Short bowel syndrome (SBS) occurs from either surgical resection or malfunction of a significant amount of small bowel. An estimated 42-50% of patients with SBS will develop kidney stones in their lifetime.1,2 Both uric acid and calcium oxalate stones are common. Increased kidney stone risk stems from a combination of possible factors including inability to maintain adequate hydration, reduced alkali absorption, enteric hyperoxaluria, hypomagnesemia, altered gut microbiome, and poor food and beverage intake. Treatment must be individualized to each patient’s 24-hour urine collection results as the cause of kidney stones will differ based on etiology of SBS and natural variations. Evidence based treatments for stone prevention in SBS include improving hydration status, oral calcium to reduce oxalate absorption, reducing dietary fat and/or oxalate, alkali supplementation, and the correction of hypomagnesemia. Dietary recommendations should be made by a registered dietitian after a complete nutrition assessment to ensure the recommendations are appropriate.
Introduction
Short bowel syndrome (SBS) is defined as “a clinical condition associated to having less than 200 centimeters of residual small bowel (SB) in continuity, measured from the duodenojejunal flexure (ligament of Treitz), with or without colon, in an adult and for children (<18 years), less than 25% of the normal length SB for their respective age.” 3 SBS can result when surgical resection of the bowel leaves the remaining bowel with an insufficient length to support adequate digestion and absorption of oral nutrients. Additionally, SBS can occur as a consequence from dysfunction from the remaining bowel, even if the length is sufficient. Most often, SBS arises due to bowel resection resulting from trauma, inflammation, or ischemia; congenital disorders; or resulting from bariatric surgery.4
The most significant concern with SBS is malabsorption, making it challenging to maintain adequate nutrition and hydration. The extent of malabsorption largely depends on the length and location of the remaining bowel. If less than 50% of the SB is removed, the remaining bowel can adapt, minimizing risk of long-term complications.4 Complications of SBS include high volume stool or ostomy output, fluid and electrolyte imbalances, vitamin and mineral deficiencies, bone disease, hepatobiliary diseases, kidney stones, small intestinal bacterial overgrowth, and possibly the need for parenteral support.4,5 This review will focus on mechanisms of how SBS increases the risk of kidney stones and the nutrition therapies for its prevention.
Prevalence of Kidney Stones
Kidney stones occur in 43-50% of patients with SBS.1,2 This is remarkably higher than the estimated 10% of the general population with kidney stones.6 Reduced kidney function is also common; one study found 28% of patients with SBS developed some level of renal impairment.7 Kidney stones, along with infections and dehydration are likely responsible for kidney damage.
Both uric acid and calcium oxalate kidney stones are common in SBS, highlighting the need for metabolic urine testing to direct prevention.8,9 Patients with a SB ostomy may be at greatest risk of uric acid stones due to massive bicarbonate loss, leading to acidic urine and those with some colon-in-continuity are at higher risk of developing calcium oxalate stones.1,10
Mechanism of Stone Formation
Kidney stones are prevalent in SBS due to a combination of factors stemming from malabsorption and dehydration. The exact cause of stone formation is different for each patient depending on the amount and location of bowel that is remaining and natural variations across people.
Reduced Fluid Absorption
The hallmark of SBS is high volume stool or ostomy output and difficulty maintaining hydration due to endogenous losses of both fluid and electrolytes. Additionally, poor appetite and GI symptoms related to eating and drinking can contribute to reduced fluid intake. Limited absorption/resorption of oral fluids and endogenous secretions are problematic in many with SBS and often leads to reduced urine volume and increased saturation of lithogenic compounds. Reducing urine saturation is key to prevent all types of kidney stones.
Patients with a proximal SB ostomy have the most difficulty with enteric fluid absorption and often struggle with chronic dehydration leading to kidney injury and kidney stones.10 Patients with SBS that have their distal ileum and/or some colon-in-continuity tend to have more efficient fluid absorption and higher urine output, though risk for dehydration persists as rapid transit of fluid through the remnant SB may exceed the absorptive capacity of the remnant SB and colon.
Inhibited Intestinal Alkali Absorption
A key tenet of calcium kidney stone prevention is maintenance of adequate urine citrate. Citrate complexes with calcium to form a soluble compound in the urine, reducing calcium available to complex with other compounds to form kidney stones.11 Kidney stone prevention may include alkalizing urine pH via medications such as potassium citrate or sodium bicarbonate and reducing the dietary acid load.11,12 Urine alkalization helps prevent uric acid stones as low urine pH is the biggest driver of uric acid kidney stone formation. For calcium-based stones, dietary or medicinal alkali helps increase urine citrate as well as alkalize urine, which may help prevent calcium oxalate kidney stone formation.
Patients with SBS tend to have low urine pH and low urine citrate, increasing risk of both uric acid and oxalate kidney stones.10 In SBS, alkali precursors such as potassium, magnesium and calcium are poorly absorbed by the residual SB, which may result in highly acidic urine predisposing patients to uric acid kidney stones.10 In addition, when alkali is not absorbed by the GI tract – from either alkali malabsorption or a high dietary acid load – the kidney will reabsorb more citrate to buffer the higher acid load, resulting in lower urine citrate.10 Examples of dietary sources of alkali and acid precursors and exact potential renal acid load (PRAL) values are provided in Table 1.
Enteric Hyperoxaluria
In non-stone formers, only 5-10% of dietary oxalate is absorbed. This varies widely based on dietary intake of calcium, fiber and other nutritional factors.13 The more calcium consumed, the more calcium binds with dietary oxalate in the gut causing reduced oxalate absorption and ultimately lower urine oxalate. By this mechanism, adequate dietary calcium is widely known to reduce the risk of forming oxalate kidney stones.14
Enteric hyperoxaluria is the over absorption of oxalate from the colon and can develop whenever fat malabsorption is present.15 Malabsorbed fat sequesters calcium in the SB, leaving oxalate to be absorbed in the colon and excreted in urine.15 Given the high frequency of fat malabsorption in SBS, enteric hyperoxaluria is common. The extent of bowel resection or dysfunction is correlated with the extent of hyperoxaluria.10 Enteric hyperoxaluria is of particular concern for patients with SBS that have partial or complete colon-in-continuity as oxalate is exclusively absorbed in the colon.10 There is very little risk of enteric hyperoxaluria in those with a SB ostomy (without colon-in-continuity).
Hypomagnesemia
Magnesium is a novel target for oxalate kidney stone prevention due to its ability to bind oxalate both in the intestine and urine to create a soluble complex. Both blood and urine magnesium levels tend to be lower in stone formers.16,17 Hypomagnesemia is common in patients with
SBS, especially in those without the distal ileum, where a majority of magnesium absorption occurs and likely contributes to risk of oxalate kidney stone formation.5
A 2024 study found that magnesium supplementation reduced urine oxalate in individuals with elevated baseline urine oxalate levels.18 However, in SBS, oral magnesium supplementation can worsen GI fluid losses, increasing stool/ostomy output, and thus worsening dehydration with increased risk of stone formation. Therefore, oral magnesium supplementation should be monitored closely, dose adjusted, and if necessary transitioned to parenteral supplementation to optimize fluid balance and serum magnesium levels.
Altered Gut Microbiome
There is a clear role of the gut microbiome in kidney stone formation.19,20 Most of the research has focused on the role that oxalate degrading bacteria play on reducing urine oxalate and therefore reduce oxalate kidney stone risk. The gut microbiome is altered in SBS, likely as a result of both dietary and physiological changes; it is likely that the alteration of the gut microbiome contributes to the increased prevalence of kidney stone formation. More research is needed to determine how and if the gut microbiome can be modulated to reduce kidney stone formation in patients with SBS.
Table 1. Dietary Sources of Alkali and Acid Precursors
| Dietary Precursors | Potential Renal Acid Load (mEq) |
| Alkali Producing Foods | |
| All Fruits Examples: | |
| Banana (1 medium) | 8.2 |
| Blueberries (1 cup) | 1.5 |
| Peach (1 each) | 4.7 |
| All Vegetables Examples: | |
| Broccoli (1 cup, cooked) | 5.5 |
| Green Beans (1 cup, cooked) | 3.5 |
| Tomato (1/2 cup, raw) | 3.7 |
| Acid Producing Foods | |
| All Meat & Seafood Examples | |
| Beef (4oz, cooked) | 12.9 |
| Chicken (4oz, cooked) | 16.3 |
| Cod (4oz, cooked) | 13.5 |
| Most Cheeses | |
| Example: | |
| Cheddar Cheese | 3.5 |
| Minimal Acid or Alkali Production Potential | |
| Most Beans, Nuts, Seeds, Legumes & Plant Protein Foods Examples: | |
| Black Beans (1/2 cup, cooked) | 2.6 |
| Lentils (1/2 cup, cooked) | 1.5 |
| Walnuts (1/2 cup) | 1.7 |
| Grains Examples: | |
| Whole Grain Bread (1 slice) | 1.8 |
| White Bread (1 slice) | 0.8 |
| Brown Rice (1/2 cup cooked) | 2.2 |
| Fats & Oils Examples: | |
| Olive oil (1 tablespoon) | 0.0 |
| Butter (1 tablespoon) | 0.1 |
| Milk & Yogurt Examples: | |
| 2% milk (1 cup) | 1.5 |
| Low Fat Yogurt (1 cup) | 0.4 |
Poor Oral Intake
Patients with SBS may control their stool output by limiting oral intake. As stated above, low volume of oral fluid intake contributes to dehydration, low urine volume, and kidney stone risk. Additionally, an unbalanced diet that is low in alkali precursors (fruits and vegetables) along with nutrient malabsorption can exacerbate low urine citrate and pH, all contributing to the risk of kidney stone formation.
Prevention and Treatment of Kidney Stones
Given the complexity and variation of kidney stones in patients with SBS, it is crucial to individualize interventions to prevent stone formation based on 24-hour urine collections. Table 2 provides suggested interventions based on common urine risk factors for kidney stone formation.
Improve Hydration
The American Urological Association recommends consuming adequate fluid to produce at least 2 ½ liters of urine output/day for kidney stone prevention.11 This volume of urine may be difficult to achieve for patients with SBS as increase in oral fluid intake often results in higher ostomy/stool output with reduced urine volume. Patients with SBS and low urine output (e.g., <1200 mL/24-hours) should be encouraged to sip fluids slowly throughout the day and to periodically measure 24- hour urine volume in response to oral fluid intake; small increases in urine volume can incrementally reduce kidney stone risk despite not producing the recommended amount of urine.
Table 2.
Kidney Stone Prevention Interventions Based on 24-hr Urine Collection Parameters
| Urine Collection Result | Diet and Hydration Strategies |
| Low urine volume (<2.5 liters) | • Increased oral fluids, ideally from water or unsweetened beverages • Oral rehydration solution as appropriate • IV fluids as appropriate • Avoid dietary sodium restriction • Avoid excess simple carbohydrate |
| Hyperoxaluria | • Supplemental calcium of 200-300mg/meal to be taken with meals (if no hypercalciuria) • Increase intake of calcium-rich foods with meals for a total of 1,000-1,200mg calcium/day • Limit intake of very high oxalate foods • Consider low fat diet (20-30% calories from fat) • Trial bile acid sequestrant |
| Low urine pH or citrate | • Potassium citrate, sodium bicarbonate or other citrate supplements dosed based on 24-hour urine collection pH and citrate • Consider increased dietary alkali |
| Hypomagnesemia | • Supplementation of 300-400mg/day as necessary • Monitor for increased GI losses |
Some patients with SBS, especially those with SB ostomy, can benefit from drinking oral rehydration solutions (ORS). ORS are iso-osmolar glucose-electrolyte solutions that utilize the sodium-glucose transport mechanism to pull water across the SB mucosa and help to correct fluid and electrolyte losses. Patients can purchase ORS products or make ORS at home (Table 3). In some cases, parenteral fluids are necessary to maintain adequate hydration and increase urine volume.
For those with SBS, avoidance of excess simple sugar is recommended to prevent rapid emptying of hypertonic fluid into the proximal SB; this results in jejunal water secretion to dilute the chyme to isotonicity, and often causes osmotic diarrhea with a net fluid loss (a.k.a. dumping syndrome). This is particularly important for individuals without the terminal ileum and/or cecum as these are the normal sites of significant fluid reabsorption. It is also advisable to avoid sugar-laden beverages (e.g., fruit juices, sodas), oral nutrition supplements, and concentrated sweets (e.g., cookies, cake, ice cream) to reduce the osmotic effect on the SB.
Dietary Sodium
Typically, a limit of 2,300 mg of sodium per day is recommended for calcium stone prevention for those with high urine calcium as higher dietary sodium increases renal excretion of calcium.11 However, in SBS, especially for patients with a sodium wasting SB ostomy, dietary sodium should be unrestricted to promote water absorption, urinary fluid output, and to prevent hyponatremia related to sodium loss in ostomy effluent.
Low Fat Diet
If a patient with SBS has enteric hyperoxaluria, avoiding excess dietary fat can help reduce sequestration of calcium and thereby reduce the absorption of oxalate and urine oxalate. The American Society of Parenteral and Enteral Nutrition (ASPEN) recommends 20-30% of calories from fat for patients with SBS and colon-in-continuity.4 This does not eliminate fat from the diet and allows for 44-67 grams fat/day on a 2,000 calorie diet. It is important to have a registered dietitian assess a patient’s habitual diet to determine the need for dietary changes.
Alkali Supplementation
As stated above, a major cause of kidney stones in SBS is limited absorption of alkali leading to acidic urine and low urine pH. Given the reduced absorptive capacity of alkali for patients with SBS, it is unlikely that reducing the dietary acid load will significantly impact urine citrate or pH levels. In fact, Bianco et al. found that clinical advice to increase dietary alkali to patients with SBS did not raise urine pH, but prescriptive, oral supplementation of alkali and citrate did increase urine pH (0.34 ± 0.53 vs. 0.22 ± 0.55, p=0.26 and 83 ± 256mg/day vs. 98± 166mg/day, p= 0.74, respectively).21
Table 3.
Commercial and Homemade Oral Rehydration Solutions
| Commercially Available Powders and Liquids | Homemade Beverage Recipes |
| Ceralyte 70® | Ingredients: • 1 liter water • 6 teaspoons sugar • ½ teaspoon salt Instructions: Combine all ingredients and mix until completely dissolved Add sugar-free flavoring as needed Refrigerate Sip throughout the day |
| Drip Drop® Fast Hydration | Ingredients: • ¾ cup fruit juice • 3 ¼ cups water • ¾ teaspoon table salt Instructions: Combine all ingredients and mix until completely dissolved Refrigerate Sip throughout the day |
| Liquid IV® Hydration Multiplier | Ingredients: • 2 ½ cups tomato juice • 1 ½ cups water Instructions: Combine ingredients Refrigerate Sip throughout the day |
| Trioral® Rehydration Electrolyte Powder | Ingredients: • 2 packets of Gatorlyte® powder • 4 cups of water • ¼ teaspoon of table salt Instructions: Combine all ingredients and mix until completely dissolved Refrigerate Sip throughout the day |
| Note: Patients with SBS should drink the sugar-containing oral rehydration solutions (ORS) to most efficiently promote water absorption. Do not add ice to chill ORS as it will dilute the solution changing the sodium and sugar concentration to less favorable levels. |
Oral supplementation of citrate is the most common strategy to increase urine pH and citrate levels for patients with SBS. Potassium citrate and sodium bicarbonate are most commonly prescribed. If not tolerated, over the counter citrate supplements such as Moonstone® or Litholyte® can be used in place of prescription alkali, at the discretion of the physician, to ensure adequate alkali absorption, based on 24-hour urine collection results. It is important to periodically monitor 24-hour urine collection results to determine adequacy of dosing.
Dietary Calcium
In the general kidney stone population, avoidance of calcium supplements is typically recommended due to concern about exacerbating hypercalciuria, especially when calcium supplements are taken away from meals.11,22 However, in patients with SBS, urine calcium is typically not elevated and calcium supplements with meals may help reduce oxalate absorption. All forms of calcium supplements can reduce oxalate absorption.
For those with SBS, including foods high in calcium, or taking calcium supplements, with each meal can help to reduce intestinal oxalate absorption, reduce urine calcium levels, and ultimately reduce oxalate kidney stone formation.13 For those with SBS and risk of kidney stones it is recommend they take 600-2000 mg per day, in split doses, with meals, e.g. 400-500 mg calcium per meal.20
Dietary Oxalate
Limiting dietary oxalate is frequently recommended for patients with SBS to reduce their urine oxalate levels. However, there is debate as to whether a low oxalate diet is beneficial for oxalate stone prevention due to the inevitable restriction of beneficial components that are in oxalate-containing foods such as alkali, magnesium, phytate and fiber.23 Noori et al. found urinary magnesium, citrate and pH increased in patients without SBS following a DASH (Dietary Approaches to Stop Hypertension) style diet compared to a low oxalate diet.24 Siener et al. found that by providing meals that were “balanced” with less oxalate, protein and sodium, along with more fiber and magnesium, patients with SBS had reduced urine oxalate.25 Finally, Bianco et al. found that advice to reduce dietary oxalate given in the clinic did not lower urine oxalate in a group of patients with SBS.22 As such, a strict low oxalate diet for patients with SBS should also be questioned.
Although avoidance of eating foods that are very high in oxalate is prudent for patients with enteric hyperoxaluria, a strict low oxalate diet should not be recommended as it will limit beneficial components for stone prevention and general health.23,24 Also, it is hard for patients to adhere to a prescribed amount of dietary oxalate given the difficulty of quantifying oxalate in food (especially prepackaged foods), incomplete lists of oxalate content of foods, discrepancies between lists of food oxalate composition, and the prevalence of misinformation.25 In addition, oxalate exists in both soluble and insoluble forms; soluble oxalate has a much larger impact on urine oxalate levels, yet this distinction is not usually made on food composition lists.27 Table 4 provides a short list of foods with moderate and high oxalate concentration (>70 mg oxalate per standard portion as measured by the 2023 Harvard Oxalate Table).28 Practically, ensuring adequate dietary calcium is a more effective and healthy way to reduce urine oxalate.
Table 4. Very High Oxalate Foods & Substitutes29
| Food Item | Oxalate (mg) | Lower Oxalate Substitutions | Oxalate (mg) |
| Spinach, ½ cup cooked | 547 | Kale, ½ cup cooked | 1 |
| Navy beans, ½ cup cooked | 96 | Kidney beans, ½ cup cooked | 10 |
| White potato with skin, 1 medium | 92 | Mashed or boiled potatoes, 1 cup | 30 |
| Beets, ½ cup cooked | 76 | Parsnip, ½ cup cooked | 15 |
| Almonds, 1 ounce (1/4 cup) | 72 | Pistachios, 1 ounce, ¼ cup | 9 |
Bile acid sequestrants, such as cholestyramine, are also used to bind oxalate in the SB and reduce urine oxalate.29,30 However, the use of bile acid sequestrants can lead to bile salt deficiency which will worsen fat malabsorption, hence increasing risk of oxalate absorption. Therefore, in patients with SBS it is necessary to provide clinical monitoring of the effectiveness of a bile salt sequestrant to determine if the resin improves or worsens a patient’s malabsorption.
Correction of Hypomagnesemia
Given the prevalence of hypomagnesemia, and the role that magnesium plays in oxalate stone prevention, the correction of hypomagnesemia may help prevent oxalate stones. Foods highest in magnesium include nuts, seeds, beans, and green leafy vegetables. Unfortunately, these foods may not be tolerated by some patients with SBS. In addition, dietary magnesium is unlikely to significantly raise serum magnesium levels in SBS patients with limited absorptive capacity and oral magnesium supplements may worsen stool output and dehydration. Therefore, parenteral magnesium replacement may be necessary to raise urinary magnesium levels and reduce stone formation.5
“Do No Harm”
Given the high risk of malnutrition, maldigestion, and malabsorption in patients with SBS, it is imperative that nutrition recommendations do not become so onerous that they make it more difficult for patients with SBS to balance their diet. Restrictive diets have been shown to reduce total calorie intake in frail populations.31 Ideally, nutrition recommendations should be devised, communicated and monitored by a registered dietitian to optimize patient adherence and prevent malnutrition.
Summary
Short bowel syndrome significantly increases the risk of kidney stone formation due to a combination of possible factors including reduced urine volume, magnesium, citrate, pH and increased oxalate. Kidney stone prevention interventions should be personalized to 24-hour urine collection results and patient preferences. A comprehensive nutrition assessment should be completed prior to providing dietary recommendations given the high risk of malnutrition. All patients with SBS that have or are at risk for kidney stone formation should be followed by a team that is knowledgeable in the prevention and management of kidney stones.
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