skip to main content
OSTI.GOV title logo U.S. Department of Energy
Office of Scientific and Technical Information

Title: Percutaneous Treatment of Pyocystis in Patients with Autosomal Dominant Polycystic Kidney Disease

Abstract

The course of autosomal dominant polycystic kidney disease (ADPKD) is frequently complicated by infection of a cyst within a polycystic kidney, which is a diagnostic and therapeutic dilemma damaging the clinical course of patients. The aim of this study was to demonstrate the safety and efficacy of percutaneous drainage in management of infected cysts in ADPKD patients. Between May 2003 and December 2006, percutaneous drainage was performed in 16 infected renal cysts of four kidneys in three patients (two females, one male), with a mean age of 57.3 years. Cyst dimensions, total amount of drained cyst fluid, catheterization duration, isolated microorganisms, and follow-up duration were recorded. Technical, clinical success rates were 100%; the complication rate was 0%. Diameters of cysts ranged between 3 and 8 cm. Average volume of drained fluid and average duration of catheterization for one cyst were 226 ml and 9.8 days. No recurrence was encountered but one patient (no. 3), who had pyocystis in the right kidney and was treated with catheterization, referred with left flank pain due to pyocystis in her left kidney 3 months later. Follow-up durations were 35, 47, and 11 months for patients 1, 2, and 3, respectively. For patient 3, follow-upmore » duration for the second procedure was 7 months. We conclude that percutaneous drainage with antibiotic therapy should be the initial method in management of infected cysts in ADPKD patients, with high success and low complication rates.« less

Authors:
;  [1];  [2]; ; ;  [1]
  1. Hacettepe University School of Medicine, Department of Radiology (Turkey)
  2. Hacettepe University School of Medicine, Department of Nephrology (Turkey)
Publication Date:
OSTI Identifier:
21450349
Resource Type:
Journal Article
Resource Relation:
Journal Name: Cardiovascular and Interventional Radiology; Journal Volume: 31; Journal Issue: 5; Other Information: DOI: 10.1007/s00270-007-9273-5; Copyright (c) 2008 Springer Science+Business Media, LLC
Country of Publication:
United States
Language:
English
Subject:
62 RADIOLOGY AND NUCLEAR MEDICINE; ANTIBIOTICS; CYSTS; DRAINAGE; KIDNEYS; MANAGEMENT; THERAPY; ANTI-INFECTIVE AGENTS; BODY; DRUGS; MEDICINE; ORGANIC COMPOUNDS; ORGANS; PATHOLOGICAL CHANGES

Citation Formats

Akinci, Devrim, E-mail: akincid@yahoo.com, Turkbey, Baris, E-mail: bturkbey@yahoo.co, Yilmaz, Rahmi, Akpinar, Erhan, Ozmen, Mustafa N., and Akhan, Okan. Percutaneous Treatment of Pyocystis in Patients with Autosomal Dominant Polycystic Kidney Disease. United States: N. p., 2008. Web. doi:10.1007/S00270-007-9273-5.
Akinci, Devrim, E-mail: akincid@yahoo.com, Turkbey, Baris, E-mail: bturkbey@yahoo.co, Yilmaz, Rahmi, Akpinar, Erhan, Ozmen, Mustafa N., & Akhan, Okan. Percutaneous Treatment of Pyocystis in Patients with Autosomal Dominant Polycystic Kidney Disease. United States. doi:10.1007/S00270-007-9273-5.
Akinci, Devrim, E-mail: akincid@yahoo.com, Turkbey, Baris, E-mail: bturkbey@yahoo.co, Yilmaz, Rahmi, Akpinar, Erhan, Ozmen, Mustafa N., and Akhan, Okan. 2008. "Percutaneous Treatment of Pyocystis in Patients with Autosomal Dominant Polycystic Kidney Disease". United States. doi:10.1007/S00270-007-9273-5.
@article{osti_21450349,
title = {Percutaneous Treatment of Pyocystis in Patients with Autosomal Dominant Polycystic Kidney Disease},
author = {Akinci, Devrim, E-mail: akincid@yahoo.com and Turkbey, Baris, E-mail: bturkbey@yahoo.co and Yilmaz, Rahmi and Akpinar, Erhan and Ozmen, Mustafa N. and Akhan, Okan},
abstractNote = {The course of autosomal dominant polycystic kidney disease (ADPKD) is frequently complicated by infection of a cyst within a polycystic kidney, which is a diagnostic and therapeutic dilemma damaging the clinical course of patients. The aim of this study was to demonstrate the safety and efficacy of percutaneous drainage in management of infected cysts in ADPKD patients. Between May 2003 and December 2006, percutaneous drainage was performed in 16 infected renal cysts of four kidneys in three patients (two females, one male), with a mean age of 57.3 years. Cyst dimensions, total amount of drained cyst fluid, catheterization duration, isolated microorganisms, and follow-up duration were recorded. Technical, clinical success rates were 100%; the complication rate was 0%. Diameters of cysts ranged between 3 and 8 cm. Average volume of drained fluid and average duration of catheterization for one cyst were 226 ml and 9.8 days. No recurrence was encountered but one patient (no. 3), who had pyocystis in the right kidney and was treated with catheterization, referred with left flank pain due to pyocystis in her left kidney 3 months later. Follow-up durations were 35, 47, and 11 months for patients 1, 2, and 3, respectively. For patient 3, follow-up duration for the second procedure was 7 months. We conclude that percutaneous drainage with antibiotic therapy should be the initial method in management of infected cysts in ADPKD patients, with high success and low complication rates.},
doi = {10.1007/S00270-007-9273-5},
journal = {Cardiovascular and Interventional Radiology},
number = 5,
volume = 31,
place = {United States},
year = 2008,
month = 9
}
  • The gene for autosomal dominant polycystic kidney disease (PKD1) is located on chromosome 16p, between the flanking markers D16S84 and D16S125 (26.6 prox). This region is 750 kb long and has been cloned. The authors have looked at the association of 10 polymorphic markers from the region, with the disease and with each other. This was done in a set of Scottish families that had previously shown association with D16S94, a marker proximal to the PKD1 region. They report significant association between two CA repeat markers and the disease but have not found evidence for a single founder haplotype inmore » these families, indicating the presence of several mutations in this population. Their results favor a location of the PKD1 gene in the proximal part of the candidate region. 25 refs., 1 fig., 4 tabs.« less
  • Autosomal dominant polycystic kidney disease (ADPKD) is a genetically heterogeneous disorder. At least two distinct forms of ADPKD are now well defined. In {approximately}86% of affected European families, a gene defect localized to 16p13.3 was responsible for ADPKD, while a second locus has been recently localized to 4q13-q23 as candidate for the disease in the remaining families. We present confirmation of linkage to microsatellite markers on chromosome 4q in eight Spanish families with ADPKD, in which the disease was not linked to 16p13.3. By linkage analysis with marker D4S423, a maximum lod score of 9.03 at a recombination fraction ofmore » .00 was obtained. Multipoint linkage analysis, as well as a study of recombinant haplotypes, placed the PKD2 locus between D4S1542 and D4S1563, thereby defining a genetic interval of {approximately}1 cM. The refined map will serve as a genetic framework for additional genetic and physical mapping of the region and will improve the accuracy of presymptomatic diagnosis of PKD2. 25 refs., 4 figs., 1 tab.« less
  • The PKDl gene was localized to an {approximately}480 kb interval of chromosome 16pl3. More than 20 independent transcripts were found in the interval. In view of the high new mutation rate in autosomal dominant polycystic kidney diseases (ADPKD), we anticipated the PKD1 gene would be large. The largest transcript in the region was represented by five cDNA clones located adjacent to the tuberin gene (TSC2). Two of these clones, KG8 and NKG9, contain {approximately}4.5 kb of contiguous sequence corresponding to the 3{prime} end of the 14 kb mRNA which is transcribed from telomeric to centromeric. They spans 11 exons, andmore » to evaluate the reading frame of the cDNA, we have compared the human and monkey sequence using human primers, and found 90-94% identity at the DNA level, and by observing amino acid conservation, determined the reading frame. To date, our open-reading frame of {approximately}800 amino-acids contained only a potential threonine kinase site, but no other recognizable peptide motifs or repeats, and was not homologous to sequences in Swissprot and GenBank. No Southern blot abnormalities have been detected with the cDNA probes used. However, an exon-by-exon scan of 8 exons for mutations by SSCP and genomic sequencing (predicted missense changes) has identified 3 patients with mutations not found in normals, and identify the KG8 gene as the PKD1 gene.« less
  • We describe a family in which both members of a non-consanguineous couple are affected by autosomal dominant polycystic kidney disease (ADPKD). They have three affected children without obvious clinical differences, and three affected grand-children. Two different morbid loci for this disease have been localized, PKD1 on chromosome 16p and PKD4 on chromosome 4q. There were four a priori mating possibilities for this couple: PKD1xPKD1, PKD1xPKD4 or PKD4xPKD1 and PKD4xPKD4. We demonstrate by linkage analysis that: (i) the father is heterozygous at the PKD1 locus (most probably a de novo mutation); (ii) the mother is heterozygous at the PKD4 locus. Themore » abnormal alleles segregates as follows: one child has the abnormal PKD1, another child has the abnormal PKD4 while the third child is a compound heterozygote for both abnormal PKD1 and PKD4 alleles, which were both transmitted to one offspring. The clinical status of these subjects is similar to the status of their relatives in the same age range, suggesting that both PKD1 and PKD4 are truly dominant disease. As there is no other example of such a situation for heterogeneous dominant diseases, we discuss this issue and some possible pathogenic processes by comparison with the similar problem of expressivity in homozygotes for dominant diseases.« less
  • The PKD1-gene responsible for autosomal dominant polycystic kidney disease in 85% of the families maps to chromosome 16q13. Last year the PKD2-gene was localized on chromosome 4q21-23 between the markers D4S231 and D4S231 and D4S423, an interval of about 8cM. In a collaborative effort to narrow down the PKD2-region, families with recombinants have been analyzed with several markers within the interval. First, an integrated map had to be constructed which contains previously published markers of different sources. To construct this map, cosmids and/or YACs isolated with the markers have been mapped by two-color FISH and were screened with the othermore » markers. Affected recombinants localize the disease between D4S1534 and D4S1544.« less