Abstract
Background
The natural course of native kidneys after renal transplantation (RT) or dialysis in patients with autosomal dominant polycystic kidney disease (ADPKD) remains poorly understood.
Methods
We measured the total volumes of native kidneys and liver in 78 and 68 ADPKD patients, respectively, who had pre-transplant (within 2 years) and at least one post-transplant computed tomography (CT)/magnetic resonance imaging (MRI); in 40 patients with at least two post-transplant but no pre-transplant CT/MRIs; in 9 patients on chronic hemodialysis with at least one CT/MRI before and after beginning dialysis; and in 5 patients who had no image before and more than one image after dialysis. The last imaging was used in patients with multiple studies.
Results
Mean total kidney volume (TKV) ( ± SD) prior to transplantation was 3187 ± 1779 mL in the 78 patients who had imaging before and after transplantation and decreased by 20.2, 28.6, 38.3 and 45.8% after 0.5–1 (mean 0.7), 1–3 (1.8), 3–10 (5.7) and >10 (12.6) years, respectively. In the multivariable analysis, time on dialysis prior to RT and time from baseline to transplantation were negatively associated with reduction in TKV, whereas estimated glomerular filtration rate (eGFR) after transplantation and time from transplantation were positively associated with percent reduction in TKV. In the 40 patients with imaging only after transplantation, TKV decreased by 3.2 ± 16.3% between 7.2 ± 6.0 and 11.2 ± 6.8 years after transplantation (P < 0.001). TKV was 11.2 ± 35.6% higher (P = NS) after a follow-up of 3.4 ± 2.0 years in the 9 patients with imaging before and after initiation of hemodialysis and 3.4 ± 40.2% lower (P = NS) in the 5 patients with imaging between 2.0 ± 2.1 and 3.5 ± 3.6 years after initiation of hemodialysis. In the 68 patients with liver measurements, volume increased by 5.8 ± 17.9% between baseline and follow-up at 3.7 ± 3.8 years after transplantation (P = 0.009).
Conclusions
TKV of native polycystic kidneys decreases substantially after RT. The reduction occurs mainly during the early post-transplantation period and more slowly thereafter.
Keywords: ADPKD, liver volume, renal transplantation, total kidney volume
INTRODUCTION
Nephromegaly in patients with autosomal dominant polycystic kidney disease (ADPKD) predisposes to abdominal discomfort, chronic pain, hematuria, nephrolithiasis and cyst infections [1, 2]. Cyst progression continues in some patients [3, 4] even when the patients start dialysis, but the natural course of polycystic kidneys after dialysis is not well described. Nephromegaly in patients with ADPKD also poses clinical issues following renal transplantation (RT). Clinicians treating symptomatic patients, especially those undergoing RT, must consider whether surgical removal of the native polycystic kidneys is indicated. However, indications and timing of native nephrectomy in patients with ADPKD undergoing RT are controversial and are associated with considerable morbidity and even mortality [5–7]. Decision-making is more difficult because the natural course of native polycystic kidneys and liver after RT is not well known. Very few studies have examined this question [8–10]. This study was designed to determine the natural course of native polycystic kidneys and liver after RT and to identify factors associated with volume changes of these organs.
MATERIALS AND METHODS
Study design
This is a retrospective analysis to determine the volume change of native polycystic kidneys and the liver after RT using a review of medical records and clinical imaging studies. Eligible patients had received a diagnosis of ADPKD [2, 11]. The study was approved by the Mayo Clinic Institutional Review Board.
Study participants
The Mayo Clinic Translational PKD Center (MTPC) clinical imaging database was used to identify patients meeting the diagnosis of ADPKD and availability of at least two abdominal computed tomography (CT) or magnetic resonance imaging (MRI) scans with complete coverage of both the kidneys and the liver. Patients who had at least two imaging studies were divided into four groups: those who (i) had pre-transplant and at least one post-transplant renal imaging, (ii) had at least two post-transplant but no pre-transplant imaging, (iii) had pre-dialysis and at least one post-dialysis imaging and (iv) had at least two post-initiation of dialysis but no pre-dialysis imaging. Patients who underwent pre- or concurrent transplant (or pre-dialysis) unilateral/bilateral nephrectomy (n = 74), who had major cyst or renal hemorrhage or a renal cyst infection or abscess (n = 1), who had <15 mL/min of estimated glomerular filtration rate (eGFR) at the time of last imaging (n = 3) and who underwent second RT (n = 9) were excluded. Liver volumes were measured in the group who had pre- and at least one post-transplant liver images. None of these patients had a liver resection or cyst fenestration. Pre-transplant and pre-dialysis images were obtained <24 months before transplantation or initiation of dialysis. Laboratory results within 3 months before and after the date of imaging were collected. Glomerular filtration rate (GFR) was estimated (eGFR) by the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation. A conversion factor was used for serum creatinine values of Mayo Clinic patients obtained before 18 October 2006 when the method to measure serum creatinine was changed to isotope dilution mass spectroscopy traceable [12].
Evaluation of CT and MRI and total kidney volume measurements
All Digital Imaging and Communications files from CT and MRI were retrieved and inspected to confirm complete coverage of both the kidneys and image quality. Total kidney volume (TKV) was evaluated by a single investigator (Y.J.) without knowledge of the subject's end-stage renal disease status [defined by initiation of dialysis or kidney transplant (KT)] and was determined from axial/coronal CT or MRI using Analyze software (Analyze 12.0, Biomedical Imaging Resource, Mayo Clinic, Rochester, MN). The changes in native kidney and liver volumes from baseline (within 2 weeks after transplantation and within 2 years before transplantation) to post-transplant values were determined. We used CT and MRI indistinctly as we have shown a strong correlation between the two methods (R² = 0.9998) with a mean % difference in TKV of 0.29 ± 1.68 [13].
Statistical analyses
Multivariate analysis was used to identify factors associated with changes in TKV. We included the first and the last imaging in patients with multiple follow-up studies in the multivariate analysis and to identify the slope of volume change of each group. The analysis of variance was used. The t-test was used to confirm the significance of differences between baseline and post-transplant values. Data are presented as means ± SD. All statistical analyses were conducted using SAS software, version 10.0 (SAS Institute, Inc., Cary, NC).
RESULTS
A total of 132 patients were included in the study, 118 recipients of a renal allograft and 14 patients treated with chronic hemodialysis. One hundred and eighteen of 454 patients with ADPKD transplanted at the Mayo Clinic between 1980 and 2013 met the criteria for the study. We measured TKV in 78 ADPKD patients who had pre- and at least one post-transplant renal CT or MRI and in 40 patients who had at least two post-transplant but no pre-transplant CT or MRI. TKV was also measured in nine patients on chronic hemodialysis who had pre- and at least one post-dialysis CT or MRI and in five patients who had no image before and more than one image after dialysis. The flow chart of the study enrollment is provided in Figure 1.
FIGURE 1:
Flow chart of the study enrollment.
Genetic testing had been performed in 42 of 132 patients enrolled in the study who had had genetic testing. Of these, 39 had PKD1 and 3 had PKD2 mutations. Of the 28 patients who had pre- and at least one post-transplant renal CT or MRI, all but one had PKD1 mutations.
Clinical characteristics for the patients with pre- and post-transplant imaging are shown in Table 1. The mean age (±SD) of the patients at baseline was 54.0 ± 10.1 years, and 51.3% were male; 69.2% underwent preemptive transplantation, and mean dialysis duration in the remaining patients was 8.4 ± 22.0 years; 71.8% received a kidney from a living donor, and 28.2% received a kidney from a deceased donor; 80.8, 7.7 and 11.5% of the patients were treated with tacrolimus-, cyclosporine- or sirolimus-based immunosuppressive protocols, respectively.
Table 1.
Demographic characteristics of ADPKD patients with pre- and at least one post-renal transplant renal CT or MRI
| Patient characteristic | Demographic data (n = 78) |
|---|---|
| Male sex, N (%) | 40 (51.3) |
| Age at transplant, mean ± SD range (years) | 54.0 ± 10.1 (23.70–77.73) |
| Preemptive KT (%) | 54 (69.2) |
| Dialysis duration (months) | 8.4 ± 22.0 (0–152) |
| Donor type (living/deceased), N (%) | 56 (71.8)/22 (28.2) |
| Immunosuppressive protocol, N (%) | |
| Induction | |
| Thymoglobulin | 52 (76.4) |
| Basiliximab | 8 (11.8) |
| Alemtuzumab | 8 (11.8) |
| Maintenance | |
| Tacrolimus | 63 (80.8) |
| Cyclosporine A | 6 (7.7) |
| Sirolimus | 9 (11.5) |
The interval between the pre-transplant image and RT was 6.9 ± 6.6 (range 0.6–23.5) months. The eGFR at the time of RT in the preemptive KT recipients was 7.9 ± 3.1 (interquartile range 6.5–9.5) mL/min1.73 m2. TKV prior to transplantation in the 78 patients who had imaging before and after transplantation was 3187 ± 1779 mL and decreased by 20.2, 28.6, 38.3 and 45.8% after 0.5–1 (mean 0.7), 1–3 (1.8), 3–10 (5.7) and >10 (12.6) years, respectively (Table 2, Figures 2A and 3). In the patients with the longest follow-up of 12.6 years, TKV was 2423 ± 1243 mL at baseline and 1348 ± 1097 mL at the time of the latest imaging (Table 2). The reductions in TKV at 1–3 years after transplantation were 31.7 ± 18.4% in the patients with preemptive KTs and 19.5 ± 20.5% in the patients with non-preemptive KTs, both statistically significant (P < 0.05).
Table 2.
TKV and TKV change from baseline in relation time interval from RT in ADPKD patients with pre- and at least one post-transplant renal CT or MRI
| Year time from transplantation (months) | Baseline | 0–6 | 6–12 | 12–36 | 36–120 | >120 |
|---|---|---|---|---|---|---|
| Number of patients | 78 | 14 | 14 | 40 | 31 | 8 |
| Number of images | 78 | 14 | 14 | 51 | 49 | 10 |
| Mean time from RT (months) | ||||||
| Mean | −7.2 | 4.8 | 8.4 | 21.6 | 68.4 | 151.2 |
| SD | 7.2 | 1.2 | 1.2 | 7.2 | 22.8 | 31.2 |
| Median | −4.8 | 4.8 | 8.4 | 21.6 | 62.4 | 141.6 |
| TKV % reduction rate | ||||||
| Mean | 0 | 14.5 | 20.2 | 28.6 | 38.2 | 45.8 |
| SD | 12.2 | 15.8 | 17.4 | 21.1 | 22.3 | |
| Median | 0 | 14.5 | 22.9 | 30.1 | 39.7 | 48.1 |
| TKV (mL) | ||||||
| Mean | 3187 | 3136 | 3266 | 2365 | 1611 | 1347 |
| SD | 1779 | 1871 | 1183 | 1625 | 1122 | 1097 |
| Median | 2789 | 2842 | 3047 | 2008 | 1344 | 964 |
FIGURE 2:
Change in native TKV in relation to time from transplantation and dialysis. (A) Patients who had pre- and at least one post-transplant renal image (n = 78). (B) Patients who had at least two post-transplant but no pre-transplant image (n = 40) C. Patients who had pre- and at least one post-dialysis image (solid line, n = 9) or only two or more post-dialysis images (dash line, n = 5).
FIGURE 3:
Kidney images of ADPKD patients before and after RT. (A) Serial magnetic resonance (MR) images; TKVs were 6517, 4534 and 3539 mL before and at 3 months or 3 years after transplantation, respectively. (B) Serial CT images; TKVs were 1269, 438 and 305 mL before and at 7 or 16 years after transplantation, respectively.
A multivariable model was employed to identify factors associated with changes in TKV including gender, age at transplantation, time on dialysis prior to transplantation, time from transplantation to post-transplant imaging, interval between pre-transplant imaging and transplantation, eGFR and diagnosis of hypertension or diabetes mellitus at last imaging and immunosuppressive program (calcineurin, n = 69, versus mTOR, n = 9, inhibitors). In the multivariable analysis, time on dialysis prior to RT and time from baseline image to transplantation were negatively associated with percent reduction in TKV. Estimated GFRs after transplantation and time from transplantation to last follow-up image were positively associated with percent reduction in TKV (Table 3).
Table 3.
Multivariate model to predict factors associated with change in TKV after RT in ADPKD patients with pre- and at least one post-transplant renal CT or MRI
| Variables | Estimate (95% CI) |
P-value | |
|---|---|---|---|
| Intercept | 41.5 | (28.79–54.15) | 0.002 |
| Sex (reference is male) | 1.24 | (−1.35 to 3.83) | 0.63 |
| Age at transplantation | −0.40 | (−0.61 to −0.19) | 0.07 |
| Hypertension at last imaging | 4.36 | (1.14–7.59) | 0.18 |
| Diabetes mellitus at last imaging | −0.60 | (−3.68 to 2.48) | 0.85 |
| Dialysis duration | −0.28 | (−0.39 to −0.18) | 0.01 |
| Time from transplantation to last imaging | 0.19 | (0.14–0.24) | <0.001 |
| Time interval between pre-transplant imaging and transplantation | −0.71 | (−1.04 to −0.38) | 0.03 |
| eGFRa at last imaging | 0.18 | (0.11–0.25) | 0.02 |
| Immunosuppressive regimen (reference is calcineurin inhibitors) | 2.56 | (−0.76 to 5.89) | 0.44 |
aCreatinine clearance was estimated by the CKD-EPI equation. Unit for eGFRs was mL/min/1.73 m2.
In the 40 patients who only had imaging after transplantation, TKV decreased by 3.2 ± 16.3% (P < 0.001) between 7.2 ± 6.0 and 11.2 ± 6.8 years (Figure 2B), consistent with the continuous reduction in TKV over time noted above.
In the 9 ADPKD patients on maintenance hemodialysis who had pre- and at least one post-dialysis image, TKV was 11.2 ± 35.6% higher after a mean follow-up of 3.4 ± 2.0 years, but this change was not statistically significant (Figure 2C solid line, Figure 4). In the 5 patients who only had imaging after dialysis, TKV decreased by 3.4 ± 40.2% between 2.0 ± 2.1 and 3.5 ± 3.6 years, but this change was not statistically significant (Figure 2C dash line).
FIGURE 4:
Kidney images of ADPKD before and after initiation of dialysis. (A) Serial CT images; TKVs were 4567, 8939 and 8513 mL before and 4 or 6 years after initiation of dialysis, respectively. (B) Serial MR and CT images; TKVs were 3326, 2589 and 2402 mL before and 2 or 4 years after initiation of dialysis, respectively.
Liver volume changes were measured in 68 of the 78 patients who had imaging before and after transplantation. The other 10 patients had MRI images that did not cover the whole liver. Sixty-one of the 68 patients (90%) had polycystic liver disease. Liver volume increased by 5.8 ± 17.9% from 2411 ± 1408 mL at baseline (at −0.5 ± 0.5 year) to 2511 ± 1455 mL after 3.7 ± 3.8 years of follow-up (P = 0.009, Figure 5A). No significant correlation was detected in these patients between the changes in liver volume and TKV. Multivariable analysis showed no factors associated with the change in liver volume applying the same variables used in TKV analysis.
FIGURE 5:
Liver volume changes in ADPKD patients after RT or initiation of dialysis. (A) Patients who had pre- and at least one post-transplant liver images (n = 68). (B) Patients who had images before and after initiation of dialysis (n = 6).
In the six ADPKD patients on maintenance hemodialysis with complete liver coverage, liver volume was 3.0 ± 16.1% higher after a mean follow-up of 3.2 ± 2.2 years, but this change was not statistically significant (Figure 5B).
DISCUSSION
Continuous kidney enlargement in patients with ADPKD is associated with a decline in renal function [14]. After kidney transplantation, the volume of the native polycystic kidneys has been shown to decrease, but there is little information on the time course of and the factors influencing this reduction [8–10]. In our patients, TKV decreased at a relatively fast rate during the first year after transplantation (by 20.2% after 0.7 year) and continued to decrease at a slower rate thereafter (by 38.3% after 5.7 years and by 45.8% after 12.6 years). A small but significant reduction in kidney volume (by 3.2%) was also observed in the patients who only had imaging studies available years (7.2 ± 6.0) after transplantation. Thus, the decrease in TKV occurs at a fast rate during the first year after transplantation and continues at a slower rate thereafter.
It is not clear which factors after transplantation influence the decrease in TKV. In the present analysis, time from baseline to transplantation and time on dialysis prior to RT were negatively associated with the percent reduction in TKV. Time from transplantation to last follow-up image and eGFR after transplantation were positively associated with the percent reduction in TKV. The impact of time from baseline to transplantation and time from transplantation to last follow-up likely reflect uncaptured continued kidney growth prior to transplantation (with seemingly less reduction in TKV after transplantation) and a longer period of time allowing for greater reduction in TKV after transplantation. Possibly, the rate of increase in TKV in patients with ADPKD accelerates after initiation of dialysis due to the added effect of acquired renal cystic disease associated with uremia. This could account for the negative association between time on dialysis prior to RT and the percent reduction in TKV after transplantation. Similarly, the greater reduction in TKV in the patients with better renal function after transplant may be due to more efficient elimination of effects of uremia on proliferation of the tubular epithelium, greater reduction of blood flow to the native kidneys, and progressive fibrosis. Studies measuring renal blood flow using magnetic resonance may better define its role in the reduction of TKV in the future. It is not likely that immunosuppression played a major role in the reduction of TKV since patients with reduced allograft function tend to be more immunosuppressed than those with good allograft function and the administration of cyclosporine (the main immunosuppressive agent in our patients) has been associated with the development of renal cysts [15].
A prior study by Yamamoto et al. showed that the native kidney volume decreased by more than 30% during the first year post-transplantation, with little change thereafter over 4 years [10]. In our study, time from transplantation was associated with a greater reduction in kidney volume, but as in the previous study, the reduction rate was greater during the first year. In two small studies, a reduction in kidney volume was reported in KT patients with ADPKD who were given mTOR inhibitors as immunosuppressive agents [9, 16]. We found no difference in the change of TKV between mammalian target of rapamycin (mTOR) inhibitor and calcineurin inhibitor-treated patients in this study, but the small number of patients treated with rapamycin makes this result inconclusive.
Conflicting results on changes in kidney volume in dialysis patients with ADPKD have been reported in a few studies [4, 8, 17]. One group reported that the majority of hemodialysis patients with ADPKD showed initial rapid reduction in TKV followed by a slow increase in the TKV. TKV in the nine ADPKD patients on maintenance hemodialysis in our study showed a tendency for increasing volume after a short follow-up, 3.4 ± 2.0 years. Among the five patients having at least two post-dialysis but no pre-dialysis imaging, three patients had an increase in TKV, while the other two had a decrease in TKV after 3.5 ± 3.6 years of follow-up. Prospective studies of the changes of polycystic kidneys after dialysis and a comparative study with the kidney volume changes after transplantation will aid in identifying the factors influencing the decrease in the TKV.
One of the most common extrarenal manifestations of ADPKD is hepatic cysts with an overall prevalence of 83% [18]. The natural course of polycystic liver disease is continued cystic growth. The rates of increase in liver volume of placebo-treated patients in clinical trials for polycystic liver disease have been 0.9–1.6% in 6–12 months [19, 20]. The rate of increase in liver volume in patients with ADPKD after RT in two small studies was about 8.6–21.4% in 12–36 months [9, 10]. However, the rate of increase in liver volume was only 5.8% for a mean follow-up of 3.7 ± 3.8 years in this study. No factors including administration of an mTOR inhibitor were associated with change in liver volume.
Decision-making on whether and when native nephrectomy should be performed in patients with ADPKD undergoing RT requires thoughtful consideration of risks and benefits [5–7]. Native nephrectomy in ADPKD is associated with significant morbidity and mortality. Hand-assisted laparoscopic nephrectomy has a lower risk, but is not always feasible [21, 22]. Furthermore, bilateral nephrectomy commits patients to dialysis while recovering from the surgery or awaiting transplant. Therefore, routine nephrectomy prior to transplantation is no longer recommended, and on average, less than one-third of patients in published series undergo pre-transplant nephrectomies [5, 23–25]. Indications include insufficient space for insertion of a kidney graft, intractable pain, recurrent and/or severe infection, recurrent and/or severe bleeding, symptomatic nephrolithiasis and suspicion of renal cancer. The results of our study along with those of the study by Yamamoto et al. [10] indicate that decisions for or against nephrectomy should take into account that native kidney volume declines after transplantation.
The volume of native polycystic kidneys decreases substantially after RT. The reduction rate is relatively fast in the early post-transplantation period but slows considerably thereafter. Shorter duration of dialysis prior to transplantation and higher GFR in the transplanted kidney are associated with greater reduction.
CONFLICT OF INTEREST STATEMENT
None declared.
ACKNOWLEDGEMENTS
This study was supported, in part, by a grant from the National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health (DK090728).
REFERENCES
- 1.Gabow PA. Autosomal dominant polycystic kidney disease. N Engl J Med 1993; 329: 332–342 [DOI] [PubMed] [Google Scholar]
- 2.Torres VE, Harris PC, Pirson Y. Autosomal dominant polycystic kidney disease. Lancet 2007; 369: 1287–1301 [DOI] [PubMed] [Google Scholar]
- 3.Milutinovic J. Massive growth of kidneys in patients with autosomal dominant polycystic kidney disease treated with chronic hemodialysis. Am J Kidney Dis 1989; 14: 365–368 [DOI] [PubMed] [Google Scholar]
- 4.Ishikawa I, Saito Y. Volume changes in autosomal dominant polycystic kidneys after the initiation of hemodialysis. Nephron 1993; 65: 649–650 [DOI] [PubMed] [Google Scholar]
- 5.Fuller TF, Brennan TV, Feng S et al. End stage polycystic kidney disease: indications and timing of native nephrectomy relative to kidney transplantation. J Urol 2005; 174: 2284–2288 [DOI] [PubMed] [Google Scholar]
- 6.Kanaan N, Devuyst O, Pirson Y. Renal transplantation in autosomal dominant polycystic kidney disease. Nat Rev Nephrol 2014; 10: 455–465 [DOI] [PubMed] [Google Scholar]
- 7.Chapman AB, Devuyst O, Eckardt KU et al. Autosomal Dominant Polycystic Kidney Disease (ADPKD): Executive Summary from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney Int 2015; 88: 17–27 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Thaysen JH, Thomsen HS, Sass A et al. Volume changes in polycystic kidneys during chronic dialysis and after renal transplantation. Acta Med Scand 1985; 217: 197–204 [DOI] [PubMed] [Google Scholar]
- 9.Qian Q, Du H, King BF et al. Sirolimus reduces polycystic liver volume in ADPKD patients. J Am Soc Nephrol 2008; 19: 631–638 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10.Yamamoto T, Watarai Y, Kobayashi T et al. Kidney volume changes in patients with autosomal dominant polycystic kidney disease after renal transplantation. Transplantation 2012; 93: 794–798 [DOI] [PubMed] [Google Scholar]
- 11.Pei Y, Obaji J, Dupuis A et al. Unified criteria for ultrasonographic diagnosis of ADPKD. J Am Soc Nephrol 2009; 20: 205–212 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Rule AD, Larson TS. Do we need another equation to estimate GFR from serum creatinine in renal allograft recipients? Nephrol Dial Transplant 2008; 23: 2427–2428; author reply 2428 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13.Irazabal MV, Rangel LJ, Bergstralh EJ et al. Imaging classification of autosomal dominant polycystic kidney disease: a simple model for selecting patients for clinical trials. J Am Soc Nephrol 2015; 26: 160–172 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 14.Grantham JJ, Torres VE, Chapman AB et al. Volume progression in polycystic kidney disease. N Engl J Med 2006; 354: 2122–2130 [DOI] [PubMed] [Google Scholar]
- 15.Calvo-Garcia MA, Campbell KM, O'Hara SM et al. Acquired renal cysts after pediatric liver transplantation: association with cyclosporine and renal dysfunction. Pediatr Transplant 2008; 12: 666–671 [DOI] [PubMed] [Google Scholar]
- 16.Shillingford JM, Murcia NS, Larson CH et al. The mTOR pathway is regulated by polycystin-1, and its inhibition reverses renal cystogenesis in polycystic kidney disease. Proc Natl Acad Sci U S A 2006; 103: 5466–5471 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17.Ishikawa I, Tateishi K, Kitada H et al. Regression of adult type polycystic kidneys during chronic intermittent hemodialysis. Is it a universal phenomenon? Nephron 1984; 36: 147. [DOI] [PubMed] [Google Scholar]
- 18.Bae KT, Zhu F, Chapman AB et al. Magnetic resonance imaging evaluation of hepatic cysts in early autosomal-dominant polycystic kidney disease: the Consortium for Radiologic Imaging Studies of Polycystic Kidney Disease cohort. Clin J Am Soc Nephrol 2006; 1: 64–69 [DOI] [PubMed] [Google Scholar]
- 19.van Keimpema L, Nevens F, Vanslembrouck R et al. Lanreotide reduces the volume of polycystic liver: a randomized, double-blind, placebo-controlled trial. Gastroenterology 2009; 137: 1661–1668 e1–2 [DOI] [PubMed] [Google Scholar]
- 20.Hogan MC, Masyuk TV, Page LJ et al. Randomized clinical trial of long-acting somatostatin for autosomal dominant polycystic kidney and liver disease. J Am Soc Nephrol 2010; 21: 1052–1061 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 21.Verhoest G, Delreux A, Mathieu R et al. Transperitoneal laparoscopic nephrectomy for autosomal dominant polycystic kidney disease. JSLS 2012; 16: 437–442 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 22.Lipke MC, Bargman V, Milgrom M et al. Limitations of laparoscopy for bilateral nephrectomy for autosomal dominant polycystic kidney disease. J Urol 2007; 177: 627–631 [DOI] [PubMed] [Google Scholar]
- 23.Rozanski J, Kozlowska I, Myslak M et al. Pretransplant nephrectomy in patients with autosomal dominant polycystic kidney disease. Transplant Proc 2005; 37: 666–668 [DOI] [PubMed] [Google Scholar]
- 24.Jacquet A, Pallet N, Kessler M et al. Outcomes of renal transplantation in patients with autosomal dominant polycystic kidney disease: a nationwide longitudinal study. Transpl Int 2011; 24: 582–587 [DOI] [PubMed] [Google Scholar]
- 25.Patel P, Horsfield C, Compton F et al. Native nephrectomy in transplant patients with autosomal dominant polycystic kidney disease. Ann R Coll Surg Engl 2011; 93: 391–395 [DOI] [PMC free article] [PubMed] [Google Scholar]