Acute Kidney Injury
Neoplasms, Cystic, Mucinous, and Serous
Kidney Failure, Chronic
Decreased expression of the pro-apoptotic protein Par-4 in renal cell carcinoma. (1/5944)Par-4 is a widely expressed leucine zipper protein that confers sensitization to apoptosis induced by exogenous insults. Because the expression of genes that promote apoptosis may be down-regulated during tumorigenesis, we sought to examine the expression of Par-4 in human tumors. We present here evidence that Par-4 protein levels were severely decreased in human renal cell carcinoma specimens relative to normal tubular cells. Replenishment of Par-4 protein levels in renal cell carcinoma cell lines conferred sensitivity to apoptosis. Because apoptosis may serve as a defense mechanism against malignant transformation or progression, decreased expression of Par-4 may contribute to the pathophysiology of renal cell carcinoma. (+info)
Surgery-related factors and local recurrence of Wilms tumor in National Wilms Tumor Study 4. (2/5944)OBJECTIVE: To assess the prognostic factors for local recurrence in Wilms tumor. SUMMARY BACKGROUND DATA: Current therapy for Wilms tumor has evolved through four studies of the National Wilms Tumor Study Group. As adverse prognostic factors were identified, treatment of children with Wilms tumor has been tailored based on these factors. Two-year relapse-free survival of children in the fourth study (NWTS-4) exceeded 91%. Factors once of prognostic import for local recurrence may lose their significance as more effective therapeutic regimens are devised. METHODS: Children evaluated were drawn from the records of NWTS-4. A total of 2482 randomized or followed patients were identified. Local recurrence, defined as recurrence in the original tumor bed, retroperitoneum, or within the abdominal cavity or pelvis, occurred in 100 children. Using a nested case-control study design, 182 matched controls were selected. Factors were analyzed for their association with local failure. Relative risks and 95% confidence intervals were calculated, taking into account the matching. RESULTS: The largest relative risks for local recurrence were observed in patients with stage III disease, those with unfavorable histology (especially diffuse anaplasia), and those reported to have tumor spillage during surgery. Multiple regression analysis adjusting for the combined effects of histology, lymph node involvement, and age revealed that tumor spillage remained significant. The relative risk of local recurrence from spill was largest in children with stage II disease. The absence of lymph node biopsy was also associated with an increased relative risk of recurrence, which was largest in children with stage I disease. The survival of children after local recurrence is poor, with an average survival rate at 2 years after relapse of 43%. Survival was dependent on initial stage: those who received more therapy before relapse had a worse prognosis. CONCLUSIONS: This study has demonstrated that surgical rupture of the tumor must be prevented by the surgeon, because spills produce an increased risk of local relapse. Both local and diffuse spills produce this risk. Stage II children with local spill appear to require more aggressive therapy than that used in NWTS-4. The continued critical importance of lymph node sampling in conjunction with nephrectomy for Wilms tumor is also established. Absence of lymph node biopsy may result in understaging and inadequate treatment of the child and may produce an increased risk of local recurrence. (+info)
Profound variation in dihydropyrimidine dehydrogenase activity in human blood cells: major implications for the detection of partly deficient patients. (3/5944)Dihydropyrimidine dehydrogenase (DPD) is responsible for the breakdown of the widely used antineoplastic agent 5-fluorouracil (5FU), thereby limiting the efficacy of the therapy. To identify patients suffering from a complete or partial DPD deficiency, the activity of DPD is usually determined in peripheral blood mononuclear cells (PBM cells). In this study, we demonstrated that the highest activity of DPD was found in monocytes followed by that of lymphocytes, granulocytes and platelets, whereas no significant activity of DPD could be detected in erythrocytes. The activity of DPD in PBM cells proved to be intermediate compared with the DPD activity observed in monocytes and lymphocytes. The mean percentage of monocytes in the PBM cells obtained from cancer patients proved to be significantly higher than that observed in PBM cells obtained from healthy volunteers. Moreover, a profound positive correlation was observed between the DPD activity of PBM cells and the percentage of monocytes, thus introducing a large inter- and intrapatient variability in the activity of DPD and hindering the detection of patients with a partial DPD deficiency. (+info)
Methylation-associated silencing of the tissue inhibitor of metalloproteinase-3 gene suggest a suppressor role in kidney, brain, and other human cancers. (4/5944)Tissue inhibitor of metalloproteinase-3 (TIMP-3) antagonizes matrix metalloproteinase activity and can suppress tumor growth, angiogenesis, invasion, and metastasis. Loss of TIMP-3 has been related to the acquisition of tumorigenesis. Herein, we show that TIMP-3 is silenced in association with aberrant promoter-region methylation in cell lines derived from human cancers. TIMP-3 expression was restored after 5-aza-2'deoxycytidine-mediated demethylation of the TIMP-3 proximal promoter region. Genomic bisulfite sequencing revealed that TIMP-3 silencing was related to the overall density of methylation and that discrete regions within the TIMP-3 CpG island may be important for the silencing of this gene. Aberrant methylation of TIMP-3 occurred in primary cancers of the kidney, brain, colon, breast, and lung, but not in any of 41 normal tissue samples. The most frequent TIMP-3 methylation was found in renal cancers, which originate in the tissue that normally expresses the highest TIMP-3 levels. This methylation correlated with a lack of detectable TIMP-3 protein in these tumors. Together, these data show that methylation-associated inactivation of TIMP-3 is frequent in many human tumors. (+info)
Isolation and characterization of a rat homologue of the human tuberous sclerosis 1 gene (Tsc1) and analysis of its mutations in rat renal carcinomas. (5/5944)In the Eker rat, a germ-line mutation in the homologue of the human tuberous sclerosis gene (Tsc2) causes renal cell carcinomas (RCs) with a complete penetrance in all heterozygotes. Tsc2 mutations have also been found in a subset of chemically induced non-Eker rat RCs. Because tuberous sclerosis patients with alteration of either of the two predisposing genes (TSC1 and TSC2) show identical symptoms, the products of these two genes are thought to be involved in a common biological pathway. In this study, to analyze the possible overlap between the functions of Tsc2 and Tscl gene products, we isolated and characterized a rat homologue of the TSC1 gene (Tsc1). The rat Tsc1 gene, which has an identical exon-intron structure to that of human TSC1 and is localized on rat chromosome 3, has been shown to encode a protein (hamartin) that is highly homologous to the human counterpart with an approximately 86% amino acid sequence identity. Using PCR-single-strand conformational polymorphism analysis, we identified two splicing donor site mutations in one chemically induced rat RC (1 of 15). This suggests that alterations of the Tsc1 gene may be involved in the development of a subset of rat RCs. (+info)
Presentation of renal tumor antigens by human dendritic cells activates tumor-infiltrating lymphocytes against autologous tumor: implications for live kidney cancer vaccines. (6/5944)The clinical impact of dendritic cells (DCs) in the treatment of human cancer depends on their unique role as the most potent antigen-presenting cells that are capable of priming an antitumor T-cell response. Here, we demonstrate that functional DCs can be generated from peripheral blood of patients with metastatic renal cell carcinoma (RCC) by culture of monocytes/macrophages (CD14+) in autologous serum containing medium (RPMI) in the presence of granulocyte macrophage colony-stimulating factor and interleukin (IL) 4. For testing the capability of RCC-antigen uptake and processing, we loaded these DCs with autologous tumor lysate (TuLy) using liposomes, after which cytometric analysis of the DCs revealed a markedly increased expression of HLA class I antigen and a persistent high expression of class II. The immunogenicity of DC-TuLy was further tested in cultures of renal tumor infiltrating lymphocytes (TILs) cultured in low-dose IL-2 (20 Biologic Response Modifier Program units/ml). A synergistic effect of DC-TuLy and IL-2 in stimulating a T cell-dependent immune response was demonstrated by: (a) the increase of growth expansion of TILs (9.4-14.3-fold; day 21); (b) the up-regulation of the CD3+ CD56- TcR+ (both CD4+ and CD8+) cell population; (c) the augmentation of T cell-restricted autologous tumor lysis; and (d) the enhancement of IFN-gamma, tumor necrosis factor-alpha, granulocyte macrophage colony-stimulating factor, and IL-6 mRNA expression by TILs. Taken together, these data implicate that DC-TuLy can activate immunosuppressed TIL via an induction of enhanced antitumor CTL responses associated with production of Thl cells. This indicates a potential role of DC-TuLy vaccines for induction of active immunity in patients with advanced RCC. (+info)
A possible contributory role of BK virus infection in neuroblastoma development. (7/5944)The tumor suppressor protein p53 is aberrantly localized to the cytoplasm of neuroblastoma cells, compromising the suppressor function of this protein. Such tumors are experimentally induced in transgenic mice expressing the large tumor (T) antigen of polyomaviruses. The oncogenic mechanisms of T antigen include complex formation with, and inactivation of, the tumor suppressor protein p53. Samples from 18 human neuroblastomas and five normal human adrenal glands were examined. BK virus DNA was detected in all neuroblastomas and none of five normal adrenal glands by PCR. Using DNA in situ hybridization, polyomaviral DNA was found in the tumor cells of 17 of 18 neuroblastomas, but in none of five adrenal medullas. Expression of the large T antigen was detected in the tumor cells of 16 of 18 neuroblastomas, but in none of the five adrenal medullas. By double immunostaining BK virus T antigen and p53 was colocalized to the cytoplasm of the tumor cells. Immunoprecipitation revealed binding between the two proteins. The presence and expression of BK virus in neuroblastomas, but not in normal adrenal medulla, and colocalization and binding to p53, suggest that this virus may play a contributory role in the development of this neoplasm. (+info)
Immunohistochemical detection of JC virus in nontumorous renal tissue of a patient with renal cancer but without progressive multifocal leukoencephalopathy. (8/5944)We performed immunohistochemical staining on the nontumorous renal tissue of 45 patients with renal cancer but without progressive multifocal encephalopathy using JCV-specific antibody. For one patient we found positive staining of the nuclei of the renal collecting ducts. Immunoelectron microscopic examination of the positive cell nuclei revealed electron-dense polyomavirus-like particles. (+info)
Kidney neoplasms refer to abnormal growths or tumors that develop in the kidneys. These tumors can be either benign (non-cancerous) or malignant (cancerous). Kidney neoplasms are also known as renal neoplasms or renal tumors. There are several types of kidney neoplasms, including: 1. Renal cell carcinoma (RCC): This is the most common type of kidney cancer and accounts for about 80-90% of all kidney neoplasms. 2. Wilms tumor: This is a type of kidney cancer that is most common in children. 3. Angiomyolipoma: This is a benign tumor that is made up of fat, smooth muscle, and blood vessels. 4. Oncocytoma: This is a benign tumor that is made up of cells that resemble normal kidney cells. 5. Papillary renal cell carcinoma: This is a type of kidney cancer that is less common than RCC but has a better prognosis. 6. Clear cell renal cell carcinoma: This is a type of kidney cancer that is the most common in adults and has a poor prognosis. The diagnosis of kidney neoplasms typically involves imaging tests such as ultrasound, CT scan, or MRI, as well as a biopsy to confirm the type and stage of the tumor. Treatment options for kidney neoplasms depend on the type, size, and stage of the tumor, as well as the overall health of the patient. Treatment options may include surgery, radiation therapy, chemotherapy, or targeted therapy.
Kidney diseases refer to a wide range of medical conditions that affect the kidneys, which are two bean-shaped organs located in the back of the abdomen. The kidneys play a crucial role in filtering waste products from the blood and regulating the body's fluid balance, electrolyte levels, and blood pressure. Kidney diseases can be classified into two main categories: acute kidney injury (AKI) and chronic kidney disease (CKD). AKI is a sudden and severe decline in kidney function that can be caused by a variety of factors, including dehydration, infection, injury, or certain medications. CKD, on the other hand, is a progressive and chronic condition that develops over time and is characterized by a gradual decline in kidney function. Some common types of kidney diseases include glomerulonephritis, which is an inflammation of the glomeruli (the tiny blood vessels in the kidneys), polycystic kidney disease, which is a genetic disorder that causes cysts to form in the kidneys, and kidney stones, which are hard deposits that can form in the kidneys and cause pain and other symptoms. Treatment for kidney diseases depends on the underlying cause and severity of the condition. In some cases, lifestyle changes such as diet modification and exercise may be sufficient to manage the condition. In more severe cases, medications, dialysis, or kidney transplantation may be necessary. Early detection and treatment of kidney diseases are essential to prevent complications and improve outcomes.
Pancreatic neoplasms refer to abnormal growths or tumors that develop in the pancreas, a gland located in the abdomen behind the stomach. These neoplasms can be either benign (non-cancerous) or malignant (cancerous). Pancreatic neoplasms can occur in various parts of the pancreas, including the exocrine gland (which produces digestive enzymes), the endocrine gland (which produces hormones), and the ducts (which carry digestive juices from the pancreas to the small intestine). Symptoms of pancreatic neoplasms can vary depending on the location and size of the tumor, but may include abdominal pain, weight loss, jaundice (yellowing of the skin and eyes), nausea, vomiting, and unexplained fatigue. Diagnosis of pancreatic neoplasms typically involves imaging tests such as CT scans, MRI scans, or ultrasound, as well as blood tests and biopsies. Treatment options may include surgery, chemotherapy, radiation therapy, or a combination of these approaches, depending on the type and stage of the neoplasm.
In the medical field, neoplasms refer to abnormal growths or tumors of cells that can occur in any part of the body. These growths can be either benign (non-cancerous) or malignant (cancerous). Benign neoplasms are usually slow-growing and do not spread to other parts of the body. They can cause symptoms such as pain, swelling, or difficulty moving the affected area. Examples of benign neoplasms include lipomas (fatty tumors), hemangiomas (vascular tumors), and fibromas (fibrous tumors). Malignant neoplasms, on the other hand, are cancerous and can spread to other parts of the body through the bloodstream or lymphatic system. They can cause a wide range of symptoms, depending on the location and stage of the cancer. Examples of malignant neoplasms include carcinomas (cancers that start in epithelial cells), sarcomas (cancers that start in connective tissue), and leukemias (cancers that start in blood cells). The diagnosis of neoplasms typically involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy (the removal of a small sample of tissue for examination under a microscope). Treatment options for neoplasms depend on the type, stage, and location of the cancer, as well as the patient's overall health and preferences.
Acute kidney injury (AKI) is a sudden and rapid decline in kidney function that occurs within a short period of time, usually within 7 days. It is a medical emergency that requires prompt diagnosis and treatment to prevent further damage to the kidneys and other organs. AKI can be caused by a variety of factors, including dehydration, blood loss, kidney infections, kidney stones, certain medications, and exposure to toxins. It can also be a complication of other medical conditions, such as heart failure, sepsis, and pneumonia. The severity of AKI is typically classified into three stages based on the level of kidney function decline. Stage 1 is mild and may not require any specific treatment, while stage 2 and 3 are more severe and may require hospitalization and dialysis. AKI can have serious consequences if left untreated, including permanent kidney damage, high blood pressure, fluid and electrolyte imbalances, and even death. Therefore, early detection and prompt treatment are crucial for preventing complications and improving outcomes for patients with AKI.
Neoplasms, cystic, mucinous, and serous are types of tumors that can occur in various organs of the body. Cystic neoplasms are tumors that are filled with fluid or semi-solid material. They can be benign or malignant and can occur in various organs, including the liver, kidneys, ovaries, and pancreas. Mucinous neoplasms are tumors that produce a thick, gelatinous substance called mucus. They can be benign or malignant and are most commonly found in the ovaries, appendix, and colon. Serous neoplasms are tumors that produce a clear, watery fluid called serous fluid. They can be benign or malignant and are most commonly found in the ovaries, peritoneum, and pleura. It's important to note that not all cystic, mucinous, and serous neoplasms are cancerous, and some may be benign and not require treatment. However, it's important to have any suspicious cystic, mucinous, or serous neoplasm evaluated by a medical professional to determine the best course of action.
Chronic kidney failure, also known as chronic renal failure, is a condition in which the kidneys are unable to function properly over a long period of time. This can be caused by a variety of factors, including diabetes, high blood pressure, and glomerulonephritis. Chronic kidney failure is typically diagnosed when the kidneys are functioning at less than 60% of their normal capacity, and the condition has been present for at least three months. As the kidneys become less functional, they are unable to filter waste products from the blood, leading to a buildup of toxins in the body. This can cause a range of symptoms, including fatigue, weakness, nausea, and difficulty concentrating. Treatment for chronic kidney failure typically involves managing the underlying cause of the condition, as well as managing symptoms and complications. This may include medications to control blood pressure and blood sugar levels, as well as dietary changes and other lifestyle modifications. In some cases, dialysis or kidney transplantation may be necessary to help the body remove waste products and maintain proper fluid balance.
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Plasma cell neoplasms1
- Transplant recipients have elevated risk for plasma cell neoplasms (PCNs, comprising multiple myeloma and plasmacytoma), but little is known about risk factors in the transplant setting. (medscape.com)
- The death of ESPN sportscaster Stuart Scott has generated interest in cancer deaths in the U.S. Cancer is the second leading cause of death in the U.S. The number of cancer deaths are available from the multiple cause of death option on the CDC WONDER database using the C00-C97 ICD Code, "Malignant Neoplasms. (cdc.gov)
- Malignant neoplasms [Levy BS and Wegman DH 2011]. (cdc.gov)
- kidney neoplasms aspiration biopsy renal cell carcinoma Acta Cytologica Accuracy of Fine Needle Aspiration in Distinguishing Subtypes of Renal Cell Carcinoma Andrew. (karger.com)
- RR CC was named for its morphologic resemblance to pediatric malignant rhabdoid tumor (MRT) of the kidney, which is a highly aggressive tumor characterized by cells that resemble rhabdomyoblasts and by genetic alterations involving chromosome 22, particularly the hSNF5/INI1 gene on 22q11.2. (medscape.com)
- This study will investigate the genetic cause of Birt Hogg-Dube (BHD) syndrome and the relationship of this disorder to kidney cancer. (nih.gov)
- People with BHD are at increased risk of developing kidney cancer. (nih.gov)
- Kidney cancer, prostate cancer / M. Linehan and W. Dahut. (nih.gov)
- Renal oncology focuses on the management and treatment of kidney cancer through surgery, immunotherapy, targeted therapy, radiation, and chemotherapy. (healthgrades.com)
- In the United States in 2023, about 81,800 new cases of kidney cancer and renal pelvis cancer will occur, along with an estimated 14,890 deaths. (peacehealth.org)
- 2 ] RCC is distinct from kidney cancer that involves the renal pelvis or renal medulla, and it only applies to cancer that forms in the lining of the kidney bed (i.e., in the renal tubules). (peacehealth.org)
- Non-RCCs of the kidney, including cancer of the renal pelvis or renal medulla, are not addressed in this summary. (peacehealth.org)
- For more information on sporadic kidney cancer, see Renal Cell Cancer Treatment and Transitional Cell Cancer of the Renal Pelvis and Ureter Treatment. (peacehealth.org)
- Kidney cancer and renal pelvis cancer account for about 4.2% of all adult malignancies in the United States. (peacehealth.org)
- To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world. (asn-online.org)
- Renal carcinomas associated with Xp11.2 translocations/ TFE3 gene fusions, briefly Xp11.2 renal cell carcinomas (RCCs), are recently introduced rare subtypes of renal neoplasms characterized by chromosomal translocations involving the TFE3 gene. (karger.com)
- His work has also changed practice relative to treating acute kidney injury (AKI), publishing a series of landmark studies examining the epidemiology of AKI. (asn-online.org)
- Diagnosing a neoplasm that is metastatic to the pancreas by fine-needle aspiration (FNA) cytology is often challenging. (karger.com)
- [ 13 ] As a result, one concern has been that the association of PCN with transplantation (kidney transplantation in particular) could largely be due to reverse causation, that is, that the PCN is actually the cause of end-stage renal disease but is diagnosed only after transplantation. (medscape.com)
- Here we report a rare case of Caroli's disease limited to one liver segment, which was initially misdiagnosed as an intraductal papillary neoplasm of the bile duct. (e-cmh.org)
- In a series of seminal publications, he improved understanding regarding how the loss of kidney function directly contributes to increased oxidative stress, inflammation, insulin resistance and endothelial dysfunction, and ultimately cardiovascular risk in kidney disease. (asn-online.org)
- Dr. Himmelfarb helped develop microphysiological systems (MPS) for kidney disease modeling and drug efficacy and toxicity testing. (asn-online.org)
- In this report, we present a case of Caroli's disease that was misdiagnosed as an intraductal papillary neoplasm of the bile duct (IPNB) and was treated with segmentectomy. (e-cmh.org)
- The kidneys are exposed to exogenous or endogenous xenobiotics in their role as primary defenders against harmful xenobiotics entering the bloodstream. (cdc.gov)
- Prognostic determinants at diagnosis include the stage of the RCC, whether the tumor is confined to the kidney, primary tumor size, Fuhrman nuclear grade, and multifocality. (peacehealth.org)
- Dr. Himmelfarb's research spans diverse areas that have propelled major advances in kidney research and care. (asn-online.org)
- Evaluate the light microscopic features of the neoplasm. (medscape.com)
- Dr. Jonathan Himmelfarb is currently Professor of Medicine, adjunct Professor of Bioengineering, Director of the Kidney Research Institute, Co-Director of Center for Dialysis Innovation, and holds the Joseph W. Eschbach MD Endowed Chair for Kidney Research in the Department of Medicine, Division of Nephrology, University of Washington. (asn-online.org)
- As the inaugural Director of the Kidney Research Institute (KRI), Dr Himmelfarb has built a highly successful, team science based clinical and translational research program, and has led efforts to engage patients as participants in the design of research, as well as developed and mentored physician scientists who are conducting groundbreaking clinical and basic research. (asn-online.org)