The impact of nephrectomy on liver and contralateral kidney volume in patients with ADPKD; a case series

Abstract

Purpose

A substantial number of patients with autosomal dominant polycystic kidney disease (ADPKD) undergo nephrectomy. A decrease in intra-abdominal pressure after nephrectomy might hypothetically accelerate the growth of other polycystic organs and accelerate the rate of eGFR decline of the remaining kidney. In this case-series, we investigated the change in kidney and liver volume in patients before and after nephrectomy, and in a control group without nephrectomy.

Methods

In this retrospective case series kidney and liver volumes were measured using an automated stereological approach (MRI) or manual tracing (CT). Additionally, change in eGFR was investigated in patients before and after nephrectomy in whom this procedure did not result in an immediate need to start kidney replacement therapy (KRT).

Results

Twelve patients were included in the nephrectomy-KRT group and ten in the KRT-only control group. Kidney volume growth rates before start of KRT were similar between both groups (nephrectomy-KRT: 6.3 [95% CI: 4.0 to 8.4]; KRT-only: 6.7 [3.5 to 9.7] %/year, difference p = 0.8). After start of KRT, kidney volume significantly decreased in both groups (nephrectomy-KRT: −3.7 [−6.3 to −0.7]; KRT-only: −5.2 [−8.9 to −1.3] %/year, difference p = 0.5). The change in liver volume was not statistically different between both groups. In four additional patients in whom nephrectomy did not immediately lead to the start of KRT, the rate of eGFR decline of the remaining kidney did not change after the procedure.

Conclusion

In patients who did and did not undergo nephrectomy at the time they reached the need for KRT, kidney volume seemed to decrease after the procedure. In the two patients who had a nephrectomy of a functional kidney without direct start of KRT, nephrectomy did not seem to lead to accelerated eGFR decline of the remaining kidney. Due to the small sample size of this case series, these results have to be validated preferably in a large prospective multicenter study.

Supplementary Information

The online version contains supplementary material available at https://doi.org/10.1186/s12882-026-05237-w.

Introduction

A substantial number of patients with autosomal dominant polycystic kidney disease (ADPKD) undergo nephrectomy [1, 2]. The primary indication for nephrectomy is lack of space for a kidney allograft due to massive enlargement of the native kidneys [3]. Other indications are recurrent cyst infections, persistent cyst bleeding, refractory pain and volume-related gastrointestinal complaints such as abdominal fulness, early satiety and weight loss [4, 5]. Nephrectomy is most often performed when patients are near the start of kidney replacement treatment (KRT), as the resultant loss of eGFR will expedite the start of KRT, which patients and clinicians want to avoid as much as possible [3]. The specific impact of nephrectomy on this has not been investigated [6]. Based on observations in a patient from our expertise center, we hypothesized that the resultant decrease in intra-abdominal pressure after nephrectomy could lead to accelerated growth of the polycystic liver and contralateral kidney, and consequently an accelerated decrease in kidney function. To investigate this hypothesis, we assessed in a case series the effect of nephrectomy on growth rate of the polycystic liver and contralateral kidney, and on the rate of eGFR decline. Because nephrectomy is often performed around the time patients reach kidney failure for which KRT is started, and that the rate of kidney growth changes after having reached kidney failure, we sought a control group of patients with ADPKD in whom KRT was initiated but nephrectomy was not performed and in whom serial imaging was available before as well as after start of KRT.

Materials and methods

Study population

In this retrospective case series, we investigated all patients seen between 2013 and 2025 in our ADPKD expertise center at the University Medical Center Groningen who had given informed consent for the use of their patient data (n = 494) (Fig. 1). Of these patients, 43 had undergone nephrectomy and 451 had not. For the analysis of the effect of nephrectomy on kidney and liver growth, we included patients who had undergone nephrectomy and had sufficient imaging (CT or MRI) to calculate growth before as well as after nephrectomy (n = 16). Sufficient imaging to calculate growth rate was defined as ≥ 2 scans minimally six months before and after nephrectomy (or ≥ 1 scan before and after when an additional scan was within one month of nephrectomy). Because it is known that TKV can decrease after kidney failure with start of KRT [7–10], the included patients were divided into a group who had undergone nephrectomy close to (<1 year) the start of KRT (nephrectomy-KRT group, n = 12) and a group in whom nephrectomy did not lead to the immediate start of KRT (nephrectomy-only, n = 4). In the nephrectomy-only group, we also assessed the changes in kidney function decline before and after nephrectomy. Patients in the nephrectomy-KRT group were compared to controls in whom KRT was initiated but who did not undergo nephrectomy and who had serial imaging available to calculate volume growth before and after KRT (KRT-only group, n = 10). Only patients with polycystic livers (>10 liver cysts [11]) and imaging of the liver before and after start of KRT were included in the analysis of changes in liver volume. None of the included patients underwent renal embolization before nephrectomy. The use of these patient data was approved by the Institutional Review Board of the University Medical Center Groningen (METc 2013/040 and RR 202200061).

Fig. 1.

Flowchart of patient inclusion

Data collection

Kidney volume was measured using MRI or CT scans. For MRI scans, T2-weighted coronal images were used to determine kidney volume measurements through an automated stereological approach [12, 13]. For CT scans, volumes were manually calculated by tracing the kidney circumference [14]. A total of 118 MRI and 36 CT scans were analyzed. Twenty-seven percent of subjects only had volume assessment in MRI scans, while 32% had 1 CT scan to supplement the assessments from the MRI scans. All other subjects, similar amounts of CT and MRI measurement or more CT to MRI measurements were used. For accurate growth rate assessment before and after nephrectomy and KRT, similar scan modalities before and after this time point were used. For example, in one patient, two MRI scans before KRT and two CT scans after KRT were used to ensure this. The median time interval between scans in all subjects was 22 months, with a range between 4 and 49 months. In the nephrectomy-KRT group, the median time interval before KRT was 14 months (range: 3–66) and in KRT-only group the time interval was 16 months (3–43). After KRT the median time interval was 14 months (range 7–64) and 19 months (range: 14–26) in the nephrectomy-KRT and KRT-only groups, respectively. Of the included subjects, eGFR data were used that were obtained in the framework of routine clinical care, with measurement of creatinine and other laboratory parameters being measured using standard laboratory techniques. All study data were collected and managed using Research Electronic Data CAPture [15].

Statistical analysis

Baseline characteristics of included subjects were determined at the start of KRT or at the time of nephrectomy, whichever came first. The primary endpoint was the annual change in volume of the contralateral kidney in patients with or without nephrectomy. The secondary endpoint was change in liver volume. Both were analyzed with a linear mixed effects model, using the first available volume and an interaction term with group (nephrectomy-KRT/KRT-only) and time in years with a spline at start of KRT as fixed effects. Intercept and slope were allowed to vary randomly, with an unstructured covariance matrix. Estimates were described with 95% confidence interval. Categorical variables were tested via the Chi-squared test. All continuous variables non-normally distributed and were, therefore, described as median [interquartile range (IQR)] and tested by a Kruskal-Wallis rank sum test. A two-sided p-value < 0.05 was considered statistically significant. For linear mixed effect modeling, non-normally distributed continuous variables were logarithmically transformed and back transformed for interpretation. The change in kidney and liver growth rate as well as kidney function of patients in whom KRT was not initiated after nephrectomy were described separately. In these patients, kidney function decline was calculated using linear regression. All statistical analyses and data visualization were performed using R version 4.3.2 (Vienna, Austria).

Results

Study population

A total of 26 patients were included, of whom 12 were in the nephrectomy-KRT group, 10 in the KRT-only control group and 4 in the nephrectomy-only group. Patients in the nephrectomy-KRT group were younger compared to the KRT-only group (45 [40 - 50] vs. 56 [52 - 60] years, p = 0.01), while there was no difference in sex distribution between the groups (female: 43.3 vs. 40.0%, p = 0.9) (Table 1). Patients in the nephrectomy-KRT group had larger kidneys compared to those in the KRT-only group (TKV: 4799 [3629 – 7736] vs. 3002 [1953 – 4628] mL, p = 0.02), while there was no significant difference in liver volume although liver volume tended to be greater in the nephrectomy-KRT group (4197 [2335 – 5259] vs. 1884 [1659 – 4986] mL, p = 0.1). The type of KRT on which patients started in the nephrectomy-KRT group was more often hemodialysis (75.0%) compared to the KRT-only group (30.0%, p = 0.1). Conversely, kidney transplantation was more often the first KRT in the KRT-only group (40.0%, p = 0.7), while the other patients in this group started with peritoneal dialysis (30.0%). Almost all patients in whom transplantation was not the first KRT later underwent kidney transplantation (nephrectomy-KRT: n = 12, KRT-only: n = 8). Standard immunosuppressive therapy after kidney transplantation in our population was triple therapy with prednisolone, tacrolimus and mycophenolate mofetil (n = 17). Other immunosuppressive agents used in a triple therapy regimen were ciclosporin (n = 1) and everolimus (n = 3). In the nephrectomy-KRT group, the indication for nephrectomy was most often chronic intractable pain (58.3%), gastrointestinal complaints (50.0%) and lack of space for a kidney allograft (33.3%), with some patients having more than one reason to perform a nephrectomy. Most procedures were performed just before the start of KRT (n = 8, 66.7%), while four patients had just started KRT at the time of nephrectomy.

Table 1.

Patient characteristics at the time of nephrectomy or start of KRT, whichever occurred first

	Nephrectomy-KRT (n = 12)	KRT-only (n = 10)	Nephrectomy-only (n = 4)	p-value*
Age, yrs	45 [40–50]	56 [52–60]	49 [46–61]	0.01
Sex (Female), n (%)	4 (33.3)	4 (40.0)	3 (75.0)	0.9
Height, cm	183 [176–186]	185 [180–186]	169 [168–171]	0.8
Weight, kg	88 [81–100]	86 [81–91]	78 [68–87]	0.6
BMI, kg/m2	27 [25–28]	26 [24–27]	26 [24–28]	0.5
Presence of liver cysts (>10), n (%)	11 (91.7)	7 (70.0)	4 (100)	0.4
Total kidney volume, mL	4799 [3629–7736]	3002 [1953–4628]	4100 [1874–8659]	0.02
Liver volume, mL	4197 [2335–5259]	1884 [1659–4986]	2813 [2430–6208]	0.1
eGFR, mL/min/1.73 m2	9 [7–15]	10 [9–13]	43 [34–46]	0.9
PKD mutation, n (%)				0.1
PKD1 truncating	2 (16.7)	5 (50.0)	1 (25.0)
PKD1 non-truncating	4 (33.3)	3 (30.0)	-
PKD2	-	1 (10.0)	-
Mutation not determined	6 (50.0)	1 (10.0)	3 (75.0)
First type of KRT, n (%)
Kidney transplantation	3 (25.0)	4 (40.0)	1 (25.0)	0.8
Hemodialysis	9 (75.0)	3 (30.0)	2 (50.0)	0.1
Peritoneal dialysis	-	3 (30.0)	-	0.2
KRT not reached	-	-	1 (25.0)	-
Indications for nephrectomy, n (%)§
Pain complaints	7 (58.3)	-	3 (75.0)	-
Gastro-intestinal complaints	6 (50.0)	-	2 (50.0)	-
Lack of space for a kidney allograft	4 (33.3)	-	-	-
Recurrent/severe cyst infection	1 (8.3)	-	1 (25.0)	-
Recurrent/persistent cyst hemorrhage	2 (16.7)	-	-	-
Timing of nephrectomy
- Before KRT, n (%)	8 (66.7)	-	3 (100)**	-
Time between nephrectomy and start of KRT, months	0 [0–3]	-	31 (23–40)	-
- After start KRT, n (%)	4 (33.3)	-	-	-
Time between start of KRT and nephrectomy, months	6 [5–12]	-	-	-

§procedures could have one or more indications. *, Patient characteristics were compared between the nephrectomy-KRT and KRT-only groups. **, One patient had not reached KRT. Abbreviations: BMI, body mass index; KRT, kidney replacement therapy

Changes in kidney volume before and after nephrectomy close to reaching kidney failure

The median follow-up time and number of scans before nephrectomy and KRT were 6.5 [4.1–7.6] years and 5.0 [3.0–5.0], while after nephrectomy and start of KRT these values were 3.6 [1.7–5.1] years and 2.0 [2.0–2.0], respectively. In these patients, kidney volume increased by 5.8 [3.3 to 8.2] %/year before nephrectomy and KRT, after which it seemed to decrease with −2.8 [−5.7 to 0.3] %/year (p = 1.6 × 10⁻⁶) (Table 2, Fig. 2A). In the KRT-only group, the median follow-up before KRT was 6.2 [3.4–7.0] years (difference between group: p = 0.7), with a median number of scans of 4.0 [3.0–4.0] (difference between groups: p = 0.5). After KRT, the median follow-up time and number of scans were 3.4 [2.1–4.2] years (difference between groups: p = 0.8) and 1.0 [1.0–2.0] (difference between groups: 0.4). Patients who started with KRT without concomitant nephrectomy had an increase in kidney volume of 6.6 [3.4 to 9.6] %/year before start of KRT, which was not statistically different from the nephrectomy-KRT group difference p = 0.7). After start of KRT, kidney volume also decreased in this group (−5.1 [−8.8 to −1.2] %/year, p = 7.4 × 10⁻⁶), which was not statistically significantly different from the rate of TKV decrease in the nephrectomy-KRT group after start of KRT (difference between groups: p = 0.4). Individual changes in kidney volume are depicted in Supplemental Fig. 1A.

Table 2.

Changes in kidney and liver volume before and after nephrectomy and the start of kidney replacement therapy

Periods	Change in kidney volume, %/year		p-value
	Nephrectomy-KRT (n = 12)	KRT-only (n = 10)
Before kidney replacement therapy	5.8 [3.3 to 8.2]	6.6 [3.4 to 9.6]	0.7
After start of kidney replacement therapy	−2.8 [−5.7 to 0.3]	−5.1 [−8.8 to −1.2]	0.4
p-value	1.6 × 10−6	7.4 × 10−6

	Change in liver volume, %/year		p-value
	Nephrectomy-KRT (n = 10)	KRT-only (n = 4)
Before kidney replacement therapy	4.3 [2.7 to 5.8]	0.7 [−2.5 to 4.1]	0.1
After start of kidney replacement therapy	2.4 [0.7 to 4.2]	−1.2 [−5.6 to 3.4]	0.2
p-value	0.1	0.6

Abbreviations: KRT, kidney replacement therapy

Fig. 2.

Changes in kidney and liver volume before and after start of kidney replacement treatment. The time of start of KRT is depicted as 0 on the x-axis. Volume is depicted on the y-axis using a logarithmic scale. The blue line depicts the group in whom nephrectomy was performed just before start of KRT and the red line depicts the group without a nephrectomy. Kidney volume in the nephrectomy-KRT group is that of contralateral kidney before as well as after nephrectomy and in the KRT-only group it is the average of both native kidneys. A: changes in kidney volume. B: changes in liver volume

Changes in liver volume before KRT and after KRT

Changes in polycystic liver volume could be assessed in 10 patients of the nephrectomy-KRT group and in 4 patients of the KRT-only group. Other patients in these groups did not have polycystic livers. In the nephrectomy-KRT patients, the median follow-up before nephrectomy and start of KRT was 5.2 [3.2–7.2] years (median number of scans with measured liver volume: 3.0 [3.0–4.0]), whereas after nephrectomy and start of KRT it was 3.6 [1.6–6.0] years and 2.0 [1.0–2.0] scans. Before nephrectomy and start of KRT, liver volume increased with 4.3 [2.7 to 5.8] %/years and seemed to keep growing after nephrectomy and start of KRT (2.4 [0.7 to 4.2], p = 0.1) %/year (Table 2, Fig. 2B). In the KRT-only group, median follow-up before KRT was 5.3 [4.2–6.1] years, with a median number of scans of 4.0 [3.0–4.0] (differences between groups: p = 0.9 and p = 0.5, respectively). After KRT, the median follow-up was 3.5 [2.6–4.1] years, with a median of 1.0 [1.0–2.0] scan (differences between groups: p = 0.9 and p = 0.3, respectively). In the KRT-only group, liver volume seemed to remain stable before KRT (0.7 [−2.5 to 4.1] %/year, difference between groups: p = 0.1) as well as during KRT (−1.2 [−5.6 to 3.4], p = 0.6, difference between groups: p = 0.2). Individual liver volume trajectories are depicted in Supplemental Fig. 1B.

Changes in kidney volume and kidney function after nephrectomy in patients not starting KRT

Four patients retained sufficient kidney function after nephrectomy to avoid immediate initiation of KRT). Patient characteristics are given in Table 1. Importantly, two out of these four patients had a non-functioning polycystic kidney that was removed, as shown preoperatively by MAG3 renography. All four had sufficient eGFR measurements and imaging available for analysis. In the four patients analyzed for change in kidney function, eGFR decline before nephrectomy was −11.3, −5.0, −8.4 and −4.8 mL/min/1.73 m²/year (Fig. 3A). After nephrectomy, two patients who had a functioning polycystic kidney removed had a drop in eGFR of around half their pre-procedure kidney function (from 41 to 20 and from 51 to 29 mL/min/1.73 m², respectively), while the two who had a non-functioning polycystic kidney removed had virtually no drop in eGFR (from 44 to 42, and from 15 to 14 ml/min/1.73 m², respectively). After the nephrectomy, eGFR slope of the remaining kidney was not accelerated in each of these four patients with values of −3.9, −1.9, −6.3 and −4.4 mL/min/1.73 m²/year, respectively (with the latter two being the patients who had a non-functioning polycystic kidney removed). In these patients, kidney growth rate of the contralateral kidney was 14.1, 4.5, 7.3 and 8.9%/year before, and 18.9, 19.4, 10.4 and 21.6%/year after nephrectomy, respectively. Liver growth could not be analyzed in one patient because the liver was not fully depicted on the scans that were performed. Liver growth in the other patients showed an increase in two (from 5.2 to 15.9 and 0.9 to 3.3%/year pre- versus post-nephrectomy) and a slight decrease in the other (from 1.9 to 0.6%/year pre- versus post-nephrectomy).

Fig. 3.

Changes in single kidney volume and kidney function decline after nephrectomy not resulting in kidney failure. A: changes in kidney function decline. The dashed lines are the kidney function decline before nephrectomy extrapolated to after nephrectomy. B: changes in kidney volume. The colored dotted lines represent the start of KRT per patient. Volume is depicted on the y-axis using a logarithmic scale

Sensitivity analyses

As a sensitivity analysis, we analyzed kidney growth rates per KRT modality. Because the above-mentioned analyses showed that the nephrectomy-KRT and KRT-only groups showed a comparable pattern in changes in kidney volume, these groups were combined for this analysis (Supplemental Table 1). Patients who underwent kidney transplantation within a year of start KRT were placed in the transplantation group (n = 12). Patients with a kidney transplantation as well as those starting with hemodialysis (n = 7) had an increase in TKV before the start of KRT that was not significantly different (4.2 [1.9 to 6.3] %/year, and 8.2 [4.9 to 11.7] %/year, respectively, p = 0.2) and a not significantly different decrease in TKV thereafter (−3.3 [−5.8 to −0.2] %/year, and −6.3 [−9.9 to −2.7] %/year, respectively, p = 0.2). In patients on peritoneal dialysis (n = 3), kidney volume increased before KRT (9.0 [4.7 to 13.1] %/year) but did not significantly decrease after KRT was initiated (3.5 [−5.5 to 13.8] %/year, p = 0.4). As an additional sensitivity analysis, we compared the growth rate between the right and left kidney in the KRT-only group. This analysis showed an overall similar growth rate between the separate kidneys before KRT (7.4 (CI: 3.5–11.1) years vs. 6.0 (2.6–9.1) years) as well as after KRT (−3.9 (−7.6–0.2) years vs −5.7 (−8.9 - −2.1) years.

Discussion

In this case series describing data of 26 patients with ADPKD, we found no effect of nephrectomy close to the start of KRT on the change in kidney volume compared to controls who started KRT without nephrectomy. Furthermore, the rate of liver growth in patients with polycystic livers seemed not different between patients who had a nephrectomy versus those who did not have nephrectomy. In patients who did not start KRT immediately after nephrectomy, the rate of kidney function decline of the remaining kidney was not different before versus post-nephrectomy.

We primarily analyzed the effect of nephrectomy on polycystic liver and contralateral kidney volume. To our knowledge, this has not been investigated in detail and with a long follow-up before. In a Japanese study, 5 of the 33 included patients with ADPKD underwent nephrectomy, with conflicting findings regarding change in kidney volume (−60 to 3%/year) [9]. An Italian study by Veroux et al. found a decrease in kidney volume of −15% 12 months after combined unilateral nephrectomy and kidney transplantation, but this reduction was not statistically significant due to a broad range in kidney volume growth [16]. Our study, with a longer follow-up before and after nephrectomy, showed that overall kidney volume significantly decreased after having reached kidney failure and start KRT in patients with as well as without nephrectomy.

Several studies have already reported that kidney volume reduces after reaching kidney failure and start of KRT [8–10]. However, the rate of decrease ranges widely in these studies from −4.6%/year to −14.6%/year with a follow-up time from 3 to 10 years. In these patients the total reduction in kidney volume after start of KRT was −40.6 to −58.4%. On the other hand, a Japanese study found that kidney volume only dropped by approximately −5% in 95 patients on dialysis with a median follow-up time of 6 years [7]. In all these studies, patients with nephrectomies were excluded. In our study, we also observed a decrease in total kidney volume after start of KRT of −3.6%/year for the total study population without difference in patients with or without nephrectomy.

The physiological mechanism behind this decrease in kidney volume after KRT may be caused by a reduction in blood flow through the native kidneys after the start of KRT, resulting in renal atrophy. This mechanism is also described in non-ADPKD kidneys, for example in cases with renal artery stenosis [17]. On the other hand, the use of immunosuppressive medication may play also a role in kidney volume reduction. In non-ADPKD transplant patients, native kidney volume may also decrease after the start of immunosuppressive medication. In transplanted patients with ADPKD, three small-scale studies investigated the effect of the mTOR inhibitor sirolimus on kidney volume. Of these studies, two found a significant reduction in native kidney volume, while the other study found a trend toward reduction [18–20]. However, multiple other RCT’s in patients with ADPKD without a transplantation showed no difference in TKV growth during mTOR inhibition, greatly reducing the likelihood that these agents affect kidney volume [6].

Although kidney volume typically decreases after reaching kidney failure and the initiation of KRT, a small number of patients may still experience kidney volume growth. In the current case series, kidney growth continued only in two patients after reaching kidney failure (both in the KRT-only group). Thus, nephrectomy close to the start of KRT should not be a risk factor for the development of volume-related complaints. Performing routine imaging in patients with ADPKD after nephrectomy and start of KRT seems therefore not needed [9, 16]. A more appropriate strategy would be to monitor development of volume-related complaints by using validated ADPKD-related questionnaires, such as the ADPKD-Pain and Discomfort questionnaire and the Polycystic Liver Disease Questionnaire [21, 22]. Only in case an increase in complaints is observed, imaging may be helpful to objectify any possible increase in kidney and/or liver volume.

We also investigated the effect of reaching kidney failure with start of KRT on liver volume growth and found no effect of nephrectomy. Due to the small number of patients in this analysis, these findings should be interpreted as exploratory. In literature, there is no consensus whether this could affect liver volume growth. Two studies showed in annual increase of 1.6 and 7.1%/year, while another study showed a decrease of 0.7%/year [7–9]. It may be that in female patients, start of menopause around time of kidney failure could influence these findings. The decrease in estrogen concentration after menopause has been found to stop liver volume growth or to lead even to a decrease in liver volume [23].

Among patients who did not reach kidney failure immediately after nephrectomy, a variable increase in kidney growth of the contralateral kidney was observed. However, we did not observe an acceleration in the rate of kidney function decline of the remaining kidney after nephrectomy. These observations in eGFR are in line with the hypothesis that both kidneys contribute equally to a patients’ kidney function as well as to their kidney function decline. Two patients had non-functioning kidney, as determined preoperatively on MAG3 renography. In these patients, nephrectomy caused neither an acute reduction in kidney function nor a significant change in the rate of kidney function decline after surgery (−8.4 to −6.3 and −4.4 to −4.8 mL/min/1.73 m²/year). In two patients who had a functional kidney removed, an immediate decrease in eGFR of approximately half their preoperative kidney function was observed and their total eGFR decline also reduced by around half (−11.3 to −3.9 and −5.0 to −1.9 mL/min/1.73 m²/year). This indicates that the kidney function decline of the remaining kidney, which becomes visible after nephrectomy, did not change after this procedure. Both the findings in the patients in whom a functional and non-functional was removed are, thus, in line with the hypothesis. Nonetheless, it should be emphasized that these findings are observed in only a small number of patients and that therefore validation in a larger cohort of patients with ADPKD is required.

Our report has limitations, the main one being the relatively small study population, as well as the lack of standardized moments of imaging and kidney function measurements. Due to the small study population in the case series, the estimates of growth rates come with an appreciable uncertainty. In addition, some baseline characteristics differed between the study groups, introducing the possibility of selection bias. In our case series, patients in het nephrectomy-KRT group were younger, larger kidney and liver volumes, and had a significantly higher proportion receiving hemodialysis as their initial KRT modality which could indicate more severe disease. This could result in more kidney and liver growth in these patients, although this was not observed when comparing growth rate before KRT. Strengths are the relatively long follow-up of patients who underwent nephrectomy, both before and after this procedure, and the use of linear mixed modeling to increase statistical power.

In this case series, we did not observe that a nephrectomy in patients with ADPKD led to accelerated growth of the contralateral kidney or the liver, nor in an accelerated loss of kidney function. However, due to a relatively small number of patients, validation of our results preferably in a large prospective multicenter study is needed for a definitive conclusion.

Electronic supplementary material

Below is the link to the electronic supplementary material.

Author contributions

Paul Geertsema: Conceptualization, Methodology, Writing and Editing, Data Analysis, Approval; Thomas Bais: Methodology, Writing and Editing, Approval; Benjamin H.J. Doornweerd: Methodology, Writing and Editing, Approval; Maatje van Gastel: Methodology, Writing and Editing, Approval; Esther Meijer: Methodology, Writing and Editing, Approval; Robert A. Pol: Methodology, Writing and Editing, Approval; Ron T. Gansevoort: Conceptualization, Methodology, Funding and Resources, Supervision Approval; Niek F. Casteleijn: Conceptualization, Methodology, Supervision, Approval.

Funding

No funding or financial support was received for this specific study.

Data availability

The data underlying this article will be shared upon reasonable request with the corresponding author.

Declarations

Ethical approval

This study was performed in accordance with the Declaration of Helsinki. Written informed consent was obtained from all patients. The use of these patient data was approved by the Institutional Review Board of the University Medical Center Groningen (METc 2013/040 and RR 202200061).

Competing interests

The authors declare no competing interests.