Overview of Kidney Disease in Patients With Cancer

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Overview of kidney disease in patients with cancer

AUTHORS: Mitchell H Rosner, MD, Mark A Perazella, MD, FACP, Colm C Magee, MD, MPH, FRCPI
SECTION EDITORS: Gary C Curhan, MD, ScD, Jeffrey S Berns, MD
DEPUTY EDITORS: Albert Q Lam, MD, Sonali M Shah, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2024.

This topic last updated: Sep 06, 2023.
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:
● (See "Kidney disease in multiple myeloma and other monoclonal gammopathies:

Etiology and evaluation".)

Treatment and prognosis".)
● (See "Diagnosis and treatment of monoclonal gammopathy of renal significance".)
● (See "Kidney disease following hematopoietic cell transplantation".)
● (See "Nephrotoxicity of chemotherapy and other cytotoxic agents".)
https://www-uptodate-com.bibliotecavirtual.udla.edu.ec/contents/overview-of-kidney-disease-in-patients-with-cancer/print?search=cancer&sourc… 1/38
● (See "Nephrotoxicity of molecularly targeted agents and immunotherapy".)
EPIDEMIOLOGY AND PROGNOSIS
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.
Overall risk has been addressed in the following observational studies:
● 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 163,071 patients undergoing systemic treatment of cancer in Ontario,

Canada between 2007 and 2014, nearly 1 in 10 patients experienced a hospitalization
or received dialysis for AKI [8]. Notably, the annual incidence of AKI increased from 18
to 52 per 1000 person-years over the study period. Malignancies with the highest five-
year incidence of AKI were multiple myeloma (26 percent), bladder cancer (19 percent),
leukemia (15 percent), and kidney cancer (14 percent). Advanced cancer stage, chronic
kidney disease (CKD), and diabetes were all associated with an increased risk of AKI,
and AKI risk was accentuated during the 90-day period following systemic therapy.
● 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
disease following hematopoietic cell transplantation" and 'AKI after nephrectomy'

below.)
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
<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'.)
ASSESSMENT OF KIDNEY FUNCTION IN PATIENTS WITH CANCER
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".)
Several classes of anticancer drugs may increase serum creatinine concentrations by

impairing tubular secretion of creatinine [29]. These drugs, which can be associated with an
erroneously reduced eGFR, include the following:
● Cyclin-dependent kinase 4 and 6 (CDK 4/6) inhibitors
● Poly-adenosine diphosphate ribose polymerase (PARP) inhibitors
● 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)
● Mesenchymal-epithelial transition (MET) inhibitors
ACUTE KIDNEY INJURY IN PATIENTS WITH CANCER
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'.)
● (See "NSAIDs: Acute kidney injury".)
● (See "Major side effects of angiotensin-converting enzyme inhibitors and angiotensin II

receptor blockers", section on 'Reduction in GFR'.)
● (See "Clinical manifestations of hypercalcemia", section on 'Kidney'.)
Among patients who have undergone myeloablative allogeneic hematopoietic cell

transplantation (HCT), a hepatorenal-like syndrome secondary to sinusoidal obstruction
syndrome (veno-occlusive disease) can occur. (See "Kidney disease following hematopoietic
cell transplantation", section on 'Transplant-specific causes' and "Hepatic sinusoidal
obstruction syndrome (veno-occlusive disease) in adults".)
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).

Etiology and evaluation", section on 'Light chain cast nephropathy'.)

Treatment and prognosis", section on 'Light chain cast nephropathy (myeloma kidney)'.)
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.
● (See "Tumor lysis syndrome: Pathogenesis, clinical manifestations, definition, etiology

and risk factors".)
● (See "Tumor lysis syndrome: Prevention and treatment".)
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
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'.)
Thrombotic microangiopathy — Thrombotic microangiopathy (TMA) is a well-described

complication of cancer and its therapy [41-43]. TMA may be associated with the primary
cancer or, more likely, with therapeutic regimens such as gemcitabine or vascular endothelial
growth factor (VEGF) inhibitors (such as bevacizumab) [43]. TMA associated with VEGF
inhibitors has a better prognosis after stopping the causative agent than do other forms of
drug-induced TMA [44]. TMA may also occur in the setting of HCT, where it is often
associated with calcineurin inhibitor use and can coexist with graft-versus-host disease
(GVHD) and radiation nephropathy [45].
● (See "Diagnostic approach to suspected TTP, HUS, or other thrombotic microangiopathy

(TMA)".)
● (See "Pathophysiology of TTP and other primary thrombotic microangiopathies

(TMAs)".)
● (See "Drug-induced thrombotic microangiopathy (DITMA)".)
● (See "Kidney disease following hematopoietic cell transplantation", section on

'Thrombotic microangiopathy'.)
Nephrotoxic anticancer agents — Drug-induced nephrotoxicity is a significant cause of

AKI among patients with cancer treated with conventional chemotherapeutic agents,
targeted therapies, and immunotherapies ( table 2) [3,46,47]. These drugs can promote
kidney injury through a variety of mechanisms that may affect the glomeruli, tubules,
interstitium, and/or renal microvasculature [3,46-49]. Importantly, the nephrotoxicity of
these agents may be exacerbated by the concurrent or proximate use of other nephrotoxins
such as iodinated contrast [50]. As previously noted, drug discontinuation due to

nephrotoxicity can limit effective tumor regression and eradication.
The nephrotoxicity of specific anticancer agents is discussed in more detail elsewhere:
● (See "Nephrotoxicity of chemotherapy and other cytotoxic agents".)
● (See "Cisplatin nephrotoxicity".)
● (See "Ifosfamide nephrotoxicity".)
● (See "Therapeutic use and toxicity of high-dose methotrexate", section on 'Renal

toxicity'.)
● (See "Intraperitoneal chemotherapy for treatment of ovarian cancer", section on

'Nephrotoxicity'.)
● (See "Treatment-related toxicity in testicular germ cell tumors", section on 'Renal

insufficiency'.)
● (See "Toxicities associated with immune checkpoint inhibitors", section on 'Kidney'.)
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.
● Proliferative/crescentic glomerulonephritis – Both membranoproliferative and

rapidly progressive glomerulonephritis have been described in isolated patients with
solid tumors and lymphomas, although the etiologic relationship between these
conditions is not proven [53,54]. There is some evidence that malignancy is more
frequent in patients diagnosed with ANCA vasculitis compared with the general
population or with those who have other forms of vasculitis [55]. A high percentage of
patients over the age of 50 years who are diagnosed with C3 glomerulopathy have an
underlying monoclonal gammopathy. Thus, monoclonal gammopathies should be

excluded as the cause in such patients [56].
• (See "Membranoproliferative glomerulonephritis: Classification, clinical features, and

diagnosis", section on 'Monoclonal gammopathies'.)
• (See "Granulomatosis with polyangiitis and microscopic polyangiitis: Clinical

manifestations and diagnosis".)
• (See "Diagnosis and treatment of monoclonal gammopathy of renal significance",

section on 'Patients with C3 glomerulopathy with monoclonal gammopathy'.)
Postrenal causes — Urinary tract obstruction should be considered as a cause of AKI in

patients with cancer, especially those with malignancies of the bladder, prostate, uterus, or
cervix. Conversely, malignancy should be considered in any patient not known to have
cancer who presents with bilateral urinary tract obstruction that is not associated with kidney
stones.
Intratubular obstruction — Intratubular obstruction can be caused by crystals composed

of uric acid, xanthine, hypoxanthine, or calcium phosphate (in TLS); light chain casts; or
crystallization of certain drugs (such as high-dose methotrexate). Maintaining a high urine
output with intravenous fluids in "at-risk" patients is the best way to avoid intratubular
precipitation in these settings.
● (See "Tumor lysis syndrome: Pathogenesis, clinical manifestations, definition, etiology

and risk factors".)
● (See "Tumor lysis syndrome: Prevention and treatment".)

Etiology and evaluation", section on 'Light chain cast nephropathy'.)

Treatment and prognosis", section on 'Light chain cast nephropathy (myeloma kidney)'.)
● (See "Crystal-induced acute kidney injury".)
● (See "Therapeutic use and toxicity of high-dose methotrexate", section on 'Renal

toxicity'.)
Extrarenal obstruction — Ureteric obstruction can be caused by a wide range of

malignancies (most commonly arising in the gastrointestinal and genitourinary tracts) and
usually indicates metastatic disease. The diagnosis is usually established by imaging studies
(eg, kidney ultrasound), which typically show dilatation of the collecting system in one or
both kidneys (hydronephrosis). Ureteral obstruction due to retroperitoneal tumor or fibrosis

(which can be secondary to malignancy) may not be associated with severe hydronephrosis
and may require invasive techniques to establish the diagnosis. Patients with cancer may
also develop urinary tract obstruction that is unrelated to the malignancy (eg, benign
prostatic hyperplasia in men).
● (See "Clinical manifestations and diagnosis of urinary tract obstruction (UTO) and
hydronephrosis".)
● (See "Clinical manifestations and diagnosis of retroperitoneal fibrosis", section on

'Diagnostic approach'.)
● (See "Clinical manifestations and diagnostic evaluation of benign prostatic

hyperplasia".)
● (See "Management of urinary tract obstruction".)
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.
Special AKI populations
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".)
CHRONIC KIDNEY DISEASE IN PATIENTS WITH CANCER
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)
● Nephrotoxic anticancer agents (see "Nephrotoxicity of chemotherapy and other

cytotoxic agents" and "Nephrotoxicity of molecularly targeted agents and
immunotherapy")
● 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")
● Chronic obstructive nephropathy (see "Clinical manifestations and diagnosis of

retroperitoneal fibrosis" and "Clinical manifestations and diagnosis of urinary tract
obstruction (UTO) and hydronephrosis" and "Chronic kidney disease (newly identified):
Clinical presentation and diagnostic approach in adults")
● Kidney irradiation
A discussion of the causes, clinical manifestations, and evaluation of CKD is presented in

more detail elsewhere. (See "Chronic kidney disease (newly identified): Clinical presentation
and diagnostic approach in adults".)
Special CKD populations
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 "Definitive surgical management of renal cell carcinoma", section on 'Overview of

the surgical approach'.)
● (See "Overview of the treatment of renal cell carcinoma", section on 'Localized renal cell
carcinoma'.)
Among patients who undergo nephrectomy for localized RCC, approximately 25 to 30

percent have preexisting CKD [61,67]. This high prevalence may reflect the presence of risk
factors that are common to both RCC and CKD, such as older age, male sex, smoking,
obesity, diabetes, and hypertension [12,68-72]. Assessment of the non-neoplastic tissue
obtained from tumor nephrectomy specimens may provide important information about the
cause of CKD and risk of progression in these patients [73-75]. In one study, for example,
medical kidney disease (most frequently, diabetic kidney disease and hypertensive
nephropathy) was identified in 15 percent of tumor nephrectomy specimens; 74 percent of
these cases also showed evidence of severe arteriolosclerosis [73]. Another study of tumor
nephrectomy specimens found that larger glomeruli in the deep cortex and wider distal
tubular diameters in the superficial cortex were independent predictors of progressive CKD
[76].
PROTEINURIA OR NEPHROTIC SYNDROME IN PATIENTS WITH CANCER
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
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'.)
Paraneoplastic glomerular diseases — The development of proteinuria and of the

nephrotic syndrome has been associated with several malignancies ( table 3). Among the
cancer-associated glomerular diseases, membranous nephropathy (MN) and minimal
change disease (MCD) are the most common. An association with malignancy has also been
described with membranoproliferative glomerulonephritis, immunoglobulin A (IgA)
nephropathy [77], IgA vasculitis (Henoch-Schönlein purpura [HSP]) [78], and amyloid A (AA)
amyloidosis [79]. (See "Membranoproliferative glomerulonephritis: Classification, clinical
features, and diagnosis", section on 'Rare causes'.)
Membranous nephropathy — MN is the most common glomerular disease in patients

with cancer [80,81]. MN may be associated with solid tumors (such as carcinomas of the
lung, prostate, or gastrointestinal tract) or, less frequently, with a hematologic malignancy
(such as chronic lymphocytic leukemia [CLL]); it may also occur after hematopoietic cell
transplantation (HCT). Typically, these patients are more likely to be negative for anti-
phospholipase A2 receptor (PLA2R) or thrombospondin type-1 domain-containing 7A
(THSD7A) antibodies, which may be a clue to an underlying malignancy. There is a strong
association between malignancy and nerve epidermal growth factor-like 1 (NELL1)-
associated MN [82]. (See "Membranous nephropathy: Pathogenesis and etiology", section on
'Malignancy' and "Kidney disease following hematopoietic cell transplantation", section on
'Nephrotic syndrome'.)
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
"Minimal change disease: Etiology, clinical features, and diagnosis in adults", section on
'Malignancies'.)
Chemotherapy-associated glomerular disorders — A number of agents used in the

treatment of cancer have been associated with the development of proteinuria and/or the
nephrotic syndrome. Kidney biopsy is recommended in these cases to determine the
associated pathology and to guide therapy. These include the following:
● Bisphosphonates – Collapsing focal segmental glomerulosclerosis (FSGS) has been

associated with exposure to high doses of intravenous bisphosphonates, particularly
pamidronate, in patients with cancer. Such patients typically present with nephrotic
syndrome and kidney failure. Stopping the bisphosphonate may improve kidney
function, but most patients have residual kidney disease, and some progress to end-
stage kidney disease (ESKD). (See "Risks of therapy with bone antiresorptive agents in
patients with advanced malignancy", section on 'Proteinuria and kidney injury'.)
● Interferons – Chronic therapy with interferon-alpha, -beta, or -gamma has been

associated with the development of FSGS not otherwise specified (NOS), collapsing
FSGS, and MCD. The onset of proteinuria and/or nephrotic syndrome may occur days to
years after the initiation of interferon treatment. Discontinuation of interferon
generally leads to complete remission of nephrotic syndrome in patients with MCD;
however, remission is less consistent in those with collapsing FSGS or FSGS NOS.
● Mechanistic (previously called mammalian) target of rapamycin (mTOR) inhibitors –

Sirolimus has been associated with proteinuria and collapsing FSGS. In addition, rare
cases of membranoproliferative glomerulonephritis, MN, and IgA nephropathy have
reported in patients treated with sirolimus. (See "Pharmacology of mammalian
(mechanistic) target of rapamycin (mTOR) inhibitors", section on 'Proteinuria'.)
● Immune checkpoint inhibitors – Antibody-induced lupus nephritis has been reported in

patients treated with the checkpoint inhibitor, ipilimumab [85]. (See "Toxicities
associated with immune checkpoint inhibitors", section on 'Kidney'.)
Disorders associated with monoclonal gammopathy — Proteinuria or nephrotic

syndrome can occur in patients who have multiple myeloma or other monoclonal
gammopathies. (See "Kidney disease in multiple myeloma and other monoclonal
gammopathies: Etiology and evaluation", section on 'Albuminuria or nephrotic syndrome'.)
Amyloidosis — Amyloidosis is a group of diseases characterized by the extracellular

deposition of Congo red-positive fibrils in soft tissues. In immunoglobulin (Ig)-associated
amyloidosis, the fibrils can consist of monoclonal light chains (AL), heavy chains (AH), or both
light and heavy chains (AHL). AL amyloidosis is by far the most common, accounting for more
than 94 percent of cases [86]. Patients with Ig-associated amyloidosis typically present with
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".)
Monoclonal immunoglobulin deposition disease — Monoclonal immunoglobulin

deposition disease (MIDD) is characterized by the deposition of nonamyloid monoclonal light
and/or heavy chains within basement membranes. MIDD is pathogenetically similar to Ig-
associated amyloidosis except that the light (or heavy) chain fragments do not form fibrils,
and the deposits are Congo red negative. Three subtypes of MIDD have been reported based
upon the composition of the deposits: light chain deposition disease (LCDD), heavy chain
deposition disease (HCDD), and light and heavy chain deposition disease (LHCDD). MIDD is
most frequently associated with multiple myeloma but can also occur in patients with
Waldenström macroglobulinemia, CLL, and nodal marginal zone lymphoma [87,88]. MIDD
typically presents with proteinuria, kidney function impairment, and hypertension.
● (See "Monoclonal immunoglobulin deposition disease".)

Etiology and evaluation", section on 'Monoclonal immunoglobulin deposition disease'.)
Less common causes — Other monoclonal gammopathy-associated disorders that can

cause proteinuria and nephrotic syndrome include the following:
● Monoclonal cryoglobulinemia (see "Kidney disease in multiple myeloma and other

monoclonal gammopathies: Etiology and evaluation", section on 'Less common causes
of albuminuria')
● Membranoproliferative glomerulonephritis (eg, proliferative glomerulonephritis with

monoclonal immunoglobulin deposition [PGNMID], C3 glomerulopathy associated with
monoclonal gammopathy)
• (See "Membranoproliferative glomerulonephritis: Classification, clinical features, and

diagnosis", section on 'Monoclonal gammopathies'.)
• (See "Kidney disease in multiple myeloma and other monoclonal gammopathies:

Etiology and evaluation", section on 'Membranoproliferative glomerulonephritis'.)
● Crystalline podocytopathy (see "Kidney disease in multiple myeloma and other

monoclonal gammopathies: Etiology and evaluation", section on 'Less common causes
of albuminuria')
● Fibrillary glomerulonephritis and immunotactoid glomerulopathy (see "Glomerular

diseases due to nonamyloid fibrillar deposits")
● Membranous-like nephropathy with masked immunoglobulin G (IgG)-kappa (see

"Membranous nephropathy: Pathogenesis and etiology", section on 'Membranous-like
nephropathy with masked IgG-kappa')
ELECTROLYTE DISORDERS IN PATIENTS WITH CANCER
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.
Spurious electrolyte disorders — Several electrolytes can be erroneously increased or

decreased due to various artifactual laboratory abnormalities [89]. This laboratory effect can
complicate the interpretation and management of some patients with cancer.
Pseudohyponatremia, pseudohypokalemia, pseudohyperkalemia,
pseudohypophosphatemia, and pseudohyperphosphatemia are examples of this
phenomenon. Recognizing these forms of pseudo–electrolyte disorders is necessary to
prevent incorrect and potentially life-threatening interventions.
● (See "Causes of hyponatremia without hypotonicity (including pseudohyponatremia)",

section on 'Pseudohyponatremia'.)
● (See "Causes of hypokalemia in adults".)
● (See "Causes and evaluation of hyperkalemia in adults", section on

'Pseudohyperkalemia'.)
● (See "Hypophosphatemia: Causes of hypophosphatemia".)
● (See "Overview of the causes and treatment of hyperphosphatemia", section on

'Pseudohyperphosphatemia'.)
Hyponatremia — Hyponatremia is the most common electrolyte disorder encountered in

patients with malignancy, occurring in up to 47 percent of hospitalized patients with cancer
[90,91]. Hyponatremia in these patients is associated with increased hospital length of stay,
increased mortality, and poor response to therapy [92]. The causes of hyponatremia among
patients with cancer include all of the causes of hyponatremia among patients without
cancer. There are two major mechanisms of hyponatremia in patients with cancer:
● 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".)
● 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.
• (See "Pathophysiology and etiology of the syndrome of inappropriate antidiuretic

hormone secretion (SIADH)", section on 'Malignancies'.)
• (See "Nephrotoxicity of chemotherapy and other cytotoxic agents", section on

'Cyclophosphamide'.)
• (See "Nephrotoxicity of chemotherapy and other cytotoxic agents", section on 'Vinca

alkaloids'.)
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.
Rarely, hyponatremia is reported as a side effect of several molecularly targeted

chemotherapeutic agents. (See "Nephrotoxicity of molecularly targeted agents and
immunotherapy".)
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".)
Hypernatremia — Arginine vasopressin disorders (previously known as diabetes insipidus),

with polyuria and polydipsia, can occur in patients with cancer. Hypernatremia will develop if
the patient does not have access to or cannot drink water:
● 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".)
● Hypercalcemia in patients with cancer can lead to reversible arginine vasopressin

resistance (AVP-R, previously known as nephrogenic diabetes insipidus). (See
"Hypercalcemia of malignancy: Mechanisms" and "Arginine vasopressin resistance

(nephrogenic diabetes insipidus): Clinical manifestations and causes".)
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".)
Hypercalcemia — Hypercalcemia is a relatively common complication of malignancy that is

most often caused by the release of parathyroid hormone-related peptide (PTHrP) or local
osteolysis (mediated by cytokines) ( table 4) [95]. Rarely, hypercalcemia is due to ectopic
production of 1,25-dihydroxyvitamin D (calcitriol) in patients with lymphoma. Tumors that
secrete PTHrP include squamous cell carcinomas; renal cell carcinoma (RCC);
adenocarcinomas of the breast, prostate, and ovary; and certain lymphomas. Local osteolytic
mechanisms are seen with multiple myeloma, lymphomas, and breast cancer. (See
"Hypercalcemia of malignancy: Mechanisms".)
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].
Treatment of cancer-associated hypercalcemia centers on aggressive intravenous hydration

to increase renal calcium excretion and to treat concomitant volume depletion, followed by
therapy with either a bisphosphonate, calcitonin, or denosumab to decrease bone release of
calcium [95]. Patients with abnormal kidney function who are receiving denosumab should
be monitored closely for hypocalcemia [97]. Glucocorticoids may be used in patients with
lymphoma and endogenous overproduction of calcitriol. (See "Treatment of hypercalcemia".)
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'.)
Hypokalemia — Hypokalemia can result from gastrointestinal losses (due to vomiting or

diarrhea induced by chemotherapy) or from renal losses (due to ifosfamide, cisplatin, or
diuretics, or, in some patients with leukemia, associated with lysozymuria) [98,99].
Hypokalemia may also be caused by the paraneoplastic secretion of ectopic
adrenocorticotropic hormone (ACTH) in the setting of neuroendocrine tumors, most
commonly arising in the lung (bronchial carcinoid tumors), small-cell lung cancer, lung
adenocarcinomas, and medullary thyroid tumors [100]. (See "Causes of hypokalemia in
adults".)
Spurious hypokalemia (pseudohypokalemia) may occur in patients with a large number of

metabolically active blood cells, such as those with acute myeloid leukemia and a marked
leukocytosis. (See "Causes of hypokalemia in adults", section on 'Increased blood cell
production'.)
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'.)
Of particular importance in this patient population is pseudohyperkalemia, usually in the

setting of marked leukocytosis or thrombocytosis [101]. This is due to a shift of potassium
out of platelets or leukocytes after a blood draw and when a blood clot has formed. The
measurement of a plasma sample, rather than a serum sample, for potassium levels should
be considered in the patient with marked thrombocytosis or leukocytosis to avoid this
occurrence. (See "Causes and evaluation of hyperkalemia in adults", section on
'Pseudohyperkalemia'.)
Hypophosphatemia — Hypophosphatemia can occur in patients with cancer who develop

proximal tubular dysfunction due to toxic light chains in multiple myeloma. In such patients,
hypophosphatemia may be accompanied by other abnormalities including glucosuria,
hypouricemia, aminoaciduria, and renal tubular acidosis (Fanconi syndrome). (See
"Hypophosphatemia: Causes of hypophosphatemia", section on 'Fanconi syndrome' and
"Kidney disease in multiple myeloma and other monoclonal gammopathies: Etiology and
evaluation", section on 'Light chain proximal tubulopathy'.)
Hypophosphatemia is also a common side effect of imatinib, a molecularly targeted agent

that is used for treatment of chronic myelogenous leukemia, and gastrointestinal stromal
tumors. (See "Nephrotoxicity of molecularly targeted agents and immunotherapy", section
on 'Imatinib'.)
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'.)
Hyperphosphatemia — Hyperphosphatemia can occur in patients with TLS and is caused by

the release of intracellular phosphate from lysed tumor cells. (See "Tumor lysis syndrome:
Pathogenesis, clinical manifestations, definition, etiology and risk factors", section on
'Hyperphosphatemia' and "Overview of the causes and treatment of hyperphosphatemia",
section on 'Tumor lysis syndrome'.)
In patients with multiple myeloma and Waldenström macroglobulinemia, circulating

monoclonal proteins can interfere with the laboratory measurement of phosphate, resulting
in spuriously elevated serum phosphate levels (pseudohyperphosphatemia). (See "Overview
of the causes and treatment of hyperphosphatemia", section on
'Pseudohyperphosphatemia'.)
Hypomagnesemia — Tubular dysfunction due to chemotherapy drugs, particularly cisplatin,

ifosfamide, and the inhibitors of the epidermal growth factor receptor (EGFR) pathway, can
lead to urinary magnesium wasting and hypomagnesemia. Particularly with cisplatin, this
can persist for years after drug administration.
● (See "Cisplatin nephrotoxicity", section on 'Hypomagnesemia'.)
● (See "Hypomagnesemia: Causes of hypomagnesemia".)
● (See "Treatment-related toxicity in testicular germ cell tumors", section on 'Electrolyte

disorders'.)
SOCIETY GUIDELINE LINKS
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
● Assessment of kidney function – 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. The assessment of kidney function
among patients with cancer is similar to that in patients without cancer. (See
'Assessment of kidney function in patients with cancer' above.)
● Kidney complications in patients with cancer – 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.
• Acute kidney injury – AKI is a common occurrence in patients with cancer. In

general, the same etiologies of AKI that occur in the general population can affect
patients with cancer; however, certain causes of AKI are specific to this group. AKI in
patients with cancer can be divided into prerenal, intrinsic renal, or postrenal
causes. (See 'Postrenal causes' above and 'Acute kidney injury in patients with
cancer' above.)
• 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.)
• Proteinuria or nephrotic syndrome – Patients with cancer may present with

proteinuria and the nephrotic syndrome, which can be caused by the underlying
malignancy (paraneoplastic) or its treatment. The most common paraneoplastic
glomerular diseases are membranous nephropathy (MN) and minimal change
disease (MCD). Proteinuria and nephrotic syndrome may be the presenting features
of disorders associated with monoclonal gammopathies, including amyloidosis and
monoclonal immunoglobulin deposition disease (MIDD). Chemotherapy-associated
glomerular diseases may present at various times during treatment, and therefore,
patients receiving these drugs should be monitored for the development of
proteinuria and/or kidney function impairment. (See 'Proteinuria or nephrotic
syndrome in patients with cancer' above.)
• Electrolyte disorders – 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.
Common abnormalities include hyponatremia, hypernatremia, hypercalcemia,
hypokalemia, hyperkalemia, hypophosphatemia, hyperphosphatemia, and
hypomagnesemia. (See 'Electrolyte disorders in patients with cancer' above.)
Use of UpToDate is subject to the Terms of Use.
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Topic 7173 Version 49.0
GRAPHICS
Etiologies of acute kidney injury in the cancer patient
Prerenal causes Intrinsic renal causes Postrenal causes
Volume depletion Glomerular Obstructive uropathy

Decreased oral intake Monoclonal Retroperitoneal fibrosis
Gastrointestinal losses gammopathy-associated
Sepsis proliferative
glomerulonephritis
Hypercalcemia
Rapidly progressive
Medications
glomerulonephritis
ACE inhibitors or
Tubulointerstitial
angiotensin receptor
blockers Acute interstitial nephritis
Diuretics Acute tubular necrosis
Iodinated contrast Light chain cast

nephropathy
NSAIDs
Lysozymuria
Sinusoidal obstruction
syndrome (venoocclusive Nephrotoxic anticancer
disease) agents
Tumor infiltration of the
kidney
Tumor lysis syndrome
Vascular
Thrombotic
microangiopathy
ACE: angiotensin-converting enzyme; NSAIDs: nonsteroidal anti-inflammatory drugs.
Graphic 112218 Version 1.0
Anticancer drug-related nephrotoxicity
Clinical renal Renal

Drug Prevention*
syndrome histopathology
Cytotoxic drugs
Cyclophosphamide Hyponatremia None Intravenous fluids

(SIADH) Mesna
Hemorrhagic cystitis
Gemcitabine AKI Thrombotic Not available

Hematuria microangiopathy
Hypertension
Proteinuria
Ifosfamide AKI Acute tubular injury Dose adjustment

NDI Intravenous fluids
Proximal
tubulopathy
(Fanconi syndrome)
Methotrexate AKI Acute tubular injury Intravenous fluids

Crystalline Urinary
nephropathy alkalinization
Mitomycin C AKI Thrombotic Not available

Hematuria microangiopathy
Hypertension
Proteinuria
Nitrosoureas Chronic kidney Chronic interstitial Intravenous fluids

disease nephritis
Pemetrexed AKI Acute tubular injury Intravenous fluids

NDI Interstitial fibrosis
Proximal
tubulopathy
(Fanconi syndrome)
Platinum agents AKI Acute tubular injury Dose adjustment

(cisplatin, Hypomagnesemia Intravenous fluids
carboplatin,
NDI Intravenous
oxaliplatin)
Proximal magnesium
tubulopathy
(Fanconi syndrome)
Salt wasting
Vinca alkaloids Hyponatremia None Not available

(SIADH)
Targeted agents
ALK inhibitors AKI Acute interstitial Not available

(crizotinib) Electrolyte disorders nephritis
Renal microcysts Acute tubular injury
Anti-VEGF agents AKI Thrombotic Not available

(aflibercept, Hypertension microangiopathy
bevacizumab)
Proteinuria
BRAF inhibitors AKI Acute interstitial Not available

(dabrafenib, Electrolyte disorders nephritis
vemurafenib) Acute tubular injury
EGFR inhibitors Hypomagnesemia None Not available

(cetuximab,
erlotinib, gefitinib,
panitumumab)
Imatinib AKI Acute tubular injury Not available

Chronic kidney
disease
Rituximab AKI (tumor lysis Acute tubular injury Hypouricemic

syndrome) Crystalline (uric agents (allopurinol,
acid) nephropathy rasburicase)
Intravenous fluids
Tyrosine kinase AKI Acute interstitial Not available

inhibitors (axitinib, Hypertension nephritis
pazopanib, Acute tubular injury
Proteinuria
sorafenib,
Focal segmental
regorafenib,
glomerulosclerosis
sunitinib)
Thrombotic
microangiopathy
Immunotherapy agents
Chimeric antigen Capillary leak None Glucocorticoid

receptor (CAR) T syndrome with AKI prophylaxis
cells Electrolyte disorders Chemotherapy to
reduce tumor
burden
CTLA-4 inhibitors AKI Acute interstitial Not available

(ipilimumab, Proteinuria nephritis
tremelimumab) Lupus-like
glomerulonephritis
Minimal change
disease
Interferons (alpha, AKI Focal segmental Not available

beta, gamma) Nephrotic-range glomerulosclerosis
proteinuria Thrombotic
microangiopathy
Interleukin-2 AKI None Intravenous fluids

Capillary leak
syndrome
PD-1 inhibitors AKI Acute interstitial Not available

(nivolumab, Proteinuria nephritis
pembrolizumab, Acute tubular injury
cemiplimab)
IgA nephropathy
Minimal change
disease
Focal segmental
glomerulosclerosis
C3 glomerulopathy
Membranous
glomerulonephritis
PD-L1 inhibitors AKI Acute interstitial Not available

(atezolizumab, nephritis
durvalumab,
avelumab)
Other drugs
Deferasirox AKI Acute interstitial Not available

nephritis
Acute tubular injury
Fanconi syndrome
Pamidronate AKI Acute tubular injury Dose adjustment

Nephrotic syndrome Focal segmental Increase infusion
glomerulosclerosis time
Sirolimus AKI Focal segmental Not available

Proteinuria glomerulosclerosis
Zoledronate AKI Acute tubular injury Dose adjustment

Nephrotic syndrome Focal segmental
glomerulosclerosis
(rare)
SIADH: syndrome of inappropriate antidiuretic hormone; AKI: acute kidney injury; NDI: nephrogenic
diabetes insipidus; ALK: anaplastic lymphoma kinase; VEGF: vascular endothelial growth factor; EGFR:
epidermal growth factor receptor; CTLA-4: cytotoxic T-lymphocyte-associated protein 4; PD-1:

programmed cell death-1; PD-L1: programmed cell death-1 ligand-1.
* In addition to minimizing exposure to other nephrotoxins.
Malignancies associated with glomerular diseases
Malignancy Glomerular diseases reported
Lung cancer* MN, MCD, MPGN, IgAN, FSGS, CGN, TMA
Colon cancer MN, MCD, CGN
Stomach cancer MN
Pancreas cancer MN, MCD, IgAN
Bladder cancer MCD
Renal cell cancer AAA, CGN, IgAN, MCD, FSGS, MPGN
Prostate cancer MN, CGN
Breast cancer MN, FSGS, MPGN, TMA
Esophageal cancer MPGN, FSGS
Gastrointestinal stromal tumor AAA
Gastric cancer MPGN, CGN, TMA
Spleen sarcoma AAA
Head and neck cancer MN, IgAN
Wilm's tumor MN, MPGN
Teratoma MN
Ovarian cancer MN, MCD
Cervical cancer MN
Endometrial cancer MN
Tongue cancer IgAN
Mesothelioma MCD
Melanoma MN, MPGN
Skin cancers (basal or squamous cell) MN
Pheochromocytoma MN
Thymoma MCD, FSGS, CGN, MPGN
Hodgkin lymphoma MCD, MN, MPGN, IgAN, FSGS, CGN, AAA, Anti-
GBM
Non-Hodgkin lymphoma MN, MCD, MPGN, IgAN, FSGS
CLL MN, MCD, MPGN, FSGS, CGN
AML MN, FSGS
CML MN, MCD, MPGN
Monoclonal gammopathy MPGN, C3 glomerulopathy
T cell leukemia FSGS
MN: membranous nephropathy; MCD: minimal change disease; MPGN: membranoproliferative

glomerulonephritis; IgAN: IgA nephropathy; FSGS: focal segmental glomerulosclerosis; CGN:
crescentic glomerulonephritis; TMA: thrombotic microangiopathy; AAA: AA amyloidosis; GBM:
glomerular basement membrane; CLL: chronic lymphocytic leukemia; AML: acute myeloid leukemia;
CML: chronic myeloid leukemia.
* 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.
Malignancies associated with hypercalcemia
Humoral hypercalcemia (secretion of PTHrP):
Squamous cell carcinomas
Renal cell carcinomas
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
Ectopic PTH secretion:

Ovarian carcinoma
Lung carcinomas
Neuroectodermal tumor
Thyroid papillary carcinoma
Rhabdomyosarcoma
Pancreatic carcinoma
CML: chronic myeloid leukemia; PTH: parathyroid hormone; PTHrP: parathyroid hormone-related
protein.

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27/2/24, 21:59 Overview of kidney disease in patients with cancer - UpToDate

Official reprint from UpToDate®

Literature review current through: Jan 2024.

● (See "Kidney disease in multiple myeloma and other monoclonal gammopathies:

● (See "Kidney disease in multiple myeloma and other monoclonal gammopathies:

● (See "Diagnosis and treatment of monoclonal gammopathy of renal significance".)

● (See "Kidney disease following hematopoietic cell transplantation".)

● (See "Nephrotoxicity of chemotherapy and other cytotoxic agents".)

● (See "Nephrotoxicity of molecularly targeted agents and immunotherapy".)

EPIDEMIOLOGY AND PROGNOSIS

Overall risk has been addressed in the following observational studies:

● In a study of 163,071 patients undergoing systemic treatment of cancer in Ontario,

disease following hematopoietic cell transplantation" and 'AKI after nephrectomy'

ASSESSMENT OF KIDNEY FUNCTION IN PATIENTS WITH CANCER

Several classes of anticancer drugs may increase serum creatinine concentrations by

● Cyclin-dependent kinase 4 and 6 (CDK 4/6) inhibitors

● Poly-adenosine diphosphate ribose polymerase (PARP) inhibitors

● Mesenchymal-epithelial transition (MET) inhibitors

ACUTE KIDNEY INJURY IN PATIENTS WITH CANCER

● (See "NSAIDs: Acute kidney injury".)

● (See "Major side effects of angiotensin-converting enzyme inhibitors and angiotensin II

● (See "Clinical manifestations of hypercalcemia", section on 'Kidney'.)

Among patients who have undergone myeloablative allogeneic hematopoietic cell

● (See "Kidney disease in multiple myeloma and other monoclonal gammopathies:

● (See "Kidney disease in multiple myeloma and other monoclonal gammopathies:

● (See "Tumor lysis syndrome: Pathogenesis, clinical manifestations, definition, etiology

● (See "Tumor lysis syndrome: Prevention and treatment".)

Thrombotic microangiopathy — Thrombotic microangiopathy (TMA) is a well-described

● (See "Diagnostic approach to suspected TTP, HUS, or other thrombotic microangiopathy

● (See "Pathophysiology of TTP and other primary thrombotic microangiopathies

● (See "Drug-induced thrombotic microangiopathy (DITMA)".)

● (See "Kidney disease following hematopoietic cell transplantation", section on

Nephrotoxic anticancer agents — Drug-induced nephrotoxicity is a significant cause of

such as iodinated contrast [50]. As previously noted, drug discontinuation due to

The nephrotoxicity of specific anticancer agents is discussed in more detail elsewhere:

● (See "Nephrotoxicity of chemotherapy and other cytotoxic agents".)

● (See "Nephrotoxicity of molecularly targeted agents and immunotherapy".)

● (See "Cisplatin nephrotoxicity".)

● (See "Ifosfamide nephrotoxicity".)

● (See "Therapeutic use and toxicity of high-dose methotrexate", section on 'Renal

● (See "Intraperitoneal chemotherapy for treatment of ovarian cancer", section on

● (See "Treatment-related toxicity in testicular germ cell tumors", section on 'Renal

● (See "Toxicities associated with immune checkpoint inhibitors", section on 'Kidney'.)

● Proliferative/crescentic glomerulonephritis – Both membranoproliferative and

underlying monoclonal gammopathy. Thus, monoclonal gammopathies should be

• (See "Membranoproliferative glomerulonephritis: Classification, clinical features, and

• (See "Granulomatosis with polyangiitis and microscopic polyangiitis: Clinical

• (See "Diagnosis and treatment of monoclonal gammopathy of renal significance",

Postrenal causes — Urinary tract obstruction should be considered as a cause of AKI in

Intratubular obstruction — Intratubular obstruction can be caused by crystals composed

● (See "Tumor lysis syndrome: Pathogenesis, clinical manifestations, definition, etiology

● (See "Tumor lysis syndrome: Prevention and treatment".)

● (See "Kidney disease in multiple myeloma and other monoclonal gammopathies:

● (See "Kidney disease in multiple myeloma and other monoclonal gammopathies:

● (See "Crystal-induced acute kidney injury".)

● (See "Therapeutic use and toxicity of high-dose methotrexate", section on 'Renal

Extrarenal obstruction — Ureteric obstruction can be caused by a wide range of

both kidneys (hydronephrosis). Ureteral obstruction due to retroperitoneal tumor or fibrosis

● (See "Clinical manifestations and diagnosis of retroperitoneal fibrosis", section on

● (See "Clinical manifestations and diagnostic evaluation of benign prostatic

● (See "Management of urinary tract obstruction".)

Special AKI populations

CHRONIC KIDNEY DISEASE IN PATIENTS WITH CANCER