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Carriazo, S.;  Perez-Gomez, M.V.;  Cordido, A.;  García-González, M.A.;  Sanz, A.B.;  Ortiz, A.;  Sanchez-Niño, M.D. Dietary Care for ADPKD Patients. Encyclopedia. Available online: https://encyclopedia.pub/entry/26756 (accessed on 05 December 2025).
Carriazo S,  Perez-Gomez MV,  Cordido A,  García-González MA,  Sanz AB,  Ortiz A, et al. Dietary Care for ADPKD Patients. Encyclopedia. Available at: https://encyclopedia.pub/entry/26756. Accessed December 05, 2025.
Carriazo, Sol, Maria Vanessa Perez-Gomez, Adrian Cordido, Miguel Angel García-González, Ana Belen Sanz, Alberto Ortiz, Maria Dolores Sanchez-Niño. "Dietary Care for ADPKD Patients" Encyclopedia, https://encyclopedia.pub/entry/26756 (accessed December 05, 2025).
Carriazo, S.,  Perez-Gomez, M.V.,  Cordido, A.,  García-González, M.A.,  Sanz, A.B.,  Ortiz, A., & Sanchez-Niño, M.D. (2022, August 31). Dietary Care for ADPKD Patients. In Encyclopedia. https://encyclopedia.pub/entry/26756
Carriazo, Sol, et al. "Dietary Care for ADPKD Patients." Encyclopedia. Web. 31 August, 2022.
Dietary Care for ADPKD Patients
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This entry is adapted from the peer-reviewed paper 10.3390/nu11071576

Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic nephropathy, and tolvaptan is the only therapy available. Recent studies have identified a chronic shift in energy production from mitochondrial oxidative phosphorylation to aerobic glycolysis (Warburg effect) as a contributor to cyst growth, rendering cyst cells exquisitely sensitive to glucose availability. Therefore, low calorie or ketogenic diets have delayed preclinical ADPKD progression.

autosomal dominant polycystic kidney disease diet water ketogenic glycolysis phosphate

1. Background

Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic nephropathy and is a sizable contributor to end-stage kidney disease (ESRD) among those younger than 70-year-old [1][2]. Dietary intervention is a key part of the care of chronic kidney disease (CKD) patients and aims at preventing CKD progression, limiting the negative impact of CKD complications (e.g., hypertension, hyperkalemia, metabolic acidosis), or complications derived from the cause of CKD (e.g., glycemia control in diabetes) while preserving the nutritional status [3].

2. Autosomal Dominant Polycystic Kidney Disease (ADPKD)

ADPKD is an inherited systemic disorder characterized by bilateral renal cysts that destroy normal renal tissue structure, leading to progressive loss of functioning nephrons and ESRD [4]. ADPKD is the fourth most frequent cause of ESRD, after diabetes, hypertension, and glomerular disease [5] and, thus, the most common genetic cause of ESRD [6]. The average prevalence is estimated at around 2.7 to 9.3 per 10,000 [7][8].
According to the Kidney Disease: Improving Global Outcomes (KDIGO 2012) definition of CKD, patients with ADPKD are classified as having CKD even when glomerular filtration rate (GFR) or urinary albumin creatinine ratio (UACR) are normal. Thus, CKD is defined as abnormalities of the kidney structure or function, present for >3 months, with implications for health [9]. A single criterion among the following allows the diagnosis of CKD: GFR < 60 mL/min/1.73 m2 or UACR ≥ 30 mg/g or abnormalities in urine sediment or tubular disorders, or pathologic abnormalities detected by histology or imaging [9][10]. Imaging allows the diagnosis of CKD caused by ADPKD even when all other parameters are normal [10]. Thus, dietary advice for CKD patients applies to all ADPKD patients, unless specified otherwise. Additionally, specific dietary interventions may provide added benefit to ADPKD patients, as discussed below.
ADPKD is characterized by enlarged kidneys in which the normal parenchyma is replaced by multiple cysts [11]. This distorts the physiological corticomedullary osmotic gradient that is required for urine concentration. Thus, urine concentration defects develop very early in the disease course, promoting polyuria, antidiuretic hormone (ADH, arginine-vasopressin, AVP) resistance and a reactive increase in AVP secretion which is best estimated by assessing copeptin, which is co-secreted with AVP but has a longer half-life [12].
ADPKD is caused by mutations in PKD1 (which encodes Polycystin 1) and PKD2 (which encodes Polycystin 2/TRPP2) [13][14], or more rarely, GANAB or DNAJB11 [15][16]. Polycystins are crucial to maintain the phenotype of the tubular epithelium through the function of primary cilia. Defective polycystin function leads to enhanced proliferation and apoptosis, remodeling of epithelial cell membrane, and development of a secretory rather than resorptive phenotype [17]. Some of the altered intracellular signaling pathways resulting from PKD mutations were described years ago. Thus, polycystins regulate intracellular calcium homeostasis and cyclic adenosine monophosphate (cAMP) levels [11][18]. Decreased intracellular calcium and increased cAMP levels promote cell proliferation and fluid secretion, the drivers of cyst growth [18][19][20]. This information led to the development of therapeutic approaches for ADPKD. AVP increases cAMP production in tubular cystic epithelial cells through activation of vasopressin-2 receptors (V2R) [4]. Currently, the V2R blocker tolvaptan is the only approved drug for ADPKD, following the demonstration in placebo-controlled clinical trials of a protective effect against renal cyst growth, as assessed by the total kidney volume (TKV) and against the progressive loss of GFR [21]. Since AVP is secreted in response to dehydration, an increased water intake has been advocated in ADPKD patients, based on the demonstrated role of AVP in ADPKD progression and on positive experiences in experimental PKD. Additionally, somatostatin decreases cAMP production and somatostatin agonists have also been tested clinically, although with less success than tolvaptan [22][23], potentially because of the downregulation of receptors associated with cyst growth [24].

3. Diet in CKD

Dietary modifications play an important role in patients with non-communicable diseases [25]. The long-life expectancy in countries such as Spain, Greece, Italy, and Japan is thought to have a strong dietary influence [26][27][28]. Dietary intervention has a key role in patients with CKD and has been associated with better preservation of eGFR [25]. Therefore, different guidelines recommend considering referral to a dietitian from early stages of CKD to improve clinical outcomes [9][29][30]. In patients with advanced CKD, a diet without an optimal intake of calories, protein, sodium, and phosphate may exacerbate CKD-related clinical and metabolic abnormalities and reduce drug therapy effectiveness [31]. Thus, interventions to be considered and individualized according to patient characteristics, include reduction of protein, phosphorus, potassium, and sodium intake and limitation of the fixed acid load, with a strict follow-up to avoid malnutrition related with these restrictions. Additional consideration may relate to the cause of CKD, such as a good glycometabolic control [32].

4. Diet in ADPKD: Current Guidelines

4.1. Protein

KHA-CARI ADPKD guidelines [33] recommend a moderate protein diet (0.75–1.0 g/kg/day), as a low protein diet (<0.6 g/kg/day) has not shown to slow the rate of ADPKD progression and may increase the risk of malnutrition. The 2015 KDIGO Controversies Conference on ADPKD [34] did not recommend any specific protein intake for ADPKD patients and referred to the 2012 KDIGO guideline on CKD that recommends to lower protein intake to 0.8 g/kg/day, when eGFR is <30 mL/min/1.73 m2.

4.2. Water and Fluid Intake

Given the preclinical evidence of the therapeutic potential of AVP suppression and the clinical success of tolvaptan, an increased water intake to reduce serum osmolarity has been considered as a means to suppress AVP secretion [35][36]. However, water intake is still open to debate given the lack of clinical trials demonstrating any impact on ADPKD progression in humans.
KHA-CARI ADPKD guidelines suggest that patients with ADPKD should drink fluid to satisfy thirst, as there is no evidence that high fluid intake is beneficial for reducing cyst growth [33]. Chebib and Torres recommend moderately enhanced hydration over 24 h (including during the night if waking up) with the aim of maintaining an average urinary osmolality of <280 mOsm/kg so as to keep AVP secretion suppressed [37]. The water prescription in liters is (24-h urine solute load in mOsm/280) + insensible losses (0.5 L). Thus, optimal water intake depends critically on daily solute intake, discussed below, which is usually estimated at 10 mOsm/kg body weight but varies greatly with diet. For example, a recent general population study recorded values up to 1300 mOsm/day [38]. An individual ingesting solute to excrete 1300 mOsm/day will thus require total water intake (including in food) of (1300/280) + 0.5 = 4.6 L. Since repeat collection of such an amount of urine to assess mean 24-h urine osmolality is impractical, it is recommended to assess first morning urine osmolality, and plasma copeptin if available [37]. However, the optimal assessment will be 24-h urinary osmolality which will be in line with the recommendation by the same authors to assess 24-h sodium excretion. Di Iorio [39] indicted that the optimal fluid intake has not yet been defined.
PREVENT-ADPKD trial, (the Randomised Controlled Trial to Determine the Efficacy and Safety of Prescribed Water Intake to Prevent Kidney Failure Due to Autosomal Dominant Polycystic Kidney Disease), aimed to evaluate the impact of prescribed water intake on the rate of change in height-corrected total kidney volume in ADPKD patients, prescribed water intake to reduce 24-hour urine osmolality to 270 mOsmol/kg did not reduce copeptin or slow the growth of total kidney volume over 3 years versus ad libitum water intake irrespective of 24-hour urine osmolality. A 24-hour urine osmolality <300 mOsmol/kg was achieved in 45/86 (52.3%) of patients randomized to prescribed water intake and in 15/86 (17.4%) of patients randomized to ad libitum water intake [40].
For patients on tolvaptan, water intake is mainly driven by thirst. Thus, although preemptive water drinking is recommended, serum sodium and osmolality usually increase, indicating that patients drink according to thirst.

4.3. Salt

Spanish guidelines for the management of ADPKD recommend a diet with <6 g salt daily (<2.3 g/d sodium, ≤100 mmol sodium/day) to prevent and to treat hypertension similar to essential hypertensive patients and in line with general CKD guidelines [41], as do KHA-CARI ADPKD guidelines similar for early CKD [33]. The Canadian Expert consensus on Assessing Risk of Disease Progression and Pharmacological Management of ADPKD [42] recommended salt restriction similar to hypertensive subjects, according to Hypertension Canada guidelines, that is, around 5 g of salt or 87 mmol of sodium per day [43]. The guidelines specifically mention that in patients treated with tolvaptan, a sodium restricted diet of ≤2.4 g/day (≤100 mmol/day) is recommended. It is somewhat surprising that sodium restriction is again mentioned in the context of tolvaptan to emphasize similar sodium targets as in the general ADPKD population. The 2015 KDIGO Controversies Conference on ADPKD [34] also highlighted the importance of a sodium-restricted diet for blood pressure control in ADPKD. However, limitation of sodium intake may also be interesting from the osmole load point of view. Despite these recommendations and dietary instructions in the Consortium for radiologic imaging studies of polycystic kidney disease (CRISP) study, mean sodium intake was approximately 4.3 g/day (179 mmol/d) and remained constant over time [44]. Similar baseline values were observed in the HALT-PKD randomized clinical trials (RCTs) of renin-angiotensin system (RAS) blockade and blood pressure control, but in these trials sodium intake decreased to 3.5–3.8 g/d (145–160 mmol/d) during the trial and higher sodium intake was associated with faster increase in TKV or decrease in GFR in study A and B, respectively, but results were not consistent across both post-hoc analyses [45].

4.4. Osmole Intake

As indicated in the prior sections, osmole intake is also a determinant of the need to secrete AVP to maintain serum osmolarity. Thus, a lower osmole intake will reduce the water needed to keep AVP suppressed. A key component of the osmole load is sodium intake, which may account for 15–30% of urinary osmoles.
A low-osmolar diet in association with adjusted water intake to achieve urine osmolality of ≤280 mOsm/kg water significantly reduced AVP secretion (assessed as copeptin levels) in a small group (n = 34) of ADPKD patients followed for two weeks as compared to no intervention [46]. Patients received individually adjusted water intake to achieve urine osmolality of ≤280 mOsm/kg, and a low sodium (60 mmol, 1.5 g/day), low protein (0.8 g/kg), and low urea (i.e., avoidance of preservatives, food additives, bulking agents, and chewing gum) diet. The dietary intervention led to a reduction in water intake required to lower copeptin. However, it was likely associated with milder thirst, thus potentially keeping the effort needed to drink without thirst unchanged. In any case, patients achieved a 17% decrease in osmol excretion, urine osmolality decreased by 40% (from 426 ± 193 to 258 ± 117 mOsm/kg water) but was unchanged in the control group (from 329 ± 159 to 349 ± 139 mOsm/kg water) and copeptin levels decreased significantly by 14% vs. no change in controls. Although conceptually innovative, the researchers believe clinical translation will be difficult given that the effort required to increase water intake to a large extent is largely replaced by an effort to change multiple dietary components, thus negatively impacting compliance. Also unanswered is whether the achieved decrease in AVP secretion is clinically relevant in humans.
Among society guidelines, osmolality recommendations were only found in the 2018 Canadian Guideline. This is the most recently updated guidelines and includes considerations about tolvaptan. The guidelines recommend that patients on tolvaptan should be referred to a dietician in order to minimize osmolal and sodium intake [42].

4.5. Caffeine

In cultured human PKD cells, caffeine increased cAMP accumulation [47]. However, the key question is whether the modulation of cAMP by caffeine has any clinical relevance, and what caffeine intake thresholds may be associated with clinical impact. Preclinical studies have assessed caffeine doses that are hardly clinically relevant. In murine Pkd1-deficient PKD, a high caffeine intake (150 mg/kg/d) accelerated disease progression, TKV, and decreased renal function [48], but this was not observed in rat PKD fed 400 mg/m2 body surface area [49]. Randomized clinical trials is needed to address the issue, but only observational studies are available that so far have not supported the clinical relevance of caffeine. In the tolvaptan era, a new question is whether caffeine intake should be a concern for patients on a drug that lowers intracellular cAMP levels.
Caffeine consumption has been evaluated in clinical studies. In a cross-sectional study, caffeine intake was not directly associated with renal volume in patients with ADPKD. The study had major shortcomings, including the cross-sectional nature, the use of ultrasound to estimate kidney volume, and low patient numbers (n = 102). In any case, caffeine intake from coffee, regular or diet soft drinks, teas, and chocolate bars was lower in ADPKD patients than in healthy controls (86 vs. 134 mg/d, approximately 1.2 and 2.0 mg/kg, respectively), likely due to prior awareness of the potential impact of caffeine restriction [50]. Thus, mean caffeine intake was just below 1 cup of coffee per day in ADPKD patients and just above that in controls. It is important to keep this perspective in mind since it implies that a high caffeine intake is uncommon in general populations. A retrospective analysis of the CRISP cohort (consortium for radiologic imaging studies of polycystic kidney disease) found no significant association between caffeine consumption from coffee, tea, and caffeinated beverages on progression of height adjusted total kidney volume (htTKV), mGFR, or time to ESRD or death in 239 patients followed for 12.5 years [51]. In the Swiss prospective ADPKD, a cohort of 151 patients was studied between 2006 and 2014. After multivariate adjustment, no statistically significantly differences in htTKV or eGFR were found between coffee drinkers and non-coffee drinkers [52].
Based on the scanty amount of good quality clinical information available, guidelines are quite conservative. KHA CARI guidelines [33] indicate that ≤200 mg/d caffeine intake (i.e., ≤2 cups of coffee or ≤4 cups of tea) could be ingested for cardiovascular health as in the general population, despite the absence of existing data associating cyst growth in ADPKD with caffeine intake. The KDIGO controversies conference for ADPKD indicated that avoiding high caffeine intake has been proposed, without defining “high caffeine” [34]. Spanish guidelines for ADPKD patients recommend avoiding drugs that stimulate cAMP accumulation, like caffeine in patients with moderate-to-severe polycystic liver disease [41]. While some guidelines do not mention other sources of caffeine beyond coffee and tea, patients should be reminded of potentially high contents in energy drinks.

4.6. Other Dietary Components

Guidelines do not discuss other dietary components beyond the recommendations to maintain a normal body weight as for the general population. In this regard, in the HALT PKD trial, overweight body mass and particularly obesity were strong independent predictors of TKV growth and GFR decline in early-stage ADPKD [53]. However, recent opinion pieces discuss dietary phosphate [37]. Although there are no prospective randomized studies on the effect of phosphorus in cardiovascular and renal outcomes in ADPKD, Chebib and Torres recommend a moderate daily phosphate restriction (800 mg) along with moderate protein restriction, based on observational studies in CKD discussed above [37]. While the researchers agree with recommendations based on the excess dietary phosphate in western diets and known potential risks of excess phosphate [54], Chebib and Torres point out to an unclear rational, citing evidence that in ADPKD patients with preserved GFR hypophosphatemia is more frequent than in the general population and this was associated with high FGF23 levels and a renal phosphate leak. In this regard, FGF-23 levels are higher in patients with ADPKD than other causes of CKD at the same eGFR [55]. In this regard, in a post-hoc analysis of the HALT-PKD study, higher serum FGF23 levels did not provide independent information on the outcomes [56].

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Subjects: Urology & Nephrology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register : Sol Carriazo ,
Maria Vanessa Perez-Gomez
, Adrian Cordido , Miguel Angel García-González , Ana Belen Sanz , Alberto Ortiz , Maria Dolores Sanchez-Niño
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Update Date: 31 Aug 2022
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