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      Nephrotic syndrome associated with gemcitabine use in a patient with ovarian cancer

      case-report

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Summary

          Background:

          Here we present a patient who developed nephrotic syndrome associated with gemcitabine use.

          Case Report:

          Gemcitabine therapy was initiated following tumor recurrence in a patient with ovarian cancer, who was previously treated twice with carboplatin and paclitaxel. Radiological findings waned and tumor marker concentrations decreased after gemcitabine treatment. However, edema and ascites development was observed on the fifth treatment cycle. Laboratory results revealed increased blood urea nitrogen and creatinine levels, decreased serum albumin concentrations, and increased 24-hour urinary protein excretion. Renal biopsy findings were compatible with membranous glomerulonephritis. Gemcitabine administration was stopped and the cyclophosphamide and steroid therapy were initiated. The symptoms and findings disappeared after the cessation of gemcitabine and immunosuppressive treatment.

          Conclusions:

          Gemcitabine treatment may be associated with proteinuria to the extent of nephrotic syndrome.

          Related collections

          Most cited references11

          • Record: found
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          Action of 2',2'-difluorodeoxycytidine on DNA synthesis.

          L Hertel, Lisa Huang, S. A. Paul Chubb … (1991)
          The action of the new deoxycytidine analogue 2',2'-difluorodeoxycytidine (dFdC) on DNA synthesis was investigated in whole cells and in vitro assay systems with purified DNA polymerases. DNA synthesis in human lymphoblastoid CEM cells was inhibited by dFdC in a concentration-dependent manner that could not be reversed by exogenous deoxynucleosides. The analogue was incorporated into cellular DNA; most of the incorporated dFdC 5'-monophosphate (dFdCMP) residues were in internucleotide linkage. In vitro DNA primer extension assays demonstrated that dFdC 5'-triphosphate (dFdCTP) competed with deoxycytidine triphosphate for incorporation into the C sites of the growing DNA strand. The ratios of the apparent Km values for the incorporation of dFdCTP and dCTP into a C site of M13mp19 DNA were 21.8 and 22.9 for DNA polymerases alpha and epsilon, respectively. The apparent Ki values of dFdCTP were 11.2 microM for DNA polymerase alpha and 14.4 microM for polymerase epsilon. After dFdCMP incorporation, the primer was extended by one deoxynucleotide before a major pause in the polymerization process was observed. This was in contrast to the action of arabinosylcytosine 5'-triphosphate, which caused both DNA polymerases alpha and epsilon to pause at the site of incorporation. The 3'----5' exonuclease activity of DNA polymerase epsilon was essentially unable to excise nucleotides from DNA containing dFdCMP at either the 3'-end or at an internal position, whereas arabinosylcytosine monophosphate was removed from the 3'-terminus at 37% the rate for deoxynucleotides. The cytotoxic activity of dFdC was strongly correlated with the amount of dFdCMP incorporated into cellular DNA. Our results demonstrate qualitative and quantitative differences in the molecular actions of dFdC and arabinosylcytosine on DNA metabolism, but are consistent with an important role for such incorporation in the toxicity of dFdC.
          Article 0 comments Cited 102 times – based on 0 reviews     Review now
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            Comparison of the cellular pharmacokinetics and toxicity of 2',2'-difluorodeoxycytidine and 1-beta-D-arabinofuranosylcytosine.

            S Plunkett, L Hertel, G B Grindey … (1988)
            2',2'-Difluorodeoxycytidine (dFdC) is a new deoxycytidine analogue with good activity against human leukemic cell lines and murine solid tumors, while the activity of 1-beta-D-arabinofuranosylcytosine (ara-C) is established in experimental systems and for the treatment of human adult leukemia. This study compared the cellular metabolism and cytotoxic properties of dFdC and ara-C in Chinese hamster ovary cells. In wild-type cells, dFdC was significantly more cytotoxic than ara-C after both 4- and 18-h incubations. The 5'-triphosphate of dFdC (dFdCTP) was the major cellular metabolite (85-90%), reaching cellular concentrations up to 20-fold greater than those observed for ara-C 5'-triphosphate at equimolar concentrations of the parent drug. A deoxycytidine kinase-deficient mutant neither accumulated dFdCTP nor showed any cytotoxic response up to drug concentrations of 100 microM. The cytotoxicity of dFdC could be competitively reversed by deoxycytidine further suggesting that dFdC, like ara-C, required phosphorylation by deoxycytidine kinase for biological activity. Several explanations for the different cellular accumulation of the drug triphosphates were established: (a) nucleoside transport studies demonstrated that the membrane permeation of dFdC was 65% more rapid than that of ara-C; (b) deoxycytidine kinase had a higher affinity for dFdC (Km = 3.6 microM) than for ara-C (Km = 8.8 microM), while the Km for deoxycytidine was 1.4 microM; (c) the elimination of intracellular dFdCTP was biphasic with t1/2 alpha = 3.9 and t1/2 beta greater than 16 h while the degradation of ara-CTP was monophasic and significantly faster (t1/2 = 0.7 h). The comparatively long half-life of dFdCTP was related to the prolonged inhibition of DNA synthesis after removal of exogenous nucleoside. Together these factors contribute to the more potent cytotoxicity of dFdC compared with ara-C.
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              Gemcitabine: current status of phase I and II trials.

              Keith S. Kaye (1994)
              Article 0 comments Cited 11 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Am J Case Rep
                Journal ID (iso-abbrev): Am J Case Rep
                Journal ID (publisher-id): amjcaserep
                Title: The American Journal of Case Reports
                Publisher: International Scientific Literature, Inc.
                ISSN (Electronic): 1941-5923
                Publication date Collection: 2012
                Publication date (Electronic): 19 November 2012
                Volume: 13
                Pages: 268-270
                Affiliations
                [1 ]Mersin State Hospital Clinic Of Medical Oncology, Mersin, Turkey
                [2 ]Department of Pathology, Mersin University Faculty Of Medicin, Mersin, Turkey
                [3 ]Department of Nephrology, Mersin University Faculty Of Medicine, Mersin, Turkey
                [4 ]Department of Medical Oncology, Mersin University Faculty Of Medicine, Mersin, Turkey
                Author notes
                Author’s address: Alper Ata, Mersin State Hospital Clinic Of Medical Oncology, Mersin, Turkey, e-mial: dralperata@ 123456yahoo.co
                Article
                Publisher ID: 883583
                DOI: 10.12659/AJCR.883583
                PMC ID: 3614261
                PubMed ID: 23569546
                SO-VID: 1dce341e-5e9b-4c4e-aa5c-8e745a90b8d5
                Copyright © © Am J Case Rep, 2012
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.

                History
                Date received : 30 June 2012
                Date accepted : 20 July 2012
                Categories
                Subject: Case Report

                Keywords: gemcitabine,nephrotic syndrome,ovarian cancer
                Data availability:
                Keywords: gemcitabine, nephrotic syndrome, ovarian cancer

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