Home About us Current issue Ahead of Print Back issues Submission Instructions Advertise Contact Login   

Search Article 
  
Advanced search 
 
Saudi Journal of Kidney Diseases and Transplantation
Users online: 1109 Home Bookmark this page Print this page Email this page Small font sizeDefault font size Increase font size 
 

ORIGINAL ARTICLE Table of Contents   
Year : 2006  |  Volume : 17  |  Issue : 4  |  Page : 511-515
Retrospective Analysis of Factors Affecting the Progression of Chronic Renal Failure in Adult Polycystic Kidney Disease


1 Alnoor hospital, Mekka, Saudi Arabia
2 Hera General Hospital, Mekka, Saudi Arabia
3 King Abdulaziz hospital, Mekka, Saudi Arabia

Click here for correspondence address and email
 

   Abstract 

Autosomal dominant polycystic kidney disease (ADPKD) is the commonest congenital cystic renal disease. Factors such as hypertension, urinary tract infection, hematuria, and proteinuria may affect the progression to chronic renal failure in ADPKD patients. Therapeutic interventions, such as the use of angiotensin converting enzyme inhibitors (ACEI) or diet modification, may impact the natural progression of the disease. We aim in this study to review a registry of ADPKD patients in order to compare the slow and fast progressors and identify possible predictors of progression and interventions that slow the progression of this disease. Sheffield Kidney Institute (SKI), one of the largest kidney institutes in Northern Europe, has registered a large number of ADPKD patients since 1981. SKI's computer network contains a wide range of information on these patients. We selected 94 adult polycystic patients from the SKI for retrospective analysis of factors affecting progression to chronic renal failure. Patients who doubled their s. creatinine in 0 36 months were considered fast progressors (FP), while those who doubled their s. creatinine in > 36 months were regarded as slow progressors (SP). There were 70 patients in the FP group and 24 patients in the SP group. A third group of 137 patients consisted of non-progressors (NP) who had stable s. creatinine levels during the same period. We found that the incidence of hypertension, UTI, macroscopic and microscopic hematuria, and overt proteinuria in the FP group was higher than in the SP and NP groups. Modification of some factors, such as hypertension and UTI, may decrease the rate of the deterioration of renal function.

Keywords: Adult, Polycystic, Kidney, Disease, Hypertension, Hematuria, Proteinuria, Urinary, Infection.

How to cite this article:
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;17:511-5

How to cite this URL:
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 [serial online] 2006 [cited 2021 Jul 25];17:511-5. Available from: https://www.sjkdt.org/text.asp?2006/17/4/511/32488

   Introduction Top


Autosomal dominant polycystic kidney disease (ADPKD) is the commonest congenital cystic renal disease. However, its pathogenesis and progression to chronic renal failure are not clearly understood. Factors such as hyper­tension, urinary tract infection, hematuria, and proteinuria may affect the progression to chronic renal failure in ADPKD patients. [1],[9]

Therapeutic interventions, such as the use of angiotensin converting enzyme inhibitors (ACEI) or diet modification, may impact the natural course of progression of the disease. 10],[11],[12],[13],[14]

We aim in this study to review a registry of ADPKD patients in order to compare the slow and fast progressors and identify possible predictors of progression and interventions to slow down the progression of this disease.


   Materials and Methods Top


Sheffield Kidney Institute (SKI), one of the largest kidney institutes in Northern Europe, has registered a large number of ADPKD patients since 1981. SKI is a computer network that contains a wide range of information on these patients. 94 adult polycystic patients were selected from the SKI for retrospective analysis of factors affecting progression to chronic renal failure. Patients who doubled their s. creatinine in < 36 months were consi­dered fast progressors (FP), while those who doubled the s. creatinine in over 36 months were regarded as slow progressors (SP). A third group consisted of non progressors (NP) whose renal function remained stable during the study period. There were 70 patients in the FP group, 24 patients in the SP group, and 137 patients in NP group.

The effects of gender, documented active and recurrent urinary tract infection (UTI), gross and microscopic hematuria, >300mg/ 24hrs or 2+ proteinuria, hypertension (defined as systolic values of ≥ 160 mmHg and a diastolic values ≥ 90mmHg during the time of progression prior to any replacement therapy), and use of angiotensin converting enzyme inhibitors on progression in the study groups were analyzed.

The mean systolic and mean diastolic pre­ssures were calculated for each patient from at least three readings before therapeutic intervention. The duration of hypertension prior to any replacement therapy was also calculated. In order to evaluate the severity of the hypertension, the number of drugs used to control hypertension was also com­pared among the study groups.


   Statistical Analysis Top


We compared the groups by using non­parametric tests. The significance of the differ­ences of the continuous variables (i.e. blood pressure) between the study groups was tested by the Wilcoxon Ranksum test. The significance of discontinuous variables (UTI, hematuria, and drugs) among the study groups were estimated by the Chi-squared test. The P value was set as significant if P< 0.05.


   Results Top


[Table - 1] shows the characteristics and risk factors of progression in the different study groups. There was no significant difference in the gender composition among the study groups. A total of 29 patients in the progressors group had UTIs, mostly in the FP group; 11 patients had recurrent UTIs. The prevalence of UTI in the NP group was 18 patients (13.1%). There was a significant statistical difference in the prevalence of UTI between the FP and NP groups (p value <0.01). The prevalence of proteinuria was 5.7% and 4.1% in the fast and slow progressors, respectively. In the NP group, the incidence of proteinuria was 2.9%. None of these patients had protein­uria of more than 1 g/24h. Because of this very small number, statistical tests were not performed. The prevalence of microscopic hematuria was 25.7%, 29%, and 8.7% in the FP, SP, and NP groups, respectively. On the other hand, the incidence of macroscopic hematuria in the FP group was 7.1%. This was higher than in the SP and NP groups, where the prevalence of macroscopic hema­turia was 4.1% and 1.5%, respectively. However, a statistically significant difference was found between the FP and NP groups (p<0.05). The prevalence of microscopic hematuria was not significantly different between the FP and SP groups but was sig­nificant between both of these and the NP group (p <0.01). The prevalence of recurrent hematuria was higher in the FP group than in the other groups. In the FP and SP groups, 81 out of 94 (86%) patients were hypertensive. the prevalence of hypertension was signifi­cantly lower in the NP group, since only 55 out of 137 (40%) patients were hypertensive, (p <0.001). The mean arterial pressure, mean systolic pressure, and mean diastolic pressure in the FP group were found to be slightly higher than in the SP group, but this was statistically not significant. Furthermore, the difference in duration of hypertension between the FP and SP groups was not significant. The prevalence of drug resistant hypertension (requiring 3 or more antihyper-tensives for satisfactory control of BP) was found to be slightly higher in FP group than in the SP and the NP groups. However, there was no statistically significant difference in the use of multiple antihypertensives or ACEIs bet­ween the FP and SP groups. Because of lack of data, the blood pressure values of non progressors could not be obtained.


   Discussion Top


With the limitations inherent in retrospective analysis, the factors affecting the progression of chronic kidney disease (CKD) in ADPKD were analyzed. We found that the prevalence of UTI, macroscopic and microscopic hema­turia, and overt proteinuria in the FP group was higher than in the SP and NP groups. This suggests an association between these factors and the progression of CKD in ADPKD patients.

An association with the fast progression of CKD in ADPKD patients who had macro­hematuria, especially before the age of 30 years, has been shown by other studies. [15] The same result was obtained for overt proteinuria. [16]

The prevalence of hypertension was signi­ficantly higher in the FP and SP groups than in the NP group. This implies that hyper­tension may be an important factor for the progression of CKD in ADPKD patients. Other investigators also observed the delet­erious effect of hypertension on the progression of CKD when they compared hypertensives with and without any interventions. [17],,[18],[19],[20],[21],[22]

The utilization of ACEIs was not signi­ficantly different between the FP and SP groups. This is largely due to a small number of patients in our study. The observations described in the MDRD study suggested a low benefit of the ACEIs in the prevention of progression of CKD in ADPKD patients. [14]

We found no gender effect on the progression of CKD in ADPKD patients after the GFR falls below 25 ml/min/1.73m 2 . The MDRD study reported the same conclusion on the gender effect on CKD progression. [5]

We conclude that the progression of CKD in ADPKD patients can be affected by several factors, such as hypertension, proteinuria, hematuria, and UTI. These factors may result in the rapid deterioration of renal function and progression towards end-stage renal failure. Modification of some factors, such hypertension and UTI, may decrease the rate of the deterioration of renal function[23].

 
   References Top

1.Churchill DN, Bear JC, Morgan J, Payne RH, Mc Manamon PJ, Gault MH. Prognosis of adult onset polycystic kidney disease re­evaluated. Kidney Int 1984;26:190-3.  Back to cited text no. 1    
2.Gabow PA. Autosomal dominant polycystic kidney disease- more than a renal disease. Am J Kidney Dis 1990;16: 403-13.  Back to cited text no. 2  [PUBMED]  
3.Gabow PA, Johnson AM, Kaehny WD, et al. Factors affecting the progression of renal disease in autosomal-dominant polycystic kidney disease. Kidney Int 1992;41:1311-19.  Back to cited text no. 3  [PUBMED]  
4.Gabow PA, Chapman AB, Johnson AM, et al. Renal structure and hypertension in autosomal dominant polycystic kidney disease. Kidney Int 1990;38:117-80.  Back to cited text no. 4    
5.Gretz N, Zeier M, Geberth S, Strauch M, Ritz E. Is gender a determinant for evolution of renal failure? A study in autosmal domi­nant polycystic kidney disease. American Journal of Kidney Dis 1989;14:178-83.  Back to cited text no. 5    
6.Higashihara E, Aso Y, Shimazaki J, Ito H, Koiso K, Sakai O. Clinical aspects of poly­cystic kidney disease. J Urol 1992;147:329-32.  Back to cited text no. 6  [PUBMED]  
7.Franz KA, Reubi FC. Rate of functional deterioration in polycystic kidney disease. Kidney Int 1983;23:526-9.  Back to cited text no. 7  [PUBMED]  
8.Paarfrey PS, Bear JC, Morgan J, et al. The diagnosis and prognosis of autosomal dominant polycystic kidney disease. N Engl J Med 1990;323:1085-90.  Back to cited text no. 8    
9.Torra R, Badenas C, Darnell A, et al. Linkage, clinical features and prognosis of autosomal dominant polycystic kidney disease types 1 and 2. J Am Soc Nephrol 1996;7:2142-51.  Back to cited text no. 9  [PUBMED]  
10.Simon HB, Thompson GJ. Congenital renal polycystic disease, a clinical and therapeutic study of three hundred sixty-six caases. J Am Med Assoc 1955;159:657-62.  Back to cited text no. 10  [PUBMED]  
11.Campanacci L, Fabris B, Fischetti F, Bardelli M, Vran F, Carretta R. ACE inhibition in renal disease: risks and benefits. Clin Exp Hypertens 1993;15:173-86.  Back to cited text no. 11  [PUBMED]  
12.Maschio G, Alberti D, Janin G, et al. Effect of the angiotensin-converting-enzyme inhibitor benazepril on the progression of chronic renal insufficiency. N Engl J Med 1996;334:939-44.  Back to cited text no. 12  [PUBMED]  [FULLTEXT]
13.Kanno Y, Suzuki H, Okada H, Takenaka T, Saruta T. Calcium channel blockers versus ACE inhibitors as antihypertensives in polycystic kidney disease. QJM 1996;89: 65-70.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]
14.Klahr S, Levey AS, Beck GJ, et al. The effects of dietary protein restriction and blood-pressure control on the progression of chronic renal disease. N Eng J Med 1994;330:877-84.  Back to cited text no. 14    
15.Klahr S, Breyer JA, Beck GJ, et al. Dietary protein restriction, blood pressure control, and the progression of polycystic kidney disease. J Am Soc Nephrol 1995;5:2037-47.  Back to cited text no. 15  [PUBMED]  
16.Gabow PA, Duley I, Johnson AM. Clinical profiles of gross hematuria in autosomal dominant polycystic kidney disease. Am J Kidney Dis 1992;20:140-3.  Back to cited text no. 16  [PUBMED]  
17.Chapman AB, Johnson AM, Gabow PA, Schrier RW. Overt proteinuria and micro­albuminuria in autosomal dominant poly­cystic kidney disease. J Am Soc Nephrol 1994;5(6):1349-54.  Back to cited text no. 17    
18.Alvestrand A, Gutierrez A, Bucht H, Bergstrom J. Reduction of blood pressure retards the progression of chronic renal failure in man. Nephrol Dial Transplant 1988;3:624-31.  Back to cited text no. 18  [PUBMED]  [FULLTEXT]
19.Bell PE, Hossack KF, Gabow PA, Durr JA, Johnson AM, Schrier RW. Hypertension in autosomal dominant polycystic kidney disease. Kidney Int 1988;34:683-90.  Back to cited text no. 19  [PUBMED]  
20.Gabow PA, Chapman AB, Johnson Am, et al. Renal structure and hypertension in autosomal dominant polycysti kidney disease. Kidney Int 1990;38:1177-80.  Back to cited text no. 20  [PUBMED]  
21.Gonzalo A, Gallego A, Rivera M, Orte L, Ortuno J. Shape of the relationship between hypertension and the rate of progression of renal failure in autosomal dominant poly­cystic kidney disease. Nephron 1992;62: 52-7.  Back to cited text no. 21  [PUBMED]  
22.Hansson L, Karlander LE, Lundgren W, Peterson LE. Hypertension in polycystic kidney disease. Scand J Urol Nephrol 1974;8:203-5.  Back to cited text no. 22  [PUBMED]  
23.Valvo E, Gammaro L, tessitore N, et al. Hypertension of polycystic kidney disease: mechanisms and hemodynamic alterations. Am J Nephrol 1985;5:176-81.  Back to cited text no. 23  [PUBMED]  

Top
Correspondence Address:
Ebadur Rahman Ahmed
Department of Nephrology, Alnoor Hospital, Mekka
Saudi Arabia
Login to access the Email id


PMID: 17186685

Rights and Permissions



 
 
    Tables

  [Table - 1]

This article has been cited by
1 Chronic asymptomatic pyuria precedes overt urinary tract infection and deterioration of renal function in autosomal dominant polycystic kidney disease
Hwang, J.H. and Park, H.C. and Jeong, J.C. and Ha Baek, S. and Han, M.Y. and Bang, K. and Cho, J.Y. and Yu, S.H. and Yang, J. and Oh, K.-H. and Hwang, Y.-H. and Ahn, C.
BMC Nephrology. 2013; 14(1)
[Pubmed]
2 Chronic kidney disease progression in patients with autosomal dominant polycystic kidney disease [Progresión de la enfermedad renal crónica en pacientes con enfermedad poliquística autosómica dominante]
Panizo, N. and Goicoechea, M. and de Vinuesa, S.G. and Arroyo, D. and Yuste, C. and Rincón, A. and Verdalles, U. and Ruiz-Caro, C. and Quiroga, B. and Luño, J.
Nefrologia. 2012; 32(2): 197-205
[Pubmed]
3 Is autosomal dominant polycystic kidney disease associated with asymptomatic bacterturla? [Czy u chorych z autosomala̧ dominuja̧ca̧ wielotorbielowatościa̧ nerek wystȩpuje bakteriomocz bezobjawowy?]
Pietrzak-Nowacka, N. and Giedrys-Kalemba, S. and Safranow, K. and Szymaniak, L. and Nowosiad, M. and Korzonek, M. and Sulikowski, T. and Ciechanowski, K.
Polski Merkuriusz Lekarski. 2010; 29(171): 173-176
[Pubmed]



 

Top
 
 
    Similar in PUBMED
    Search Pubmed for
    Search in Google Scholar for
  Related articles
    Email Alert *
    Add to My List *
* Registration required (free)  
 


 
    Abstract
    Introduction
    Materials and Me...
    Statistical Analysis
    Results
    Discussion
    References
    Article Tables
 

 Article Access Statistics
    Viewed4700    
    Printed93    
    Emailed0    
    PDF Downloaded533    
    Comments [Add]    
    Cited by others 3    

Recommend this journal