| Abstract|| |
Acquired cystic disease of the Kidney (ACDK) is a well documented complication of end stage renal failure in patients managed conservatively or supported by dialysis. The aim of the present study is to highlight the scope of the problem among our patients, and to evaluate the clinical characteristics of the disease. A Total of 124 patients with chronic renal failure (106 on dialysis, 18 non-dialyzed) were studied with ultrasonography by the same radiologist. ACDK was defined as the presence of four or more cysts in each kidney. The cysts should have sharp smooth wall with acoustic enhancement. In non-dialyzed patients, 5.5% had ACDK, 33.5% had one to three cysts and 61% had no cysts. Among dialysis patients 42.5% had ACDK, 26% had one to three cysts and 31.1% had no cysts. During of dialysis therapy and age were greater in patients with ACDK (74 ± 30 months. 58 ± 3 years respectively) compared to those with no cysts (11 ± 8 months. 26 ± 4 years). The major clinical complications were intracystic hemorrhage in three cases and stones in seven cases. No correlation was noted between the presence of cysts and the original kidney disease, gender, hematocrit or adequacy of dialysis. We conclude that, ACDK occurs commonly in patients with chronic renal failure; however, patients are generally older and have been on dialysis longer than patients without cysts. Ultrasound, in the hands of an experienced radiologist, is a relatively adequate screening tool for ACDK and its complications.
Keywords: Acquired cystic disease, chronic renal failure, Hemodialysis, Jordan
|How to cite this article:|
Ghanaimat M, Juman R, Nimri M, El-Lozi M. Acquired Cystic Disease of Kidney in Chronic Renal Failure in Jordan. Saudi J Kidney Dis Transpl 1998;9:4-7
|How to cite this URL:|
Ghanaimat M, Juman R, Nimri M, El-Lozi M. Acquired Cystic Disease of Kidney in Chronic Renal Failure in Jordan. Saudi J Kidney Dis Transpl [serial online] 1998 [cited 2021 Jul 28];9:4-7. Available from: https://www.sjkdt.org/text.asp?1998/9/1/4/39293
| Introduction|| |
Little attention has been paid to the fate of contracted kidneys in long term hemodialysis patients until 1977, when Dunhill, Millard and Oliver  evaluated necropsy kidney specimens in 30 long-term dialysis patients and found extensive bilateral cystic disease in 14 of them (46.6%). None of the patients had family history or clinical evidence suggestive of congenital renal cystic disease when they were started on dialysis. Complications of this condition noted by the authors included cyst rupture, cyst hemorrhage and the development of solid adenomatous or adenocarcinomatous lesion  .
Since then, the same observations have been confirmed repeatedly throughout the world ,,,, . The present study examines the prevalence, the clinical characteristics and the early detection of complications of acquired cystic disease of kidney (ACDK) in population with chronic renal failure in Jordan.
| Patients and Methods|| |
Between May, 1995 and July 1996, renal ultrasound was performed to evaluate the prevalence of ACDK in 106 patients maintained on intermittent hemodialysis in the renal unit at King Hussein Medical center, Jordan. Patients with known underlying renal cystic disease (autosomal dominant polycystic kidney disease, medullary sponge kidney, medullary cystic kedneys), or those with a family history were excluded.
The clinical characteristics of the dialysis study group are shown in [Table - 1]. Mean age was 42.8 years (range 22-61 years) and mean length of time of dialysis was 32 months (range 3-104 months).
Eighteen patients with advanced chronic renal failure who had never received any form of dialysis therapy were also studied; ten males and eighty females, with a mean age of 39 years (range 18-58 years).
Renal ultrasound was performed by the same radiologist; the number of cysts present in each kidney was recorded. Acquired renal cystic disease was defined as the presence of four or more cysts in each kidney  , ultrasonographic criteria for a firm or presumptive diagnosis of renal cysts were absence of internal echoes, a smooth sharply defined cyst wall, and the presence of acoustic enhancement  .
Clinical variables analyzed were age, sex, serum urea nitrogen, hematocrit, length of time of dialysis and original kidney disease, which was divided into five general categories: glomerular disease, tubulointerstitial disease, diabetes, hypertension, and miscellaneous.
| Statistical Methods|| |
We used chi-square (x 2 ) method to compare between the two discrete variables, dialysis or non-dialysis and between males and females. We considered p value < 0.05 as significant.
| Result|| |
The prevalence of acquired renal cystic disease in the dialysis study group is shown in [Table - 2]. Forty five (42.5%) patients had multiple bilateral cystic changes in the kidneys consistent with ACDK. Twentyeight (26.4%) patients had one to three solitary renal cysts, while 33 (31.1%) patients did not have any cysts.
The prevalence of renal cysts in the 18 nondialysis patients was significantly less than the dialysis group p < 0.05, [Table - 2]. Only one (5.5%) patient had ACDK, six (33.3%) patients had one to three cysts and 11 (61.1!) had no cysts.
Of the total 124 patients with chronic renal failure included in this study, 29 of 73 (39.7%) males had ACDK. Three was no statistically significant difference between both groups.
[Table - 3] demonstrates the clinical variables in dialysis patients. The average age was 58 ± 3 years for those with one to three cysts and 26 ± 4 years for those with no cysts. The average time of dialysis therapy was 74 ± 30 months for the group with ACDK, compared to 26 ± 6 months for those with one to three cysts and 11 ± 8 months for those with no cysts.
There were no significant differences in hematocrit, serum urea nitrogen or underlying primary renal disease in patients with ACDK compared to patients without cysts or those with one to three cysts. Of the 18 patients with advanced chronic renal failure not yet on dialysis, there were no significant differenced in gender, hematocrit, serum urea nitrogen or the primary renal disease in patients with no cysts compared to those with one to three cysts.
| Discussion|| |
The prevalence of ACDK among our dialysis patients was found to be 42.5%, which is comparable to that reported in the literature ,, . Ishikawa, et al  reported that multiple cysts were found in 43.5% of patients on dialysis for less than 3 years, and in 79.3% of patients who had been on dialysis for more than 3 years.
The mean age of our cases was 42.8 years; 25 of 79 (31.6%) patients less than 50 years of age have ACDK. This demonstrates that the incidence of ACDK is higher in older patients.
There are many reports which show male preponderance in the incidence of ACDK and suggested that male hormones had a role in predisposing or accentuating tubular epithelial hyperplasia leading to ACDK formation  . The result of our study show no significant difference in prevalence between males and females.
Most patients with ACDK have persistent symptoms. Acute pain may be a sign of retroperitoneal hemorrhage. A disproportionally high hematorcrit level accompanies the cystic process in some patients and suggests that some of these kidneys produce high amount of erythropoietin. Metastatic carcinoma sometimes may be the first clinical manifestation of renal tumors occurring in ACDK  . In our study, only five patients presented with pain; two with macroscopic hematuria, and three with stones.
Diagosis of ACDK can be established by CT scan and by sonography. Ultrasound is enexpensive, non-invasive, widely available, and in view of many authors , is a satisfactory initial screening technique. However CT scan is more sensitive in detecting small renal tumors and retroperitoneal hemorrhage , .
The pathogenesis of ACDK and renal tumors in long-term dialysis patients is unclear. Histologically, the cysts are derived from proximal tubular epithelium that retains secretory function and renotrophic growth factors have been proposed to promote cystic changes  . The lack of progression of cystic changes in transplanted patients with some patients showing regression  suggests that proliferating factors may only be present in uremic patients.
The consequences of cystic transformation are clinically very important, intracystic hemorrhage can occur due to rupture of unsupported sclerotic vessels that project into cysts. Hemoprinization and prolonged bleeding times in uremia may further contribure to the incidence and severity of hemorrhage. Subcapsular and perinephric hemorrhage have also been described , .
In our study three of 46 (6.5%) patients with ACDK had intracystic hemorrhage. Acquired renal cysts were also commonly the site of calcium oxalate deposition and can provide a nidus for formation of stones because of stagnation of fluid  , in our study seven of 46 (15.2%) patients had stones.
Incidence of single or multiple renal tumors in patients with ACDK is variable, Dunhill et al reported six of 14 (43%) patients with ACDK had tumors and one case had multiple metastasis  . Grantham et al  reported an incidence of 16.4%. however, Mickisch et al  in their rather large series of patients reported an incidence of less than 1%. In our study, none of the patients exhibited renal tumor.
The pathogenesis of renal tumors is unclear presumably they arise from the foci of proliferating tubular epithelial cells in close association with cysts or even within cysts.
In conclusion, acquired renal cystic disease occurs commonly in patients with chronic renal failure in Jordan,; more in those supported by dialysis. Patients with ACDK are generally older and have been on dialysis longer than those with no cysts, However, no correlation with gender, adequacy of dialysis, or hemtocrit was found.
| References|| |
|1.||Dunhill MS, Millard PR, Oliver D. Acquired cystic disease of the kidneys: a hazard of long-term intermittent maintenance hemodialysis. J clin Pathol 1977;30:868-77. |
|2.||Moorthy AV, Beirne GJ. Acquired cystic disease of kidney. Lancet 1978;1:663. |
|3.||McMannus JF, Hughson MD, Hennigar GR, Fits CT, Rajapopalan PR, Williams AV. Dialysis enhances renal epithelial prolifereatin. Arch Pathol Lab Med 1980;104:192-5. |
|4.||Ishikawa I, Saito Y, Onouchi Z, et al. Deveopment of acquired cystic disease and adenocacinoma of the kidney in glomerulonephritic chronic hemodialysis patients. Clin Nephrritic chronic hemodialysis patients. Cli Nephrol 1980;14:1-6. |
|5.||Feiner HD, Katz LA, Gallo GR. Acquired cystic disease of kidney in chronic dialysis patient. Urology 1981;17:260-4. [PUBMED] |
|6.||Sarasin FP, Wong JB, Levey AS, Meyer KB. Screening for acquired cystic kidney disease: a decision analytic perspective. Kidney Int 1995;48:207-19. [PUBMED] |
|7.||Narasimhan N, Golper TA, Wolfson M, Rahatzad M, Bennett WM. Clinical characteristics and diagnostic considerations in acquired renal cystic disease. Kidney Int 1986;30:748-52. [PUBMED] |
|8.||McClennan BL, Stanley RJ, Melson GL, Levitt RG, Sagel SS. CT of the renal cyst is cyst aspiration necessary? AM J Roentgenol 1979;133:671-5. |
|9.||MacDougall ML, Wiegmann TB. Incidental discovery of renal adenocarcinoma in hemodialysis patients. Am J Kidney Dis 1984;4:15(abstract). |
|10.||Kutcher R, Amodio JB, Rosenblatt R. Uremic renal cystic disease: value of sonographic screening. Radiology 1983;147:833-5. [PUBMED] [FULLTEXT]|
|11.||Jenkins DA, Temple RM, Winney RJ, Allan PL, Notgi A, Wild SR. Effect of treatment mode on the natural history of acquired cystic disease of the kidney in patients on renal replacement therapy. Nephrol Dial Transplant 1992;7:613-7. [PUBMED] [FULLTEXT]|
|12.||Grantham JJ, Levine E. acquired cystic disease: replacing one kidney disease woth another. Kidney Int 1985;28:99-105. [PUBMED] |
|13.||Taylor AJ, Cohen EP, Erickson SJ, Olson DL, Foley WD. Renal imaging in long term dialysis patients; a comparison of CT and sonography. Am J Roentgerol 1989;153:765-7. |
|14.||Vaziri ND, Darwish R, Martin DC, Hostetler J. Acquired renal cystic disease in renal transplant recipients. Nephron 1984;37:203-5. [PUBMED] |
|15.||Nishi T, bond C Jr, Brown G, Solez K, Heptinstall RH. A morphometric study of arterial intimal thickening in kidneys of dialyzed patients. Am J Path 1979;95:597-610. [PUBMED] [FULLTEXT]|
|16.||Bommer J, Waldherr R, van Kaick G, Strauss L, Ritz E. Acquired renal cysts in uemic patients-in vivo demonstration by computed tomography. Clin Nephrol 1980;14:299-303. [PUBMED] |
|17.||Mickisch O, Bommer J, Bachmann S, Waldherr R, Mann JF, Ritz E. Multicystic transformation of kidneys in chronic renal failure. Nephron 1984;38:93-9. [PUBMED] |
King Hussein Medical Center, P.O. Box 540708, Abu-Nusair, Amman
[Table - 1], [Table - 2], [Table - 3]