Glomerular hyperfiltration in children with cancer: prevalence and a hypothesis
Creators
- 1. Boston Children's Hospital, Department of Radiology, Boston, MA (United States)
- 2. Children's National Medical Center, Division of Diagnostic Imaging and Radiology, Washington, DC (United States)
- 3. Children's National Medical Center, Department of Hematology/Oncology, Washington, DC (United States)
- 4. Boston Children's Hospital, Department of Cardiology, Boston, MA (United States)
- 5. The Johns Hopkins University School of Medicine, Department of Pathology, Baltimore, MD (United States)
Description
Glomerular hyperfiltration has recently been reported in children with malignancies and has been attributed to increased solute from breakdown of tumor tissues. To evaluate the prevalence of hyperfiltration in the pediatric oncology population and explore its pathophysiological mechanism. Tc-99 m diethylenetriaminepentaacetic acid (DTPA) glomerular filtration rate (GFR) examinations (437 studies) and medical records of 177 patients <21 years of age diagnosed with a malignancy between January 2005 and October 2013 were retrospectively reviewed. Hyperfiltration was defined as a GFR ≥ 160 ml/min/1.73 m2. Seventy-seven (43.5%) patients had hyperfiltration in at least one GFR exam. A significantly higher percentage of patients with central nervous system (CNS) tumors (63.6%) had hyperfiltration when compared to other tumor types (27.3%, P < 0.001). No association was found between hyperfiltration and age, gender, race or bone marrow involvement. There was a significant trend toward decreasing hyperfiltration after the second cycle of chemotherapy (P = 0.006) and a significant increase in subjects with low GFR (<100 ml/min/1.73 m2) with increasing number of cycles of chemotherapy (P = 0.005). Glomerular hyperfiltration is common in children with malignancies at diagnosis and during initial cycles of chemotherapy. It is particularly prevalent in patients with central nervous tumors, which are frequently smaller in volume. Therefore, the pathophysiological mechanism of hyperfiltration cannot be explained solely on the basis of large tumor volume and subsequent cell breakdown. We hypothesize that host hypermetabolic state plays an important role in pathophysiology of hyperfiltration. (orig.)
Availability note (English)
Available from: http://dx.doi.org/10.1007/s00247-016-3733-5Additional details
Identifiers
Publishing Information
- Journal Title
- Pediatric Radiology
- Journal Volume
- 47
- Journal Issue
- 2
- Journal Page Range
- p. 221-226
- ISSN
- 0301-0449
- CODEN
- PDRYA5
INIS
- Country of Publication
- Germany
- Country of Input or Organization
- Germany
- INIS RN
- 48038110
- Subject category
- S62: RADIOLOGY AND NUCLEAR MEDICINE;
- Descriptors DEI
- BLOOD; CARCINOMAS; CENTRAL NERVOUS SYSTEM; CHEMOTHERAPY; CHILDREN; DIAGNOSIS; DTPA; FILTRATION; GLOMERULI; INFANTS; METABOLISM; PEDIATRICS; RADIOPHARMACEUTICALS; TECHNETIUM 99
- Descriptors DEC
- AGE GROUPS; AMINO ACIDS; ANIMALS; BETA DECAY RADIOISOTOPES; BETA-MINUS DECAY RADIOISOTOPES; BIOLOGICAL MATERIALS; BODY; BODY FLUIDS; CARBOXYLIC ACIDS; CHELATING AGENTS; CHILDREN; DISEASES; DRUGS; HOURS LIVING RADIOISOTOPES; INTERMEDIATE MASS NUCLEI; INTERNAL CONVERSION RADIOISOTOPES; ISOMERIC TRANSITION ISOTOPES; ISOTOPES; KIDNEYS; LABELLED COMPOUNDS; MAMMALS; MAN; MATERIALS; MEDICINE; NEOPLASMS; NERVOUS SYSTEM; NUCLEI; ODD-EVEN NUCLEI; ORGANIC ACIDS; ORGANIC COMPOUNDS; ORGANS; PRIMATES; RADIOACTIVE MATERIALS; RADIOISOTOPES; RADIOPROTECTIVE SUBSTANCES; RESPONSE MODIFYING FACTORS; SEPARATION PROCESSES; TECHNETIUM ISOTOPES; THERAPY; VERTEBRATES; YEARS LIVING RADIOISOTOPES