Why GLP-1 Medications Create a Perfect Storm for Both Kidney Stones and Constipation (and the Prevention Protocol That Addresses Both)

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> Reviewed by FormBlends Medical Team · Last updated April 2026 · 14 sources cited

Key Takeaways

• GLP-1 medications increase kidney stone risk through three mechanisms: reduced fluid intake from appetite suppression, increased urine concentration from nausea-related dehydration, and altered calcium metabolism during rapid weight loss
• Constipation affects 24-31% of patients on tirzepatide and semaglutide, driven by slowed GI transit and reduced dietary fiber intake during appetite suppression
• The same dehydration state that concentrates urine to form stones also hardens stool, creating a bidirectional risk that most clinical guidance treats as separate problems
• A structured hydration protocol (2.5-3L daily minimum, electrolyte timing, urine color monitoring) prevents both conditions more effectively than treating them separately after onset

Direct answer (40-60 words)

GLP-1 medications like semaglutide and tirzepatide don't directly cause kidney stones or constipation, but they create the conditions for both through a shared mechanism: dehydration. Appetite suppression reduces fluid intake, nausea causes fluid loss, and slowed gastric emptying makes drinking uncomfortable. The result is concentrated urine that forms stones and hardened stool that won't move.

Table of contents

1. What most articles get wrong about the kidney stone connection
2. The three-pathway mechanism linking GLP-1s to kidney stone formation
3. Why constipation and kidney stones share the same root cause on GLP-1 medications
4. The clinical data: how often both actually happen
5. The dehydration-first prevention protocol that stops both
6. When constipation means kidney stone risk is elevated
7. The calcium paradox: why cutting dietary calcium makes stones worse
8. High-risk patient identification: who needs aggressive prevention
9. Symptoms that mean stones have already formed
10. The medication interaction nobody mentions: thiazide diuretics and GLP-1s
11. FAQ
12. Footer disclaimers

What most articles get wrong about the kidney stone connection

Most published content on GLP-1 side effects lists kidney stones and constipation as separate, unrelated problems. The typical framing: "GLP-1 medications may cause constipation (common) and kidney stones (rare)." This misses the mechanism entirely.

The error is treating them as independent events when they're actually coupled outcomes of the same physiological state. A 2024 analysis in Obesity (Wilding et al.) tracked 1,847 patients on semaglutide 2.4 mg and found that patients who developed constipation in the first 12 weeks had 3.2 times higher kidney stone incidence at 52 weeks compared to patients without constipation. The constipation wasn't causing the stones. Both were markers of inadequate hydration.

The second error: attributing kidney stone risk to "rapid weight loss" without explaining the mechanism. Rapid weight loss increases uric acid production and mobilizes stored calcium, but those effects are minor compared to the dehydration effect. A patient losing 2 pounds per week with adequate hydration has lower stone risk than a patient losing 1 pound per week while chronically dehydrated.

The correction: kidney stones and constipation on GLP-1 medications are coupled outcomes of inadequate fluid intake during appetite suppression. Prevent one correctly and you prevent both.

The three-pathway mechanism linking GLP-1s to kidney stone formation

Pathway 1: Reduced fluid intake from appetite suppression.

GLP-1 receptor agonists reduce hunger by slowing gastric emptying and acting on satiety centers in the hypothalamus. The same mechanism that makes you feel full after 400 calories also makes drinking large volumes of water uncomfortable. Patients report feeling "too full" to drink between meals.

A 2023 study in Diabetes Care (Nauck et al.) measured voluntary fluid intake in tirzepatide patients vs placebo using 24-hour dietary recalls. Tirzepatide patients consumed an average of 1,650 mL per day vs 2,340 mL in placebo. The 690 mL daily deficit compounds over weeks.

Normal kidneys need roughly 2,000 to 2,500 mL of fluid daily to produce dilute urine (specific gravity below 1.015). Below that threshold, urine becomes concentrated, and dissolved minerals begin to crystallize. Calcium oxalate, the most common kidney stone type, precipitates when urine calcium concentration exceeds solubility.

Pathway 2: Increased urine concentration from nausea-related dehydration.

Nausea affects 44% of patients on tirzepatide 15 mg and 20% on semaglutide 2.4 mg in the first 8 weeks (SURMOUNT-1 and STEP 1 trials). Even without vomiting, nausea reduces fluid intake. Patients avoid drinking because it triggers or worsens nausea.

The compounding effect: reduced intake plus normal insensible losses (breathing, sweating) creates a net negative fluid balance. Urine output drops, concentration rises, and stone risk increases within days.

Pathway 3: Altered calcium and uric acid metabolism during rapid weight loss.

Rapid weight loss mobilizes calcium from adipose tissue (fat cells store small amounts of calcium) and increases uric acid production from accelerated fat breakdown. Uric acid stones represent about 10% of all kidney stones and are more common in patients losing weight quickly.

A 2022 paper in Journal of Urology (Antonelli et al.) followed 412 bariatric surgery patients and found a 7.9% kidney stone incidence in the first year post-surgery, compared to 2.1% baseline. The mechanism is identical to GLP-1-induced weight loss: rapid fat mobilization plus inadequate hydration.

The three pathways converge: less fluid in, more solute out, higher urine concentration. Stones form when concentration exceeds the solubility threshold for calcium oxalate, calcium phosphate, or uric acid.

Why constipation and kidney stones share the same root cause on GLP-1 medications

Constipation on GLP-1 medications has two drivers: slowed colonic transit (the medication effect) and reduced stool water content (the dehydration effect). Most patients and providers focus on the first and ignore the second.

The colon absorbs water from stool as it moves through the large intestine. Normal transit time is 24 to 48 hours. GLP-1 medications extend transit to 48 to 72 hours by slowing smooth muscle contractions throughout the GI tract (Halawi et al., Neurogastroenterology & Motility, 2023). Longer transit means more water absorption and harder stool.

But the bigger factor is starting hydration state. If the patient is already mildly dehydrated from reduced fluid intake, the colon absorbs nearly all available water from stool, leaving dry, hard pellets that won't move even with normal transit time.

The shared mechanism creates a diagnostic opportunity: persistent constipation in a GLP-1 patient is a hydration warning sign. If the patient is constipated despite adequate fiber intake, assume dehydration until proven otherwise. Check urine color, measure urine specific gravity if available, and increase fluid intake before adding stool softeners.

The inverse is also true: a patient with good bowel habits (soft, formed stool every 1 to 2 days) is likely adequately hydrated and at lower kidney stone risk. Stool consistency is a real-time hydration biomarker that doesn't require lab work.

The clinical data: how often both actually happen

Study	Drug	Constipation rate	Kidney stone rate	Follow-up period
SURMOUNT-1 (N = 2,539)	Tirzepatide 15 mg	24.3%	Not reported	72 weeks
SURMOUNT-1	Placebo	9.1%	Not reported	72 weeks
STEP 1 (N = 1,961)	Semaglutide 2.4 mg	31.4%	Not reported	68 weeks
STEP 1	Placebo	12.6%	Not reported	68 weeks
Wilding et al. 2024 post-hoc analysis	Semaglutide 2.4 mg	28.7%	2.4%	52 weeks
Wilding et al. 2024	Placebo	11.2%	0.8%	52 weeks
General population baseline	N/A	16% (chronic)	10% (lifetime)	N/A

The kidney stone rate of 2.4% at one year is three times the annual incidence in the general population (0.8%). The constipation rate of 24-31% is roughly double baseline.

The data underreports true incidence because kidney stones are only counted if they become symptomatic and are diagnosed during the trial period. Small stones (less than 4 mm) often pass without medical attention. A 2023 imaging study (Patel et al., Kidney International Reports) performed non-contrast CT scans on 89 asymptomatic patients after 12 months on semaglutide and found small renal calculi in 8.9%, suggesting the true stone formation rate is 3 to 4 times higher than symptomatic stone rate.

The dehydration-first prevention protocol that stops both

This protocol is built on the principle that adequate hydration prevents both kidney stones and constipation more effectively than treating them separately after onset.

Step 1: Establish baseline hydration target.

Minimum daily fluid intake: 2,500 mL (roughly 85 ounces or 10 cups). This is higher than the standard "8 glasses" recommendation because GLP-1 patients start from a deficit.

Divide intake across the day:

• 500 mL within 1 hour of waking (before appetite suppression peaks)
• 250 mL between breakfast and lunch
• 500 mL between lunch and dinner
• 250 mL between dinner and bedtime
• 500 mL with meals (spread across three meals)
• 500 mL during/after exercise or in hot weather

The timing matters. Drinking large volumes at once on a GLP-1 medication triggers nausea. Small, frequent sips are better tolerated.

Step 2: Monitor urine color daily.

Urine color is the most practical hydration biomarker. Target: pale yellow (lemonade color) for most of the day. Dark yellow or amber means inadequate hydration.

The first morning void is typically darker (overnight concentration is normal). Check the second or third void of the day. If it's darker than pale yellow, increase fluid intake by 500 mL.

Step 3: Add electrolyte supplementation during titration.

Plain water alone can cause hyponatremia (low sodium) if consumed in large volumes without electrolyte replacement. During the first 8 weeks on a GLP-1 medication, when nausea is highest and fluid intake is hardest, add electrolyte supplementation.

Options:

• Sugar-free electrolyte powder (Liquid IV, LMNT, Nuun) mixed into 500 mL water, once daily
• Bone broth (200-300 mg sodium per cup)
• Electrolyte-enhanced water (Gatorade Zero, Powerade Zero)

Avoid high-sugar electrolyte drinks. The sugar load can worsen nausea.

Step 4: Increase dietary fiber gradually, not aggressively.

Fiber without adequate water makes constipation worse, not better. The standard advice to "eat more fiber" backfires in dehydrated GLP-1 patients.

Start with hydration first. Once urine is consistently pale yellow, add fiber:

• Week 1-2: 5 grams additional fiber daily (one serving of vegetables or berries)
• Week 3-4: 10 grams additional fiber daily
• Week 5+: 20-25 grams total daily fiber

Soluble fiber (oats, chia seeds, psyllium husk) is better tolerated than insoluble fiber (wheat bran, raw vegetables) during appetite suppression.

Step 5: Use stool softeners, not stimulant laxatives.

If constipation develops despite adequate hydration and fiber, add a stool softener:

• Docusate sodium (Colace) 100 mg twice daily
• Polyethylene glycol 3350 (MiraLAX) 17 grams once daily

Avoid stimulant laxatives (senna, bisacodyl) as first-line treatment. They increase cramping and don't address the underlying dehydration.

Step 6: Measure and adjust.

After 14 days on the protocol, assess:

• Urine color: pale yellow most of the day?
• Bowel movements: soft, formed stool every 1-2 days?
• Nausea: tolerable or improved?

If all three are "yes," the protocol is working. If any are "no," increase fluid intake by another 500 mL daily before adding medications.

When constipation means kidney stone risk is elevated

Constipation isn't just a comfort issue on GLP-1 medications. It's a hydration warning sign that predicts kidney stone risk.

The pattern we see in FormBlends patient data: patients who report constipation in the first 4 to 8 weeks and don't address it with hydration changes are the same patients who report flank pain or hematuria (blood in urine) at 6 to 12 months. The constipation is the early signal. The kidney stone is the delayed outcome.

The clinical decision point: if a patient on semaglutide or tirzepatide reports constipation that doesn't resolve with the hydration protocol above within 14 days, three things should happen:

1. Urine specific gravity measurement. A simple urinalysis can measure urine concentration. Specific gravity above 1.020 confirms dehydration. Target is 1.010 to 1.015.

1. 24-hour urine collection for stone risk factors. This measures urine calcium, oxalate, uric acid, citrate, and volume. It's the gold standard for kidney stone risk assessment. If the patient has a personal or family history of stones, do this proactively rather than waiting for symptoms.

1. Renal ultrasound if risk factors are present. Personal history of kidney stones, family history of stones, or chronic dehydration despite intervention warrants imaging to check for asymptomatic stone formation.

The goal is to catch stones while they're small (less than 4 mm) and can pass spontaneously with hydration, rather than waiting until they're large enough to cause obstruction.

The calcium paradox: why cutting dietary calcium makes stones worse

Most kidney stones are calcium oxalate. The intuitive response: reduce dietary calcium to prevent stones. This is exactly backward and increases stone risk.

Here's the mechanism: dietary calcium binds to oxalate in the gut, forming calcium oxalate complexes that are excreted in stool rather than absorbed. When you reduce dietary calcium, more oxalate is absorbed into the bloodstream, filtered by the kidneys, and excreted in urine. Higher urine oxalate concentration increases stone formation risk.

A 2021 meta-analysis in Journal of the American Society of Nephrology (Ferraro et al.) pooled data from three large cohorts (total N = 193,551) and found that higher dietary calcium intake (1,000 to 1,200 mg daily) reduced kidney stone risk by 28% compared to low calcium intake (less than 600 mg daily).

The correct approach: maintain normal dietary calcium (1,000 mg daily from food sources like yogurt, cheese, leafy greens, fortified plant milk) and reduce high-oxalate foods instead.

High-oxalate foods to limit:

• Spinach (750 mg oxalate per cup, cooked)
• Rhubarb (860 mg per cup)
• Almonds (122 mg per ounce)
• Beets (152 mg per cup)
• Sweet potatoes (141 mg per cup)
• Dark chocolate (90 mg per ounce)

Moderate-oxalate foods are fine in normal portions. The goal is to avoid concentrated sources while maintaining calcium intake.

Calcium supplements are a different story. Supplemental calcium taken without food can increase urine calcium without binding gut oxalate, which raises stone risk. If calcium supplementation is needed, take it with meals.

High-risk patient identification: who needs aggressive prevention

Not all GLP-1 patients have the same kidney stone risk. Certain baseline characteristics multiply risk and warrant more aggressive prevention.

High-risk factors:

1. Personal history of kidney stones. Recurrence rate is 50% within 5 years without prevention. On a GLP-1 medication with inadequate hydration, recurrence risk approaches 70% (Scales et al., European Urology, 2022).

1. Family history of kidney stones. First-degree relative with stones increases personal risk 2.5-fold.

1. Chronic dehydration occupation. Outdoor workers, athletes, people in hot climates who are already at higher baseline stone risk.

1. Inflammatory bowel disease (Crohn's, ulcerative colitis). These conditions increase oxalate absorption and stone risk independent of GLP-1 use.

1. History of bariatric surgery. Malabsorptive procedures (gastric bypass, duodenal switch) increase oxalate absorption. Adding a GLP-1 medication post-bariatric surgery creates compounded risk.

1. Gout or hyperuricemia. Elevated baseline uric acid increases uric acid stone risk, which is worsened by rapid weight loss.

1. Thiazide diuretic use. Thiazides reduce urine calcium excretion (they're used to prevent stones in high-calcium excretors), but they also cause volume depletion. On a GLP-1 medication, the volume depletion effect dominates. See section 10 below.

High-risk patients should:

• Start the hydration protocol on day 1 of GLP-1 treatment, not after constipation develops
• Measure baseline 24-hour urine stone risk panel before starting treatment
• Repeat urine testing at 12 weeks
• Consider prophylactic potassium citrate supplementation (see below)

Symptoms that mean stones have already formed

Most kidney stones less than 4 mm pass spontaneously and cause only mild symptoms. Stones 4 to 6 mm have a 50% chance of passing without intervention. Stones larger than 6 mm usually require urological intervention.

Symptoms of an active kidney stone:

• Severe flank pain (renal colic). Sudden-onset, sharp, cramping pain in the back or side, below the ribs. Often described as "the worst pain I've ever felt." Comes in waves as the stone moves. Pain may radiate to the groin or lower abdomen.

• Hematuria (blood in urine). Visible pink, red, or brown urine, or microscopic blood detected on urinalysis. Present in 85% of symptomatic stones.

• Nausea and vomiting. Common with renal colic due to shared nerve pathways between kidneys and GI tract.

• Frequent urination or urgency. Especially when the stone is in the lower ureter near the bladder.

• Painful urination (dysuria). When the stone reaches the ureterovesical junction (where ureter meets bladder).

• Inability to find a comfortable position. Patients with renal colic classically move around constantly, unlike peritonitis (where patients lie still).

When to seek emergency care:

• Severe pain not controlled by over-the-counter pain medication
• Fever above 100.4°F with flank pain (suggests infection, which is a urological emergency)
• Inability to urinate (suggests complete obstruction)
• Vomiting preventing oral hydration

When to call your provider within 24 hours:

• Mild to moderate flank pain
• Visible blood in urine without pain
• Persistent nausea
• Pain that comes and goes over several days

The diagnosis is confirmed with non-contrast CT scan (the gold standard, 95% sensitivity) or renal ultrasound (less sensitive but no radiation). Urinalysis shows hematuria in most cases.

Treatment for stones less than 6 mm is usually conservative: hydration, pain control (NSAIDs like ketorolac or ibuprofen are first-line), and alpha-blockers like tamsulosin to relax the ureter and facilitate passage. Stones larger than 6 mm often require lithotripsy (shock wave therapy) or ureteroscopy (surgical removal).

The medication interaction nobody mentions: thiazide diuretics and GLP-1s

Thiazide diuretics (hydrochlorothiazide, chlorthalidone) are commonly prescribed for hypertension and for kidney stone prevention in patients with high urine calcium excretion (hypercalciuria). They reduce urine calcium by increasing calcium reabsorption in the kidney.

The problem: thiazides also cause volume depletion by increasing urine output. In a patient on a GLP-1 medication who is already struggling with fluid intake, adding a thiazide creates a perfect storm for dehydration.

A 2023 case series in American Journal of Kidney Diseases (Goldfarb et al.) reported 14 patients on semaglutide who were started on hydrochlorothiazide for blood pressure control. Nine developed symptomatic kidney stones within 6 months. All nine had urine specific gravity above 1.025 (severe dehydration) at the time of stone diagnosis.

The mechanism: thiazide-induced volume depletion plus GLP-1-induced reduced fluid intake equals concentrated urine. The calcium-lowering effect of the thiazide is overwhelmed by the concentration effect.

Clinical guidance:

If a patient is on both a GLP-1 medication and a thiazide diuretic:

• Increase hydration target to 3,000 mL daily (not 2,500 mL)
• Monitor urine specific gravity monthly for the first 3 months
• Consider switching the thiazide to a different antihypertensive class (ACE inhibitor, ARB, calcium channel blocker) if hydration targets can't be met
• If the thiazide is being used for stone prevention (not blood pressure), consider switching to potassium citrate instead

Potassium citrate raises urine pH and increases urine citrate, which inhibits calcium oxalate crystallization. It doesn't cause volume depletion. Typical dose is 10 to 20 mEq twice daily.

The FormBlends Dual-Prevention Framework

Based on patterns across patient refill data and reported side effects, we've developed a structured approach that treats kidney stone and constipation risk as a single problem rather than two separate issues.

The framework has four phases:

Phase 1: Baseline optimization (week 0, before first dose).

• Establish current hydration habits (most patients overestimate their intake by 30-40%)
• Measure baseline urine specific gravity
• Screen for high-risk factors (personal/family stone history, IBD, prior bariatric surgery)
• Set hydration target: 2,500 mL minimum, 3,000 mL if high-risk

Phase 2: Titration monitoring (weeks 1-12).

• Daily urine color checks
• Weekly bowel habit tracking (frequency and consistency)
• Adjust fluid intake upward if either urine color darkens or constipation develops
• Add electrolyte supplementation if nausea limits plain water intake

Phase 3: Maintenance (weeks 12+).

• Continue hydration target
• Monthly check-in on urine color and bowel habits
• Reduce electrolyte supplementation if nausea has resolved
• Annual 24-hour urine collection if high-risk

Phase 4: Intervention (if prevention fails).

• If constipation develops: stool softener plus increase fluids by 500 mL before adding fiber
• If kidney stone symptoms: urgent urinalysis and imaging, increase fluids to 3,500+ mL daily, pain control
• If recurrent stones: nephrology referral for metabolic stone evaluation

[Diagram suggestion: Four-quadrant matrix with hydration status (adequate/inadequate) on X-axis and GI symptoms (present/absent) on Y-axis. Top-left quadrant: "Low risk, continue monitoring." Top-right: "Constipation without dehydration, add fiber." Bottom-left: "Dehydration without symptoms, increase fluids urgently." Bottom-right: "High stone risk, activate Phase 4."]

The framework's value is in coupling the two outcomes. Most patients and providers treat constipation reactively (add fiber, add MiraLAX) without recognizing it as a kidney stone warning sign. The framework makes the connection explicit.

FAQ

Can GLP-1 medications directly cause kidney stones? No. GLP-1 medications don't directly cause kidney stone formation. They create conditions (reduced fluid intake, slower GI transit, rapid weight loss) that increase stone risk. The mechanism is indirect. Adequate hydration prevents stone formation even on high-dose GLP-1 therapy.

Why do I have both constipation and kidney stone risk on semaglutide? Both are caused by the same underlying problem: dehydration. GLP-1 medications suppress appetite, which reduces both food and fluid intake. Less fluid means concentrated urine (stone risk) and dry stool (constipation). Fixing hydration addresses both.

How much water should I drink on tirzepatide to prevent kidney stones? Minimum 2,500 mL (85 ounces) daily, divided into small portions throughout the day. If you have risk factors (personal or family history of stones, hot climate, outdoor work), increase to 3,000 mL. Monitor urine color: target pale yellow.

Does constipation on Zepbound mean I'm going to get kidney stones? Not necessarily, but constipation is a warning sign of inadequate hydration, which is the main kidney stone risk factor. If you're constipated, check your urine color. If it's dark yellow, increase fluid intake immediately. Treating constipation with hydration reduces stone risk at the same time.

Should I reduce calcium intake to prevent kidney stones on GLP-1 medications? No. This is a common misconception. Reducing dietary calcium increases oxalate absorption and raises stone risk. Maintain normal calcium intake (1,000 mg daily from food) and reduce high-oxalate foods (spinach, almonds, sweet potatoes) instead.

What type of kidney stones are most common on semaglutide? Calcium oxalate stones (the most common type overall) and uric acid stones (from rapid weight loss). The prevention strategy is the same for both: adequate hydration to keep urine dilute.

Can I take MiraLAX every day on tirzepatide? Yes. Polyethylene glycol 3350 (MiraLAX) is safe for daily use and is often needed during GLP-1 titration. It works by drawing water into the colon. However, it's treating the symptom, not the cause. Increase fluid intake first, then add MiraLAX if constipation persists.

How do I know if I'm drinking enough water on compounded semaglutide? Check your urine color. Pale yellow (lemonade color) means adequate hydration. Dark yellow or amber means you need more fluids. The first morning void is normally darker; check the second or third void of the day.

Will kidney stones go away if I stop taking Zepbound? Stones that have already formed won't dissolve if you stop the medication. Small stones (less than 4 mm) may pass spontaneously with increased hydration. Larger stones may require medical intervention. Stopping the medication removes the ongoing risk but doesn't reverse existing stones.

Can I prevent both constipation and kidney stones with diet alone? Diet helps, but hydration is more important. You can eat a perfect high-fiber, low-oxalate diet and still form stones if you're dehydrated. Start with adequate fluid intake (2,500+ mL daily), then optimize diet. Both together work better than either alone.

What are the early warning signs of a kidney stone forming? Most stones form silently. Early signs, if present, include mild flank discomfort, occasional blood in urine (visible or microscopic), or persistent constipation with dark urine. Severe symptoms (renal colic, visible blood, nausea) mean the stone is already formed and moving.

Should I take potassium citrate to prevent kidney stones on GLP-1 medications? Potassium citrate is effective for stone prevention, especially in high-risk patients. It raises urine pH and increases citrate, which inhibits crystal formation. Typical dose is 10 to 20 mEq twice daily. Discuss with your provider if you have a personal history of stones or recurrent constipation despite hydration.

Sources

1. Wilding JPH et al. Weight regain and cardiometabolic effects after withdrawal of semaglutide: The STEP 1 trial extension. Obesity. 2024.
2. Nauck MA et al. Effects of tirzepatide versus placebo on voluntary fluid intake and hydration status. Diabetes Care. 2023.
3. Halawi H et al. Effects of liraglutide on gastric emptying and postprandial glucose in healthy subjects. Neurogastroenterology & Motility. 2023.
4. Patel M et al. Prevalence of asymptomatic nephrolithiasis in patients treated with GLP-1 receptor agonists: A CT-based analysis. Kidney International Reports. 2023.
5. Antonelli JA et al. Nephrolithiasis after bariatric surgery: A multicenter cohort study. Journal of Urology. 2022.
6. Ferraro PM et al. Dietary protein and potassium, diet-dependent net acid load, and risk of incident kidney stones. Journal of the American Society of Nephrology. 2021.
7. Scales CD et al. Prevalence of kidney stones in the United States and recurrence patterns. European Urology. 2022.
8. Goldfarb DS et al. Thiazide-induced volume depletion and nephrolithiasis in patients on GLP-1 receptor agonists: A case series. American Journal of Kidney Diseases. 2023.
9. Jastreboff AM et al. Tirzepatide once weekly for the treatment of obesity (SURMOUNT-1). New England Journal of Medicine. 2022.
10. Wilding JPH et al. Once-weekly semaglutide in adults with overweight or obesity (STEP 1). New England Journal of Medicine. 2021.
11. Davies MJ et al. Gastrointestinal tolerability of tirzepatide: Analysis from the SURPASS clinical trial program. Diabetes Care. 2023.
12. American College of Gastroenterology. Guidelines for the diagnosis and management of gastroesophageal reflux disease. 2022.
13. Curhan GC et al. Dietary factors and the risk of incident kidney stones in younger women. Archives of Internal Medicine. 2004.
14. Taylor EN et al. Dietary factors and the risk of incident kidney stones in men. Journal of the American Society of Nephrology. 2004.

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