期刊论文详细信息
BMC Nephrology
Chronic asymptomatic pyuria precedes overt urinary tract infection and deterioration of renal function in autosomal dominant polycystic kidney disease
Curie Ahn3  Young-Hwan Hwang6  Kook-Hwan Oh2  Jaeseok Yang3  Suk Hee Yu4  Jeong Yeon Cho1  Kitae Bang7  Mi Yeun Han2  Seon ha Baek2  Jong Cheol Jeong2  Hayne Cho Park5  Jin Ho Hwang2 
[1] Department of Radiology, Seoul National University Hospital, Seoul, South Korea;Department of Internal Medicine, Seoul National University Hospital, 101 Daehak-no, Jongno-gu, Seoul, 110-744, South Korea;Transplantation Center, Seoul National University Hospital, Seoul, South Korea;Department of Internal Medicine, Chung-Ang University Hospital, Seoul, South Korea;Research Center for Rare Diseases, Seoul National University Hospital, Seoul, South Korea;Department of Internal Medicine, Eulji General Hospital, Seoul, South Korea;Department of Internal Medicine, Daejeon Eulji University Hospital, Daejeon, South Korea
关键词: Urinary tract infection;    Pyuria;    Glomerular filtration rate;    Chronic renal failure;    Polycystic kidney disease;   
Others  :  1083037
DOI  :  10.1186/1471-2369-14-1
 received in 2012-06-21, accepted in 2012-12-19,  发布年份 2013
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【 摘 要 】

Background

Urinary tract infection (UTI) occurs in 30%-50% of individuals with autosomal dominant polycystic kidney disease (ADPKD). However, the clinical relevance of asymptomatic pyuria in ADPKD patients remains unknown.

Methods

We retrospectively reviewed medical records of 256 ADPKD patients who registered to the ADPKD clinic at Seoul National University Hospital from Aug 1999 to Aug 2010. We defined the asymptomatic pyuria as more than 5-9 white blood cells in high-power field with no related symptoms or signs of overt UTI. Patients were categorized into 2 groups depending on its duration and frequency: Group A included non-pyuria and transient pyuria patients; Group B included recurrent and persistent pyuria patients. The association between asymptomatic pyuria and both the development of overt UTI and the deterioration of renal function were examined.

Results

With a mean follow-up duration of 65.3 months, 176 (68.8%) out of 256 patients experienced 681 episodes of asymptomatic pyuria and 50 episodes of UTI. The annual incidence of asymptomatic pyuria was 0.492 episodes/patient/year. The patients in group B showed female predominance (58.5% vs. 42.0%, P=0.01) and experienced an upper UTI more frequently (hazard ratio: 4.612, 95% confidence interval: 1.735-12.258; P=0.002, adjusted for gender and hypertension). The annual change in estimated glomerular filtration rate (ΔeGFR) was significantly larger in magnitude in group B than in group A (-2.7±4.56 vs. -1.17±5.8, respectively; P=0.01). Age and Group B found to be the independent variables for ΔeGFR and developing end-stage renal disease (16.0% vs. 4.3%, respectively; P=0.001).

Conclusions

Chronic asymptomatic pyuria may increase the risk of developing overt UTI and may contribute to declining renal function in ADPKD.

【 授权许可】

   
2013 Hwang et al.; licensee BioMed Central Ltd.

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【 参考文献 】
  • [1]Igarashi P, Somlo S: Genetics and pathogenesis of polycystic kidney disease. J Am Soc Nephrol 2002, 13(9):2384-2398.
  • [2]Brenner FCR, Barry M: Brenner & Rector’s The Kidney. 6th edition. Philadelphia, PA: WB Saunders Company; 2000.
  • [3]Fick-Brosnahan GM, Tran ZV, Johnson AM, Strain JD, Gabow PA: Progression of autosomal-dominant polycystic kidney disease in children. Kidney Int 2001, 59(5):1654-1662.
  • [4]Koslowe O, Frank R, Gauthier B, Vergara M, Trachtman H: Urinary tract infections, VUR, and autosomal dominant polycystic kidney disease. Pediatr Nephrol 2003, 18(8):823-825.
  • [5]Sklar AH, Caruana RJ, Lammers JE, Strauser GD: Renal infections in autosomal dominant polycystic kidney disease. Am J Kidney Dis 1987, 10(2):81-88.
  • [6]Schwab SJ, Bander SJ, Klahr S: Renal infection in autosomal dominant polycystic kidney disease. Am J Med 1987, 82(4):714-718.
  • [7]Chow CL, Ong AC: Autosomal dominant polycystic kidney disease. Clin Med 2009, 9(3):278-283.
  • [8]Gabow PA, Johnson AM, Kaehny WD, Kimberling WJ, Lezotte DC, Duley IT, Jones RH: Factors affecting the progression of renal disease in autosomal-dominant polycystic kidney disease. Kidney Int 1992, 41(5):1311-1319.
  • [9]Ahmed ER, Tashkandi MA, Nahrir S, Maulana A: Retrospective analysis of factors affecting the progression of chronic renal failure in adult polycystic kidney disease. Saudi J Kidney Dis Transpl 2006, 17(4):511-515.
  • [10]Idrizi A, Barbullushi M, Petrela E, Kodra S, Koroshi A, Thereska N: The influence of renal manifestations to the progression of autosomal dominant polycystic kidney disease. Hippokratia 2009, 13(3):161-164.
  • [11]Pei Y, Obaji J, Dupuis A, Paterson AD, Magistroni R, Dicks E, Parfrey P, Cramer B, Coto E, Torra R, et al.: Unified criteria for ultrasonographic diagnosis of ADPKD. J Am Soc Nephrol 2009, 20(1):205-212.
  • [12]Ramakrishnan K, Scheid DC: Diagnosis and management of acute pyelonephritis in adults. Am Fam Physician 2005, 71(5):933-942.
  • [13]Sallee M, Rafat C, Zahar JR, Paulmier B, Grunfeld JP, Knebelmann B, Fakhouri F: Cyst infections in patients with autosomal dominant polycystic kidney disease. Clin J Am Soc Nephrol 2009, 4(7):1183-1189.
  • [14]Greg Miller W, Myers GL, Ashwood ER, Killeen AA, Wang E, Thienpont LM, Siekmann L: Creatinine Measurement: State of the Art in Accuracy and Interlaboratory Harmonization. Archives of Pathology & Laboratory Medicine 2005, 129(3):297-304.
  • [15]Levey AS, Stevens LA, Schmid CH, Zhang YL, Castro AF 3rd, Feldman HI, Kusek JW, Eggers P, Van Lente F, Greene T, et al.: A new equation to estimate glomerular filtration rate. Ann Intern Med 2009, 150(9):604-612.
  • [16]Stevens LA, Schmid CH, Greene T, Zhang YL, Beck GJ, Froissart M, Hamm LL, Lewis JB, Mauer M, Navis GJ, et al.: Comparative performance of the CKD Epidemiology Collaboration (CKD-EPI) and the Modification of Diet in Renal Disease (MDRD) Study equations for estimating GFR levels above 60 mL/min/1.73 m2. Am J Kidney Dis 2010, 56(3):486-495.
  • [17]K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification Am J Kidney Dis 2002, 39(2 Suppl 1):1-266.
  • [18]Meadow SR, White RH, Johnston NM: Prevalence of symptomless urinary tract disease in Birmingham schoolchildren. I. Pyuria and bacteriuria. British medical journal 1969, 3(5662):81-84.
  • [19]Ozdem S, Bayraktar T, Oktay C, Sari R, Gultekin M: The prevalence of asymptomatic pyuria in diabetic patients: comparison of the Sysmex UF-100 automated urinalysis analyzer with Fuchs-Rosenthal hemacytometer. Clin Biochem 2006, 39(9):873-878.
  • [20]Reeders ST: Multilocus polycystic disease. Nat Genet 1992, 1(4):235-237.
  • [21]Piontek K, Menezes LF, Garcia-Gonzalez MA, Huso DL, Germino GG: A critical developmental switch defines the kinetics of kidney cyst formation after loss of Pkd1. Nat Med 2007, 13(12):1490-1495.
  • [22]Lantinga-van Leeuwen IS, Leonhard WN, van der Wal A, Breuning MH, de Heer E, Peters DJ: Kidney-specific inactivation of the Pkd1 gene induces rapid cyst formation in developing kidneys and a slow onset of disease in adult mice. Hum Mol Genet 2007, 16(24):3188-3196.
  • [23]Takakura A, Contrino L, Beck AW, Zhou J: Pkd1 inactivation induced in adulthood produces focal cystic disease. J Am Soc Nephrol 2008, 19(12):2351-2363.
  • [24]Grantham JJ: Clinical practice. Autosomal dominant polycystic kidney disease. N Engl J Med 2008, 359(14):1477-1485.
  • [25]Bastos AP, Piontek K, Silva AM, Martini D, Menezes LF, Fonseca JM, Fonseca II, Germino GG, Onuchic LF: Pkd1 haploinsufficiency increases renal damage and induces microcyst formation following ischemia/reperfusion. J Am Soc Nephrol 2009, 20(11):2389-2402.
  • [26]Happe H, Leonhard WN, van der Wal A, van de Water B, Lantinga-van Leeuwen IS, Breuning MH, de Heer E, Peters DJ: Toxic tubular injury in kidneys from Pkd1-deletion mice accelerates cystogenesis accompanied by dysregulated planar cell polarity and canonical Wnt signaling pathways. Hum Mol Genet 2009, 18(14):2532-2542.
  • [27]Takakura A, Contrino L, Zhou X, Bonventre JV, Sun Y, Humphreys BD, Zhou J: Renal injury is a third hit promoting rapid development of adult polycystic kidney disease. Hum Mol Genet 2009, 18(14):2523-2531.
  • [28]Arnaout MA: Molecular genetics and pathogenesis of autosomal dominant polycystic kidney disease. Annu Rev Med 2001, 52:93-123.
  • [29]Weimbs T: Third-hit signaling in renal cyst formation. J Am Soc Nephrol 2011, 22(5):793-795.
  • [30]Gardner KD Jr, Reed WP, Evan AP, Zedalis J, Hylarides MD, Leon AA: Endotoxin provocation of experimental renal cystic disease. Kidney Int 1987, 32(3):329-334.
  • [31]Pirson Y: Does TNF-alpha enhance cystogenesis in ADPKD? Nephrol Dial Transplant 2008, 23(12):3773-3775.
  • [32]Wu L, Tiwari MM, Messer KJ, Holthoff JH, Gokden N, Brock RW, Mayeux PR: Peritubular capillary dysfunction and renal tubular epithelial cell stress following lipopolysaccharide administration in mice. Am J Physiol Renal Physiol 2007, 292(1):F261-F268.
  • [33]Chapman AB, Guay-Woodford LM: Renal volume in children with ADPKD: size matters. Clin J Am Soc Nephrol 2009, 4(4):698-699.
  • [34]Grantham JJ, Torres VE, Chapman AB, Guay-Woodford LM, Bae KT, King BF Jr, Wetzel LH, Baumgarten DA, Kenney PJ, Harris PC, et al.: Volume progression in polycystic kidney disease. N Engl J Med 2006, 354(20):2122-2130.
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