Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder characterized by kidney cyst formation and progressive kidney function loss. It is the fourth most common cause of kidney failure, leading to potentially life-threatening kidney and extrarenal manifestations. Managing ADPKD effectively involves a multifaceted approach, and dietary interventions have emerged as a strategy to slow progression and improve outcomes. Whether you’ve just been diagnosed with autosomal dominant polycystic kidney disease (ADPKD) or been living with the condition for some time, it’s vital to maintain a healthy diet and drink plenty of fluids to maintain overall health and maximize kidney function.
The Role of Diet in ADPKD Management
Emerging evidence suggests that diet can play an important role in the progression of kidney disease, including ADPKD. Dietary interventions show promise in managing ADPKD by improving metabolic health and reducing oxidative stress. In 2018, experts recommended moderate sodium restriction, increased hydration, moderate caloric restriction, and moderate protein restriction for patients with kidney function decline. Since then, additional preclinical and clinical studies have focused on dietary manipulation.
Understanding the Metabolic Pathways in ADPKD
ADPKD is characterized by a complex interplay with multiple nutrient metabolism pathways, disrupting key cellular pathways, such as autophagy, glycolysis, fatty acid metabolism, and mitochondrial function. Mutations in the PKD1 and PKD2 genes lead to higher cAMP levels, which promote cystogenesis. PC1 and PC2 proteins modulate calcium ion influx and mitochondrial dynamics, directly influencing mitochondrial function. PC1 C-terminal tail suppresses cystic disease in a mitochondrial enzyme NNT-dependent fashion. PC2 is critical for uncoupling mitochondria from the endoplasmic reticulum. Therefore, it is conceivable that manipulation of mitochondrial bioenergetics through diet modifications (e.g., caloric restriction) may modulate PC1/2 effects on mitochondrial function.
In ADPKD, altered cellular metabolism results in increased aerobic glycolysis and extracellular lactate accumulation. Reduced OXPHOS in mitochondria stimulates glycolysis and results in increased ATP, reduced AMPK activity, and increased mTORC1 activity. Dietary interventions that reduce osmolar intake and suppress vasopressin secretion, such as water prescription and low-sodium diet, may reduce cystogenesis by inhibiting cAMP formation. Crucial signaling intermediaries, including mTOR, AMPK, SIRT-1, IGF-1, and PPARα/γ, exhibit significant roles in ADPKD pathology and metabolic response. The overactivity of the miR-17 microRNA cluster, coupled with PC-1 deficiency, contributes to mitochondrial dysfunction by repressing PPARα. These complexities underscore the intricate link between ADPKD progression and metabolic dysregulation.
General Dietary Recommendations for ADPKD
To optimize ADPKD management, patients are generally advised to follow a dietary regimen that aims to achieve or maintain an ideal body weight and includes high fluid intake, low sodium, and limited concentrated sweets. Here’s a breakdown of key components:
Read also: Managing Stage 3 Kidney Disease with Diet
Hydration
Drinking plenty of water is crucial for people with ADPKD. Generous water intake helps maintain a dilute urine and decreases the risk of kidney stones, which are seen at increased frequency in PKD patients. Drinking at least 3 quarts of water daily - 12 or more 8-ounce glasses - helps manage the disease. Less concentrated urine is easier on the kidneys. It also suppresses vasopressin, a hormone that triggers thirst and stimulates cyst growth in ADPKD. Avoiding dehydration is considered wise. In addition, generous water intake has the potential to suppress vasopressin production and decrease cAMP production in the kidney.
Your urine should generally be pale in color. This will tend to suppress vasopressin production by the brain and cAMP production in the kidneys. However, before you start upping your water intake, check with your nephrologist. “If you have a very low level of kidney functioning, high water intake can be dangerous,” says Dr. Fatica. It’s important to understand that the benefit or risk of high water intake has never been formally studied in PKD patients, and the results cannot be predicted or guaranteed. In addition, as kidney function deteriorates, generous water intake can be problematic and even dangerous.
Sodium Restriction
People with ADPKD are at a high risk for high blood pressure. Salt triggers the release of a hormone called vasopressin that is stimulated by thirst and controls how your kidneys concentrate your urine. In individuals with ADPKD, vasopressin also fuels kidney cyst growth and enlargement. Over time, this can lead to reduced kidney function. Excess sodium also increases blood pressure by retaining fluid in your blood vessels, forcing your heart to work harder.
The recommended sodium intake for individuals with ADPKD is no more than 2,300 milligrams a day, the same as for the general population. Some easy ways to limit sodium: Don’t salt your foods at the table, use salt-free spices/herbs while cooking, and check food labels for sodium content, says Maruschak. Choose fresh or frozen vegetables instead of canned vegetables. Avoid canned soups and frozen dinners that are high in sodium. Be careful with salt substitutes and “reduced sodium” foods.
Protein Intake
Protein is vital for maintaining your body’s cells, repairing muscles and supporting essential functions. However, too much protein can strain the kidneys, particularly in people with ADPKD. Experts recommend daily consumption of 0.8 to 1 gram of protein per kilogram of body weight. Diets exceeding 1.3 grams of protein per kilogram of body weight may be harmful to people with ADPKD. Conversely, individuals on dialysis may require higher protein intake to prevent malnutrition.
Read also: A Review of the Mediterranean Diet in Kidney Disease
Plant-based protein like beans and nuts are easier on the kidneys than animal proteins like meat and dairy products. This is because plant proteins produce less acid in the body than meat proteins. More acid in body can damage the kidneys. Good lean protein sources for people with ADPKD include seafood, poultry, eggs, legumes, nuts, seeds, and soy products, says Maruschak.
Limiting Concentrated Sweets
Reducing concentrated sweets is a common dietary recommendation for everyone, but it’s particularly important for people with ADPKD.
Other Nutrients to Manage
People with CKD may need to control the amount or type of one or more nutrients:
- Potassium: Potassium is important for muscle function, including the heart muscle. The amount of potassium you need is based on how well your kidneys are working and your medications. Some high-potassium foods include milk, meat, bananas, oranges and orange juice, cantaloupe, dried fruits, winter squash and salt substitutes.
- Phosphorus: As kidney function gets lower, extra phosphorus can start building up in the blood. High phosphorus levels can cause bones to get weaker. High phosphorus foods include dairy products, organ meats, colas, deli meats, and processed foods with phosphate additives. Avoid processed foods that have additives with PHOS like disodium PHOSphate.
- Calcium: Foods that are good sources of calcium are often high in phosphorus.
Specific Dietary Interventions
Several specific dietary interventions have been explored for their potential benefits in ADPKD management:
Caloric Restriction
Daily caloric restriction (approximately 30%) is a standard approach to weight loss in obesity. Caloric restriction seems particularly beneficial for patients with overweight or obesity because it promotes weight loss and improves metabolic parameters. Overweight status or obesity is strongly and independently associated with ADPKD progression in early-stage patients. Weight loss through caloric restriction is a reasonable recommendation in patients with ADPKD who are overweight or obese. It should be implemented under medical supervision and in consultation with a registered dietitian.
Read also: Nutrition and stage 2 CKD
However, caution is needed in patients with an ideal body mass index (BMI, 18.5-24.9 kg/m2). Patients with ADPKD should not restrict water intake and must maintain an adequate intake of micronutrients while restricting calorie intake. Long-term caloric restriction may not be feasible or advisable.
Intermittent Fasting and Time-Restricted Feeding
Intermittent fasting involves restricting calories (by 80%) for 1-3 nonconsecutive days per week, while time-restricted feeding limits caloric intake to a narrow feeding window of 8-10 hours per day. Time-restricted feeding is referred to the dietary intervention implemented in preclinical studies, whereas time-restricted eating is the term used in human clinical trials. Limiting feeding to an 8-hour window in the nonorthologous Han:SPRD rat model of PKD reduced cystic index and improved kidney function by induction of ketosis, partially mediated by changes in mTOR and signal transducer and activator of transcription 3 signaling. Moderate daily caloric restriction can effectively facilitate weight loss without the requirement of inducing ketosis.
However, data on intermittent fasting in ADPKD are limited to the single pilot study listed above, which compared daily caloric restriction (34% restriction daily) to intermittent fasting (80% caloric restriction for 3 nonconsecutive days per week) and found more adverse effects with intermittent fasting. Pilot data suggest that the tolerability of intermittent fasting in patients with ADPKD may pose implementation challenges. Intermittent fasting may be an alternative approach for patients with overweight or obesity, but should only be considered with medical guidance. In summary, there is insufficient evidence to recommend intermittent fasting or time-restricted eating for patients with ADPKD.
Ketogenic Diet
Ketogenic diets increase the production of ketone bodies, such as β-hydroxybutyrate (BHB) and acetoacetate. The classic ketogenic diet is a high-fat (55%-65% of dietary macronutrients), adequate-protein (1 g/kg), and low-carbohydrate (5%-10%) diet that leads to a starvation-like metabolic state. AMPK activation and metabolic substrates changes (e.g., increased ketone bodies that fuel cellular metabolism instead of glucose) contribute to the ketogenic diet's beneficial effects on insulin sensitivity, oxidative stress reduction, and cell growth and proliferation. The ketogenic diet has been used for several decades in the medical management of epilepsy and, more recently, to aid in the treatment of metabolic disorders such as obesity.
Preclinical studies have shown that a ketogenic diet can reduce cystic burden and kidney function loss, making it a promising candidate for managing ADPKD. However, it is unclear whether the benefit is through weight loss or ketosis alone. Limited efficacy and safety data are available for ADPKD. The KETO-ADPKD study showed potentially favorable short-term outcomes, including decreased cystic liver growth and an acute improvement in kidney function. The short-term increase in creatinine-based eGFR might be related to decreased animal protein (meat) intake, leading to a decreased creatinine pool size and lowered serum creatinine, rather than true GFR change. Long-term efficacy and safety data are still needed.
The Importance of a Renal Dietitian
If you have ADPKD, knowing what foods to avoid and which to eat more of can change according to the severity of your disease and your level of kidney function. To maximize your success, make sure you’re checking in with your care team, including a renal dietitian, regularly. Meeting with a dietitian is a service covered by Medicare and may also be covered by other types of insurance. You may need to call your insurance provider to see if your plan covers meeting with a dietitian.
A renal dietician can help you create an eating plan that helps you control your blood sugar, while also limiting sodium, phosphorus, potassium and fluids. They can also suggest you take a special supplement made for people with kidney disease or a special kind of vitamin D, folic acid or iron pill, to help prevent some common side effects of kidney disease, such as bone disease and anemia.
Lifestyle Adjustments
Eating habits are deeply ingrained in people’s daily lives, and the idea of changing them can feel overwhelming. But dietary changes don’t have to happen all at once. Take your time when adjusting your eating habits. Before making major dietary changes, consult with your kidney doctor or other healthcare professional. Making healthy choices at mealtimes and following simple, delicious recipes created by a dietitian specializing in PKD can make the process easier.
Transitioning to a PKD-friendly diet doesn’t have to feel overwhelming. Dietitian Diana Bruen specializes in PKD. She has seen hundreds of people use diet as an important part of an overall treatment plan designed to keep their kidneys functioning longer and preserve their overall health.
Potential Supplements
Supplementation with curcumin, ginkgolide B, saponins, vitamin E, niacinamide, or triptolide has demonstrated uncertain clinical benefit in patients with ADPKD. Notably, β-hydroxybutyrate supplements have shown promise in animal models; however, their safety and efficacy in ADPKD require further evaluation through well-designed clinical trials. Therefore, the use of these supplements is not currently recommended for patients with ADPKD.
Considerations for Patients with Both PKD and Diabetes
Normally, having PKD doesn’t make a person more likely to develop diabetes (and vice versa), but that may not be the case for those undergoing a kidney transplant. Studies suggest that high-protein diets may be beneficial for people with diabetes, but they’re not a good choice for those with PKD too.
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