Papillary Renal Cell Carcinoma: Understanding Your Pathology Report

Section Editor: Trevor Flood MD FRCPC
July 16, 2026

Papillary renal cell carcinoma is a type of kidney cancer. It starts from the cells that line the tiny tubes inside the kidney called tubules, which filter the blood and make urine. It is the second most common type of kidney cancer in adults, making up about 15 out of every 100 kidney cancers. The name comes from the way the tumor grows under the microscope: the cells form small finger-like projections called papillae, each built around a thin core of connective tissue and blood vessels.

Most papillary renal cell carcinomas are found while they are still inside the kidney, and most are cured by surgery alone. This type of kidney cancer is also more likely than other types to appear as more than one tumor in the same kidney or in both kidneys.

This article will help you understand the findings in your pathology report for papillary renal cell carcinoma, what each term means, and why it matters for your care. If your report or an older report uses the terms “type 1” or “type 2,” the section below on why these terms are no longer used explains what has changed.

What causes papillary renal cell carcinoma?

Most papillary renal cell carcinomas, the second most common type of kidney cancer, happen by chance, and there is usually no single event or exposure that explains why the tumor developed. Inside the tumor cells, the typical change is the gain of extra copies of chromosomes 7 and 17, often along with loss of the Y chromosome in men. Chromosome 7 carries a gene called MET, which normally tells kidney cells when to grow and divide. Having extra copies of MET, or a change in the gene that leaves it switched on, drives the cells to keep growing. This is a different pathway from the one that causes clear cell renal cell carcinoma, which is why the two cancers are treated with different drugs.

Several factors increase a person’s risk of developing this tumor:

Chronic kidney disease and long-term dialysis — This is a stronger risk factor for papillary renal cell carcinoma than for other kidney cancers. People on dialysis for many years often develop cysts in the kidneys (acquired cystic kidney disease), and papillary tumors can arise within them.
Smoking — Long-term tobacco use increases the risk of all types of kidney cancer.
Obesity and high blood pressure — Both are linked to a higher risk of kidney cancer.
Family history — Having a parent, brother, or sister with kidney cancer increases risk, even when no inherited syndrome is found.

Inherited conditions associated with papillary renal cell carcinoma

Hereditary papillary renal cell carcinoma (HPRC) — The inherited condition most specifically linked to this tumor. It is caused by a change in the MET gene that a person is born with, and it is passed from parent to child. People with HPRC typically develop many papillary tumors in both kidneys, often starting in middle age, and they usually have no problems outside the kidney.
Birt-Hogg-Dubé syndrome — Caused by a change in the FLCN gene. It mainly causes chromophobe renal cell carcinoma, oncocytoma, and tumors with features of both, but papillary tumors are occasionally reported.
Lynch syndrome — An inherited condition affecting the genes that repair DNA. It is best known for causing bowel and uterine cancer, and papillary kidney tumors are reported in a small number of people who have it.

An important point about inherited kidney cancer has changed in recent years. Tumors caused by hereditary leiomyomatosis and renal cell carcinoma (HLRCC), an inherited condition affecting the FH gene, used to be grouped with papillary renal cell carcinoma because they can look papillary under the microscope. They are now recognized as a separate cancer called fumarate hydratase-deficient renal cell carcinoma, which behaves differently and is managed differently.

What are the symptoms of papillary renal cell carcinoma?

Most people with papillary renal cell carcinoma, a cancer that starts in the kidney, have no symptoms. These tumors are usually found by accident when an ultrasound, CT scan, or MRI is performed for an unrelated reason, or during imaging done to monitor long-standing kidney disease. When symptoms do occur, they may include:

Blood in the urine, which can make the urine look red, pink, or brown.
Pain or a dull ache in the back or the side of the abdomen.
A lump or fullness in the abdomen or side.
Weight loss that was not intended, or fatigue.
Fever without an obvious cause.

If the tumor has spread to another part of the body (a process called metastasis), the symptoms depend on where it has spread.

How is the diagnosis made?

The diagnosis of papillary renal cell carcinoma is made when a pathologist examines kidney tissue under a microscope. The tumor is usually first seen as a mass in the kidney on an ultrasound, CT scan, or MRI. For most kidney masses, the next step is surgery to remove the tumor rather than a needle biopsy. A biopsy is more likely to be performed when the mass is small and treatment options are being weighed, when a person is not well enough for surgery, when there is more than one tumor, or when the cancer has already spread and a tissue diagnosis is needed before drug treatment can start.

Under the microscope, papillary renal cell carcinoma is made up of cells arranged along papillae, finger-like projections built around a fibrovascular core of connective tissue and small blood vessels. Two other findings are common and often mentioned in the report: foamy histiocytes, which are immune cells filled with fat that collect within the papillae, and psammoma bodies, which are tiny round deposits of calcium. Many of these tumors are surrounded by a capsule, which is one reason they are often removed completely by surgery. Some tumors grow in solid sheets or tubes rather than obvious papillae, and the diagnosis can still be made.

Because several other kidney tumors can also grow in a papillary pattern, a test called immunohistochemistry, which uses special stains to detect proteins inside cells, is often performed. Papillary renal cell carcinoma is typically positive for AMACR, CK7, and PAX8 (which confirms that the tumor started in the kidney). Pathologists also have a low threshold for adding stains called FH, 2SC, and SDHB, particularly in a younger person or when the tumor has an unusual appearance, because a normal result helps rule out fumarate hydratase-deficient renal cell carcinoma and succinate dehydrogenase-deficient renal cell carcinoma, two rare cancers that are strongly linked to inherited conditions. Other tumors that must be separated from papillary renal cell carcinoma include TFE3-rearranged renal cell carcinoma, mucinous tubular and spindle cell carcinoma, and papillary renal neoplasm with reverse polarity, a tumor that behaves in a harmless way. Once the diagnosis is confirmed, imaging of the chest and abdomen is used to look for spread.

Why type 1 and type 2 are no longer used

For many years, pathologists divided papillary renal cell carcinoma into type 1 and type 2 based on how the cells lining the papillae looked. Type 1 tumors had a single layer of small cells with pale cytoplasm; type 2 tumors had larger cells with pink cytoplasm and more abnormal nuclei, and were described as behaving more like a fast-growing cancer.

The World Health Organization removed this division in its 2022 classification, and subtyping into type 1 and type 2 is no longer recommended. The reason is that research showed the two groups were not two versions of one disease. Type 1 tumors turned out to be a consistent group driven by changes in chromosome 7 and 17 and the MET gene. Type 2 was not a real single entity at all: it was a mixture of tumors that happened to look alike, and many of them are now recognized as separate cancers with their own names, causes, and treatments, including fumarate hydratase-deficient renal cell carcinoma, TFE3-rearranged renal cell carcinoma, and succinate dehydrogenase-deficient renal cell carcinoma. What remains under the name papillary renal cell carcinoma is essentially the former type 1 group, along with tumors that do not fit any of the newly defined categories.

What this means for you depends on when your tissue was examined. Reports issued today should say only “papillary renal cell carcinoma,” sometimes with a description of the growth pattern. If your report was issued before 2022 and says “type 1,” the diagnosis is unchanged, and the tumor would still be called papillary renal cell carcinoma today. If your report says “type 2,” it is reasonable to ask whether your tumor has been reviewed under the current classification, because some tumors that were called type 2 in the past would now be given a different diagnosis, and that difference can matter for treatment, for follow-up, and for whether inherited testing should be offered. Grade and stage, described below, now carry the prognostic information that subtyping was once thought to provide.

Papillary adenoma: when a small papillary tumor is not called cancer

Not every papillary tumor in the kidney is a papillary renal cell carcinoma. A papillary adenoma is a noncancerous tumor that is made of the same kind of cells and has the same papillary growth pattern, but is 15 mm (1.5 cm) or smaller, is low grade, and has no capsule around it. Tumors above that size, or with higher grade features, are diagnosed as papillary renal cell carcinoma. Papillary adenomas are common, especially in kidneys affected by long-standing disease, and are often found by chance in the tissue around a larger tumor. They do not spread and do not require treatment. If your report mentions one or more papillary adenomas alongside your cancer, this is an expected finding and not a second cancer.

Histologic grade (WHO/ISUP grade)

Grade describes how abnormal the cells of a papillary renal cell carcinoma look under the microscope, and now that subtyping into type 1 and type 2 has been abandoned, grade is one of the most important predictors of behavior on your report. Kidney cancers are graded using the WHO/ISUP grading system, developed by the World Health Organization and the International Society of Urological Pathology, which is validated for both papillary and clear cell renal cell carcinoma. It is based mainly on how easily the nucleoli (small round structures inside the nucleus of each cell) can be seen under the microscope. It has replaced the Fuhrman grading system, which you may still see on older reports.

Grade 1 — Nucleoli are absent or cannot be seen, even at high magnification.
Grade 2 — Nucleoli can be seen at high magnification but are not visible at low magnification.
Grade 3 — Nucleoli are clearly visible at low magnification.
Grade 4 — The cells show extreme variation in size and shape, or there are giant cells, or the tumor contains sarcomatoid or rhabdoid cells (described in the next section).

Grades 1 and 2 are considered low grade, and most papillary renal cell carcinomas fall into this group. These tumors tend to grow slowly and are less likely to spread. Grades 3 and 4 are considered high grade and are more likely to spread beyond the kidney. The grade is assigned from the most abnormal area of the tumor, even if that area is small, so a tumor that is mostly low grade can still be reported as high grade. Grade helps predict how the tumor is likely to behave and is used along with stage to decide how closely a person is followed after surgery.

Sarcomatoid and rhabdoid features

Some papillary renal cell carcinomas contain areas where the tumor cells have changed their appearance completely. These changes, called sarcomatoid and rhabdoid features, matter because they identify tumors that are more likely to grow quickly and spread. They are uncommon in this type of kidney cancer, occurring in fewer than 5 out of every 100 tumors.

Sarcomatoid features — The tumor cells are replaced by long, thin, spindle-shaped cells that resemble a soft tissue cancer rather than a carcinoma.
Rhabdoid features — The tumor cells become large and round with a bright pink center and an off-to-the-side nucleus, resembling muscle cells.

If either feature is present, the tumor is automatically WHO/ISUP grade 4, and your report will state the percentage of the tumor involved. Both are associated with a higher risk of the cancer returning. Tumors with sarcomatoid features also tend to respond better than average to immunotherapy, so this finding is one of the details the medical oncology team uses when discussing drug treatment.

Multifocal and bilateral tumors

Papillary renal cell carcinoma is the type of kidney cancer most likely to appear as more than one tumor. When a single tumor is present, pathologists call it unifocal. When more than one tumor is found in the same kidney, it is called multifocal, and when tumors are present in both kidneys, they are called bilateral. Your report will describe each tumor separately, with its own size and grade, and the stage is based on the largest one.

Multiple tumors do not mean the cancer has spread. Each tumor started on its own in the kidney. Finding several of them is important for two other reasons: it raises the possibility of an inherited condition such as hereditary papillary renal cell carcinoma, particularly in a younger person or when there is a family history, and it affects surgical planning, because preserving kidney function becomes a larger consideration when both kidneys are involved.

Tumor size

Your pathology report will state the size of the papillary renal cell carcinoma, measured in centimeters, from the tissue removed at surgery. This measurement is more accurate than the size estimated on imaging beforehand, so the two numbers may not match exactly. Size matters because it is one of the main factors that determines the tumor stage (pT), and because larger tumors are more likely to be high grade and to grow outside the kidney. The important thresholds are 4 cm, 7 cm, and 10 cm. If more than one tumor was found, the size of each is reported, and the largest one is used for staging.

Tumor extension

Tumor extension describes whether a papillary renal cell carcinoma has grown outside the kidney and, if so, how far. The kidney is surrounded by a layer of fat, and outside that fat is a tough envelope called Gerota’s fascia. The adrenal gland sits on top of the kidney, and the renal vein carries blood away from the kidney into the largest vein in the body, the inferior vena cava. Your pathologist examines all of these structures in the tissue removed at surgery.

The report may describe growth into the fat around the kidney (perinephric fat), into the fat in the middle of the kidney where the blood vessels enter (renal sinus fat), into the collecting system that drains urine (the pelvicalyceal system), into the renal vein or the inferior vena cava, into the adrenal gland, or through Gerota’s fascia into other organs. Growth outside the kidney is less common in papillary renal cell carcinoma than in clear cell renal cell carcinoma, because many papillary tumors are surrounded by a capsule. When it is present, it raises the tumor stage and is associated with a higher risk of the cancer returning.

Lymphovascular invasion

Lymphovascular invasion means that cells from the papillary renal cell carcinoma are seen inside small blood vessels or lymphatic channels within or around the tumor. Blood vessels carry blood throughout the body, and lymphatic channels carry a fluid called lymph toward the lymph nodes. Tumor cells inside these vessels can be carried elsewhere, so lymphovascular invasion is associated with a higher risk of the cancer returning or spreading.

Lymphovascular invasion is not the same as growth into the renal vein, which is a large named vessel and is reported separately as part of tumor extension and stage. Lymphovascular invasion does not change the pT stage on its own, but it is one of the findings your treatment team considers when deciding how closely to follow you after surgery.

Surgical margins

A margin is the cut edge of the tissue removed during surgery for papillary renal cell carcinoma. Your pathologist examines these edges under the microscope to see whether any tumor cells reach them. Which margins are examined depends on the operation. In a partial nephrectomy, where only the tumor and a rim of surrounding tissue are removed, the margins are the kidney tissue and fat around the tumor. Partial nephrectomy is used frequently in this type of kidney cancer, because tumors are often small and because preserving kidney function matters when more than one tumor is present or when the kidneys are already damaged. In a radical nephrectomy, where the whole kidney is removed, the margins include the fat around the kidney, the renal vein, the ureter (the tube carrying urine to the bladder), and the blood vessels.

Negative margin — No tumor cells are seen at the cut edge. This suggests the whole tumor was removed and is associated with a low risk of the cancer coming back in the same place.
Positive margin — Tumor cells are present at the cut edge. This means tumor cells may have been left behind, and it is associated with a higher risk of the cancer returning at that site. A positive margin is one of the findings the surgical team uses when deciding whether more surgery or closer imaging follow-up should be considered.

Lymph nodes

Lymph nodes are small immune organs found throughout the body, including around the large blood vessels near the kidney. Cells from a papillary renal cell carcinoma can travel through lymphatic channels and settle in a lymph node. Lymph nodes are not removed routinely during kidney cancer surgery. They are usually removed only when they look enlarged on imaging or feel abnormal during the operation, so many reports will say that no lymph nodes were submitted. Papillary renal cell carcinoma involves lymph nodes somewhat more often than clear cell renal cell carcinoma does, and enlarged nodes are more likely to be sampled for that reason.

If lymph nodes were removed, your report will state how many were examined, how many contained cancer, and the size of the largest deposit of tumor within a node. It may also state whether extranodal extension is present, which means that cancer cells inside a lymph node have broken through the outer capsule of the node into the surrounding tissue. Cancer in even one lymph node is an important finding, because it is associated with a substantially higher risk of the cancer returning and it places the tumor in a higher stage group.

Examination of the non-tumor kidney

When kidney tissue is removed for papillary renal cell carcinoma, your pathologist also examines the kidney tissue away from the tumor. This part of the report deserves attention in papillary renal cell carcinoma in particular, because this tumor is so often associated with underlying kidney disease. Common findings include scarring of the small blood vessels from long-standing high blood pressure (arterionephrosclerosis), damage to the filters from diabetes (diabetic nephropathy), scarring from other chronic kidney disease, and cysts from acquired cystic kidney disease. These findings do not describe the cancer. They are reported because they help predict how well the remaining kidney will work after surgery and may lead to a referral to a kidney specialist (nephrologist).

Biomarker and molecular testing

Biomarkers are features of a tumor, usually a protein or a change in a gene, that provide information beyond the diagnosis itself. In some cancers, biomarker results decide which drug a person receives. Papillary renal cell carcinoma is not yet one of them: no biomarker test is currently required before treatment for this cancer can be chosen, and most people whose tumor is removed at an early stage will not have any molecular testing performed. The tests below are performed in specific situations, most often when the cancer has spread, when an inherited condition is suspected, or when a clinical trial is being considered.

MET and chromosome 7 and 17 changes

Most papillary renal cell carcinomas carry extra copies of chromosomes 7 and 17, and many also have a change in the MET gene that leaves the growth signal switched on. Tumors with these findings are described as MET-driven. This information is not used to select an approved drug at present, because no MET-blocking drug is approved specifically for kidney cancer. It matters for two other reasons. Finding gains of chromosomes 7 and 17 supports the diagnosis when the appearance under the microscope is not clear-cut. And MET-driven status determines eligibility for clinical trials of drugs that block MET, including savolitinib combined with durvalumab, which is being compared against standard treatment in an ongoing international trial in MET-driven papillary renal cell carcinoma. Testing is usually done by next-generation sequencing (NGS) or by a test called FISH. Results are reported as a MET alteration detected, or no alteration detected, or as gains of chromosomes 7 and 17 present or absent.

Inherited (germline) genetic testing

Germline testing looks for a gene change a person was born with, using a blood or saliva sample rather than the tumor itself. It is offered to people with papillary renal cell carcinoma who were diagnosed at a young age (usually 46 or younger), who have tumors in both kidneys or more than one tumor in the same kidney, who have a close relative with kidney cancer, or who have features suggesting a syndrome. Because papillary tumors are more often multiple than other kidney cancers, this conversation comes up more frequently here than in other types. The genes usually tested include MET (for hereditary papillary renal cell carcinoma), FH, FLCN, SDHB, SDHC, SDHD, and the mismatch repair genes associated with Lynch syndrome.

Results are reported in one of three ways: a pathogenic (disease-causing) variant, which confirms an inherited syndrome; no variant identified, which is the usual and reassuring result; or a variant of uncertain significance, which means a change was found but it is not yet known whether it matters. A pathogenic result is important for the whole family. It indicates a need for lifelong imaging of the kidneys, and it means close relatives can be offered testing of their own (called cascade testing) through a genetics clinic.

Comprehensive genomic profiling (next-generation sequencing)

Next-generation sequencing reads many genes at once from the tumor tissue. In papillary renal cell carcinoma it is generally performed only when the cancer has spread and a clinical trial or a treatment outside the standard options is being considered. Along with MET, the genes most often altered include SETD2, NF2, TERT, and the chromatin-modifying genes. Reports may state which alterations were found, that no reportable alterations were identified, or that a change of uncertain significance was detected. Sequencing also helps confirm that the tumor is a papillary renal cell carcinoma rather than one of the entities formerly grouped under type 2, which is why it is sometimes requested even when treatment will not change.

Mismatch repair, microsatellite instability, and tumor mutational burden

These tests identify tumors that respond to immunotherapy regardless of where the cancer started, an idea called a tumor-agnostic approval. Mismatch repair proteins (MLH1, PMS2, MSH2, and MSH6) are tested by immunohistochemistry and reported as intact or retained, which is the normal result, or as deficient (dMMR) when one or more proteins are lost. The related test for microsatellite instability is reported as stable (MSS) or high (MSI-H). Tumor mutational burden counts the number of mutations in the tumor and is reported as mutations per megabase, with 10 or more considered high. All three findings are uncommon in papillary renal cell carcinoma, but when present they make a person eligible for the immunotherapy drug pembrolizumab under approvals that apply across cancer types. A deficient mismatch repair result also raises the possibility of Lynch syndrome, and referral to a genetic counselor is considered when it is found.

You can learn more about the tests described here in our Biomarkers and Genetic Testing section.

Pathologic stage (pTNM)

The pathologic stage of a papillary renal cell carcinoma describes how far the cancer had grown at the time of surgery. It is written using the TNM system created by the American Joint Committee on Cancer (AJCC), currently in its 8th edition, and it is the same system used for all renal cell carcinomas. T describes the size of the tumor and how far it has grown outside the kidney, N describes whether cancer is found in nearby lymph nodes, and M describes whether the cancer has spread to a distant part of the body. The letter “p” in front means the category was assigned by a pathologist after examining the tissue. The M category is almost always determined by imaging rather than by the pathologist, so it may not appear on your report at all. When more than one tumor is present, the stage is based on the largest tumor.

Tumor stage (pT)

pT1a — The tumor is 4 cm or smaller and remains inside the kidney.
pT1b — The tumor is larger than 4 cm but not more than 7 cm and remains inside the kidney.
pT2a — The tumor is larger than 7 cm but not more than 10 cm and remains inside the kidney.
pT2b — The tumor is larger than 10 cm and remains inside the kidney.
pT3a — The tumor has grown into the renal vein or one of its branches, into the fat around the kidney or in the renal sinus, or into the collecting system that drains urine, but not beyond Gerota’s fascia.
pT3b — The tumor has grown into the inferior vena cava below the diaphragm.
pT3c — The tumor has grown into the inferior vena cava above the diaphragm, or into the wall of the vena cava.
pT4 — The tumor has grown beyond Gerota’s fascia, including growth into the adrenal gland on the same side.

Nodal stage (pN)

pN0 — No cancer was found in any of the lymph nodes examined.
pN1 — Cancer was found in one or more nearby lymph nodes.
pNX — No lymph nodes were removed or they could not be assessed. This is a common and expected result in kidney cancer surgery.

What is the prognosis?

Prognosis means the expected course of a disease. For papillary renal cell carcinoma, the strongest predictor is the stage at diagnosis. Most of these tumors are found while still confined to the kidney, and the outlook in that situation is very good: more than 9 out of 10 people with a stage I tumor are alive and free of kidney cancer five years later, and stage-for-stage, localized papillary renal cell carcinoma does at least as well as localized clear cell renal cell carcinoma. The picture is different when the cancer has spread. Advanced papillary renal cell carcinoma responds less well to drug treatment than clear cell renal cell carcinoma does, and in clinical trials of people with cancer that has spread, average survival has been measured in years rather than decades. Published survival figures for kidney cancer as a whole are dominated by clear cell cases and should be interpreted with that in mind.

The features on your pathology report that are associated with a higher risk of the cancer returning include:

High WHO/ISUP grade — Grade 3 and grade 4 tumors return more often than grade 1 and grade 2 tumors. Now that type 1 and type 2 are no longer used, grade carries much of the prognostic weight once assigned to subtype.
Sarcomatoid or rhabdoid features — Either finding identifies a tumor that is more likely to spread.
Tumor necrosis — Areas where tumor cells have died, usually because the tumor outgrew its blood supply. Necrosis seen under the microscope is an independent sign of a higher risk of the cancer returning.
Larger tumor size — Risk rises across the 4 cm, 7 cm, and 10 cm thresholds.
Growth outside the kidney — Involvement of the fat around the kidney, the renal sinus, the renal vein, or the vena cava.
Lymphovascular invasion — Tumor cells within small blood or lymphatic vessels.
Positive surgical margin — Tumor cells at the cut edge of the tissue removed.
Cancer in lymph nodes — Even a single positive node is associated with a considerably higher risk.

These features are not weighed one at a time. Urologists combine stage, grade, tumor size, and necrosis into published risk scores, such as the Leibovich score and the SSIGN score, which estimate the chance that the cancer will return after surgery. Your treatment team uses one of these scores, along with the details on your report, to decide how often you will have imaging. For people whose cancer has already spread, a separate tool called the IMDC risk model uses blood test results and the time since diagnosis rather than pathology findings.

What happens after the diagnosis?

Once papillary renal cell carcinoma has been confirmed, the findings on your pathology report, particularly the stage, the grade, whether more than one tumor was present, and the margin status, shape the next steps in your care. Kidney cancer is managed by a team that usually includes a urologist, a medical oncologist, a radiologist, and a pathologist, and may include a genetic counselor and a nephrologist.

Surgery — For tumors confined to the kidney, surgery is the main treatment and is often curative. A partial nephrectomy removes the tumor and preserves the rest of the kidney; it is used often in this type of kidney cancer because the tumors are frequently small, sometimes multiple, and often occur in people whose kidney function is already reduced. A radical nephrectomy removes the whole kidney and is considered for larger tumors or tumors involving the renal vein. For some small tumors, active surveillance with regular imaging, or an ablation procedure that destroys the tumor with heat or cold, may be discussed instead.
Treatment after surgery (adjuvant therapy) — This is an area where papillary renal cell carcinoma differs from clear cell renal cell carcinoma, and the difference is worth understanding. The immunotherapy drugs approved for use after surgery in kidney cancer, including pembrolizumab and the pembrolizumab and belzutifan combination approved in June 2026, were studied in and approved for clear cell renal cell carcinoma. They are not approved for papillary renal cell carcinoma, and no drug treatment after surgery has been shown to help in this type. For most people, the plan after surgery is imaging surveillance rather than drug treatment, and a clinical trial may be discussed for tumors at high risk of returning.
Treatment for cancer that has spread — The options here are also different from clear cell renal cell carcinoma. Cabozantinib, a drug that blocks several growth signals including MET, is the option most supported by evidence from a trial conducted specifically in papillary renal cell carcinoma. Other options the team may consider include the immunotherapy combination of ipilimumab and nivolumab, and pembrolizumab combined with lenvatinib. Because the evidence base in this type of kidney cancer is thinner than in clear cell, enrolling in a clinical trial is discussed more often, particularly for tumors that are MET-driven. Chemotherapy is not effective in this cancer and is not used.
Follow-up — Follow-up includes imaging of the abdomen and chest on a schedule set by the risk score, along with blood tests of kidney function. Because papillary tumors can be multiple, imaging pays attention to both kidneys. If the non-tumor kidney showed damage from diabetes, high blood pressure, or long-standing kidney disease, a referral to a kidney specialist may be arranged.
Genetic assessment — If you were diagnosed young, have more than one kidney tumor, or have a family history of kidney cancer, a referral to a genetics clinic may be offered so that hereditary papillary renal cell carcinoma and other inherited conditions can be looked for and family members can be tested if needed.

Questions to ask your doctor

Does my report use the terms type 1 or type 2, and if so, has my tumor been reviewed under the current classification?
What was the WHO/ISUP grade of my tumor, and what does that grade mean for me?
How large was my tumor, and what was the pathologic stage (pT and pN)?
Was there more than one tumor in my kidney, or tumors in both kidneys?
Did my tumor contain sarcomatoid or rhabdoid cells, and if so, what percentage?
Was tumor necrosis seen under the microscope?
Did the tumor grow outside the kidney, into the fat, the renal sinus, or the renal vein?
Were the surgical margins negative or positive, and if positive, where?
Were any lymph nodes removed, and did any contain cancer?
What did the report say about the non-tumor kidney, and how well is my remaining kidney working?
What risk score was calculated for my tumor, and what is my chance of the cancer returning?
Should I be referred for genetic counseling or germline testing, and should my family be tested?
Was my tumor tested for MET, and would that open any clinical trial options?
How often will I need imaging, and for how many years?