyponatremia in
adults".)
● Primary or secondary malignancies in the brain (most often, lung cancer, leukemia, or
lymphoma) can involve the hypothalamic-pituitary region and lead to arginine
vasopressin deficiency (AVP-D, previously known as central diabetes insipidus);
neurosurgery for brain tumors is also an important cause. (See "Arginine vasopressin
deficiency (central diabetes insipidus): Etiology, clinical manifestations, and
postdiagnostic evaluation".)
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Less commonly, ectopic production of adrenocorticotropic hormone (ACTH) by tumor cells (in
the setting of severe Cushing's syndrome) can cause hypernatremia [93,94].
The evaluation and treatment of hypernatremia are discussed separately. (See "Etiology and
evaluation of hypernatremia in adults" and "Treatment of hypernatremia in adults".)
PTHrP shares the same N-terminal end as parathyroid hormone (PTH) and can bind to the
same receptor, the type 1 PTH receptor. As a result, PTHrP can simulate most of the actions
of PTH, including increases in bone resorption and distal tubular calcium reabsorption and
inhibition of proximal tubular phosphate transport [96].
An abnormal total serum calcium concentration in the presence of a normal ionized calcium
concentration (pseudohypercalcemia) can occur in patients with multiple myeloma. (See
"Relation between total and ionized serum calcium concentrations", section on 'Multiple
myeloma'.)
Hyperkalemia — Hyperkalemia may result from kidney failure of any cause or tumor lysis
syndrome (TLS), which is also accompanied by hyperphosphatemia, hypocalcemia, and
hyperuricemia. (See "Tumor lysis syndrome: Pathogenesis, clinical manifestations, definition,
etiology and risk factors", section on 'Clinical manifestations'.)
A rare and indolent condition that leads to hypophosphatemia is the syndrome of tumor-
induced osteomalacia or oncogenic osteomalacia in which tumor production of phosphaturic
factors, such as fibroblast growth factor (FGF)-23, results in renal phosphate wasting and
osteomalacia [102]. Most of the malignancies associated with this syndrome are
mesenchymal tumors (ie, chondrosarcoma, osteoblastoma, and solitary fibrous
tumor/hemangiopericytoma). The mainstay of therapy for this syndrome is tumor resection,
although monoclonal antibodies targeting FGF-23 may prove to be an effective alternative.
(See "Hereditary hypophosphatemic rickets and tumor-induced osteomalacia", section on
'Tumor-induced osteomalacia'.)
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Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Chronic kidney
disease in adults" and "Society guideline links: Cancer of the kidney and ureters".)
SUMMARY
• Chronic kidney disease – Patients with cancer may develop CKD from causes that
are related or unrelated to the malignancy and its treatment. Kidney insults directly
related to cancer or its therapy include prior episodes of AKI, nephrotoxic anticancer
agents, a reduction in kidney mass following nephrectomy for renal cell (RCC) or
urothelial cancers, chronic obstructive nephropathy, and kidney irradiation. (See
'Chronic kidney disease in patients with cancer' above.)
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Topic 7173 Version 49.0
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GRAPHICS
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Cytotoxic drugs
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Targeted agents
Immunotherapy agents
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Minimal change
disease
Other drugs
SIADH: syndrome of inappropriate antidiuretic hormone; AKI: acute kidney injury; NDI: nephrogenic
diabetes insipidus; ALK: anaplastic lymphoma kinase; VEGF: vascular endothelial growth factor; EGFR:
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Stomach cancer MN
Teratoma MN
Cervical cancer MN
Endometrial cancer MN
Mesothelioma MCD
Pheochromocytoma MN
Hodgkin lymphoma MCD, MN, MPGN, IgAN, FSGS, CGN, AAA, Anti-
GBM
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* Includes small cell, non-small cell, squamous cell, and bronchogenic cancers.
Original table modified for this publication. From: Jhaveri KD, Rosner MH. Cancer and chronic kidney disease. In: Chronic
Renal Disease, 1st ed, Kimmel PL, Rosenberg ME (Eds), Academic Press 2014. p.574. Table used with the permission of Elsevier
Inc. All rights reserved.
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Bladder carcinoma
Breast carcinoma
Lung cancer
Ovarian carcinoma
Prostate carcinoma
Colorectal carcinoma
Non-Hodgkin lymphoma
CML
Leukemia
Lymphoma
Osteolytic metastases:
Breast carcinoma
Multiple myeloma
Lymphoma
Leukemia
1,25-dihydroxyvitamin D:
Lymphoma (non-Hodgkin, Hodgkin, lymphomatosis/granulomatosis)
Ovarian dysgerminomas
Lung carcinomas
Neuroectodermal tumor
Rhabdomyosarcoma
Pancreatic carcinoma
CML: chronic myeloid leukemia; PTH: parathyroid hormone; PTHrP: parathyroid hormone-related
protein.
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