The GranStone Trial

Prevention of Kidney Stones Due to Paraffin Oil Induced Granuloma: A Prospective Interventional Study

This study will investigate whether treatment with empagliflozin or losartan can reduce the risk of kidney stone formation in patients with paraffin disease, a condition caused by the injection of paraffin oil into muscle tissue for cosmetic muscle enlargement.

Paraffin disease can lead to chronic inflammation, disturbances in calcium regulation, high blood calcium levels, kidney stones, and impaired kidney function. Previous studies from Herlev-Gentofte Hospital have shown that kidney stones occur in nearly half of affected patients, while approximately one-third develop reduced kidney function. Current treatment primarily consists of high-dose corticosteroids, which can reduce blood calcium levels but cause substantial adverse effects and may not adequately control the underlying disease process.

Both empagliflozin and losartan are widely used medications with documented kidney-protective effects in other chronic kidney diseases. This randomized clinical trial will evaluate whether either treatment can prevent kidney stone formation and slow kidney-related complications in patients with paraffin disease.

The purpose of this study is to determine whether treatment with empagliflozin or losartan can prevent kidney stone formation and improve kidney health in patients with paraffin disease.

Study Overview

• Status: Not yet recruiting
• Conditions: Granuloma, Foreign-Body; Paraffinoma
• Intervention / Treatment: Drug: empagliflozin (Jardiance) 25 mg; Drug: Losartan 100 mg

Detailed Description

Cosmetic treatments are becoming increasingly popular, now also encompassing injection of different sorts of fillers. One such approach is the injection of paraffin oil into muscular regions for the sole purpose of enhancing muscular size. During the last 4 years we have experienced that injections with paraffin oil are being more widely used than anticipated. Usage is mainly seen in the younger segment of the male Danish population, causing severe morbidity including hypercalcemia, kidney stones and renal failure in patients often in their thirties. Injected paraffin oil causes foreign body reactions, leading to inflammation and granuloma formation. Granulomas are rich in macrophages capable of producing large amount of activated vitamin D (1,25OH2D3) that may cause severe hypercalcemia. Although, the link between foreign body granuloma, and hypercalcemia has been known for more than 60 years sparse evidence-based treatments exist to control calcium and vitamin D balance in these patients. Physiologically, cutaneous produced or orally absorbed 25OH2D3 (cholecalciferol) needs activation before it can activate the vitamin D receptor (VDR) and exert its actions. This activation occurs through hydroxylation by CYP27B1 in the kidneys creating the active 1,25(OH)2D3 (calcitriol). CYP27B1 is the rate-limiting step in calcitriol synthesis and is tightly regulated under physiologic conditions. Control of high 1,25(OH)2D3 is achieved by a feedback system, where 1,25(OH)2D3 stimulates the enzyme CYP24A1, which in turn hy-droxylate 1,25(OH)2D3 to the inactive 1,24,25OH2D3. Several other players, e.g. parathy-roid hormone (PTH) and fibroblast growth factor 23 (FGF23) regulate calcium homeostasis. However, in macrophages, CYP27B1 is upregulated by interleukin 2, and the inhibiting enzyme CYP24A1 is not upregulated. Therefore, granulomas can produce large amounts of 1,25OH2D3, and this production is not counteracted by the otherwise tight regulatory and physiological mechanisms. Unimpeded 1,25OH2D3 in turn increase calcium absorption from the intestines, reabsorption from the kidneys and to some extent calcium release from bones, all leading to hypercalcemia. Hypercalcemia is a late feature of accelerated 25OH2D3 activation, as several counter regulatory mechanisms will attempt to maintain normocalcemia. As a result, these patients suffer from nephrolithiasis or progressive kidney disease due to nephrocalcinosis and/or nephrolithiasis, with some patients progressing to end stage renal dis-ease (ESRD).

SGLT2 inhibitors were developed for treatment of type 2 diabetes to lower blood glucose levels but they had a more pronounced effect in patients with heart or renal failure irrespective of diabetes status. SGLT2 inhibitors could prevent or reduce eGFR decline in patients with renal failure and it appeared in some trials that it could also lower the risk of nephrolithiasis. SGLT2 inhibitors have few adverse effects in non-diabetics and may be used to prevent progression of paraffin oil disease by protecting the kidney and reducing the risk of kidney stones in these patients. ACEi's and ARB's have also been shown to reduce progression of kidney disease. Although the data on prevention of kidney stones is less convincing for ACEi/ARB's the renoprotective effects make them a potential treatment option.

Data from our cohort of patients:

During our initial investigation of 88 patients, milder symptoms of hypercalcemia were often accompanied by hypercalcuria with increased risk of kidney stones and later nephrocalcinosis and ultimately progressive renal failure and vascular calcification as seen in patients with primary hyperparathyroidism or CKD. 3 deaths have been recorded in our cohort of young men, so paraffin disease leads to significant morbidity, but presumably also increased mortality. Currently, paraffin disease is still very sparsely described in the medical literature. The number of affected individuals is presumably large because early disease causes few symptoms and many of these men rarely seek medical attention. At the section of Endocrinology at Herlev-Gentofte Hospital, there is currently more than 310 young males who injected paraffin oil prior to referral. In the first published cohort of 88 males (32 ± 7 years (mean ± SD)) who injected paraffin oil 6 years prior to their first visit, the minority (42%) have managed to maintain an apparent normal calcium metabolism (normocalcemic and normoparathyoid), while the majority have developed an abnormal calcium metabolism ranging from normocalcemic and hypoparathyroid (24%) to hypercalcemic and hypoparathyroid (34%). Renal stone formers ranging from 22 % in patients with an apparent normal calcium homeostasis to a stunning 47-48% in those with abnormal calcium homeostasis (5-10% in back-ground population). Importantly, a significant number of patients (approx. 30%) had already developed mild to severe renal impairment with reduced eGFR. Most patients tended to have increased inflammatory markers (interleukine-2 receptor (IL-2R) and/or pepti-dyldipeptidase (ACE)) - even in those with apparent normal calcium metabolism. Surgical resection may improve both local reactions and pain. However, due to granuloma formation within muscle tissue and oilmigration, it is difficult to remove all the granuloma tissue. Currently, first line of treatment for paraffin disease is prednisolone, which has proven effective in lowering calcium levels in all our patients. However, patients require relatively large (15-75 mg daily) and long term (years) doses of prednisolone to achieve and maintain normal or near normal calcium levels with many possible adverse effects. Noteworthy, after 4 years observation we have not yet seen any decrease in inflammatory markers in any male suggesting that prednisolone monotherapy is not enough when you have large amount of granuloma tissue. Paraffin disease mimics sarcoidosis, both being granulomatous diseases with hypercalcemia due to macrophage mediated 25OH2D3 activation. Interestingly, RAAS activation has been shown to contribute to sarcoidosis granuloma formation in an ex vivo model, highlighting an additional potential role for treatment with ACEi/ARB's. However, paraffin disease appears to be much more progressive, not self-limiting and require more aggressive treatment probably because the volume of granulomatous tissue is so huge.

Since ACEi's, ARB's and SGLTi's are the only drug classes consistently shown to slow progression in CKD in a non-diabetic population, we hypothesize that these treatments will be effective in a cohort of patients with hypercalcemia due to paraffin oil induced granulomatous disease. Furthermore, we hypothesize that SGLTi will have a greater effect due to the potential decrease in incident nephrolithiasis. However, the ketosis associated with this treatment may not be beneficial, which clearly justifies the face-to-face comparison.

Losartan was chosen over an ACE inhibitor due to ease of administration and proven safety in patients with severe kidney disease. Additionally, it has been suggested that ARB's have greater efficacy than ACEi's on survival in patients with granulomatous disease due to sarcoidosis.

This research project will investigate whether it is of value to initiate nephroprotective treatment with an SGLT2 inhibitor or ARB in patients with hypercalciuria due to paraffin oil induced granulomatous disease.

• Study Type: Interventional
• Enrollment (Estimated): 100
• Phase: Phase 2; Phase 3

Contacts and Locations

• Study Contact: Name: Martin B Jensen, Professor; Phone Number: +4538687318; Email: martin.blomberg.jensen@regionh.dk
• Study Contact Backup: Name: Emil B Wriedt, MD; Phone Number: +4551185797; Email: emil.brink.wriedt@regionh.dk

Study Locations

• Denmark
  • Herlev, Denmark, 2730
    • Division of Translational Endocrinology, Department of Endocrinology and Internal Medicine, Copenhagen University Hospital Herlev, Herlev
    • Principal Investigator: Martin B Jensen, Professor
    • Sub-Investigator: Emil B Wriedt, MD
    • Contact: Emil B Wriedt, MD; Phone Number: +451185797; Email: emil.brink.wriedt@regionh.dk

Participation Criteria

Eligibility Criteria

• Ages Eligible for Study: Adult; Older Adult
• Accepts Healthy Volunteers: No

Description

Inclusion Criteria:

• Signed informed consent by participant
• Male
• 18-70 years
• Paraffin granuloma disease with hypercalcemia, hypoparathyroidism, hypercalciuria or a history of nephrolithiasis

Exclusion Criteria:

• eGFR < 30 ml/min
• Cancer (past or present, except basal cell skin cancer or squamous cell skin cancer), which in the investigator's opinion could interfere with the results of the trial
• Type 1 DM
• Known chronic kidney disease in whom RAS-blockade and SGLT2-inhibition is indicated.
• Severely impaired liver function
• History of organ transplantation
• Receiving therapy with an SGLT2 inhibitor or ATII antagonist within 8 weeks prior to enrollment or previous intolerance of an SGLT2 inhibitor or ATII antagonist.
• Known history of angioedema
• Mental incapacity, language barriers or unwillingness to comply with the requirements of the protocol, which may preclude adequate understanding or cooperation during the trial, as judged by the investigator

Study Plan

How is the study designed?

Design Details

• Primary Purpose: Treatment
• Allocation: Randomized
• Interventional Model: Parallel Assignment
• Masking: Single

Number of Arms

2

Arms and Interventions

Participant Group / Arm	Intervention / Treatment
Experimental: Empagliflozin; Once daily 25 mg tablet PO	Drug: empagliflozin (Jardiance) 25 mg; Once daily 25 mg tablet PO
Active Comparator: Losartan; Once daily 100 mg tablet PO	Drug: Losartan 100 mg; Once daily 100 mg tablet PO

What is the study measuring?

Primary Outcome Measures

Outcome Measure	Measure Description	Time Frame
Image verified new or increased nephrolithiasis or nephrocalcinosis (from 0-24 months).	The individual components of the composite outcome are defined as follows: If nephrolithiasis- or nephrocalcinosis burden occurs after baseline or aggravates by more than 20% at follow-up it is counted as a positive outcome.; Any CT scans conducted as a part of a participant's routine medical care or hospital visits will also be used.; In the event that a participant undergoes more than 1 CT scan, it will be counted as a positive outcome if any of the scans shows nephrolithiasis or nephrocalcinosis accord-ing to the criteria above.; Symptomatic kidney stone as defined as visible passage of a stone in the urine accom-panied by flank/groin/abdominal pain will also be counted as a positive outcome.	From baseline to end of follow-up at 24 months

Secondary Outcome Measures

Outcome Measure	Measure Description	Time Frame
Change in calcium homeostasis after 12 and 24 months	Change in calcium homeostasis after 12 and 24 months defined by either: 1A Change in p-Calcium ion concentration (mmol/L); 1B Change in p-PTH concen-tration (pmol/L); 1C Change in urine calcium excretion (mmol/L).	From baseline to month 3, 12 and end of follow-up at 24 months
Change in estimated glomerular filtration rate (eGFR) (mL/min/1.73 m²)		From baseline to month 3, 12 and end of follow-up at 24 months
Change in p-Creatinine (μmol/L)		From baseline to month 3, 12 and end of follow-up at 24 months
Change in average daily prednisolone dosage (mg) based on cumulative average prednisolone dose.		From baseline to month 3, 12 and end of follow-up at 24 months
Change in inflammatory activity of the granulomas.	Change in inflammatory activity evaluated by changes in p-IL-2R (kU/L) and p-ACE (U/L).	From baseline to month 3, 12 and end of follow-up at 24 months
Change in physical- and mental health scores assessed by the Short-Form 36 questionnaire (SF-36).	The SF-36 consists of 36 questions designed to assess overall health status. Results are transformed onto a scale from 0 (worst possible health) to 100 (best possible health).	From baseline to end of follow-up at 24 months
Change in serum albumin (g/L)		From baseline to month 3, 12 and end of follow-up at 24 months
Change in urine albumin (mg/L)		From baseline to month 3, 12 and end of follow-up at 24 months
Changes in serum vitamin D metabolites	Changes in serum 25OHD, and 24,25(OH)2D3, and 1,25(OH)2D	From baseline to month 3, 12 and end of follow-up at 24 months
Changes in left ventricular ejection fraction (LVEF) and other indices of cardiac function as measured by transthoracic echocardiography.		From baseline to end of follow-up at 24 months
Incident or worsening signs of: Systolic- and/or diastolic dysfunction, left ventricular hypertrophy, structural heart disease including valvular pathology		From baseline to end of follow-up at 24 months
Changes in CT Hounsfield Units in the femoral neck and lumbar vertebrae		From baseline to end of follow-up at 24 months
Change in Coronary Artery Calcium Score on CT-scan	Coronary artery calcium (CAC) score measured using the Agatston method on non-contrast cardiac CT; higher scores indicate greater coronary calcified plaque burden.	From baseline to end of follow-up at 24 months
Changes in self-reported kidney stones.		From baseline to end of follow-up at 24 months
Change in BUN (mmol/L)		From baseline to month 3, 12 and end of follow-up at 24 months
Change in serum phosphate (mmol/L)		From baseline to month 3, 12 and end of follow-up at 24 months
Change in urine phosphate (mmol/L)		From baseline to month 3, 12 and end of follow-up at 24 months
Change in serum magnesium (mmol/L)		From baseline to month 3, 12 and end of follow-up at 24 months
Change in urine magnesium (mmol/L)		From baseline to month 3, 12 and end of follow-up at 24 months
Change in serum iron (µmol/L)		From baseline to month 3, 12 and end of follow-up at 24 months
Change in serum ferritin (µg/L)		From baseline to month 3, 12 and end of follow-up at 24 months
Change in serum FGF23 (ng/L)		From baseline to month 3, 12 and end of follow-up at 24 months
Change in serum Klotho		From baseline to month 3, 12 and end of follow-up at 24 months
Change in urine Ka (mmol/L)		From baseline to month 3, 12 and end of follow-up at 24 months
Change in urine Na (mmol/L)		From baseline to month 3, 12 and end of follow-up at 24 months
Change in urine pH		From baseline to month 3, 12 and end of follow-up at 24 months
Change in urine citrate (mmol/L)		From baseline to month 3, 12 and end of follow-up at 24 months
Change in urine oxalate (μmol/L)		From baseline to month 3, 12 and end of follow-up at 24 months
Change in urine bicarbonate (mmol/L)		From baseline to month 3, 12 and end of follow-up at 24 months
Change in urine uric acid (mmol/L)		From baseline to month 3, 12 and end of follow-up at 24 months

Collaborators and Investigators

• Sponsor: Martin Blomberg Jensen
• Collaborators: Copenhagen University Hospital at Herlev
• Investigators: Principal Investigator: Martin B Jensen, Professor, Herlev Hospital

Publications and helpful links

General Publications

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• Heerspink HJL, Stefansson BV, Correa-Rotter R, Chertow GM, Greene T, Hou FF, Mann JFE, McMurray JJV, Lindberg M, Rossing P, Sjostrom CD, Toto RD, Langkilde AM, Wheeler DC; DAPA-CKD Trial Committees and Investigators. Dapagliflozin in Patients with Chronic Kidney Disease. N Engl J Med. 2020 Oct 8;383(15):1436-1446. doi: 10.1056/NEJMoa2024816. Epub 2020 Sep 24.
• Brenner BM, Cooper ME, de Zeeuw D, Keane WF, Mitch WE, Parving HH, Remuzzi G, Snapinn SM, Zhang Z, Shahinfar S; RENAAL Study Investigators. Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy. N Engl J Med. 2001 Sep 20;345(12):861-9. doi: 10.1056/NEJMoa011161.
• Laurent S, Boutouyrie P, Asmar R, Gautier I, Laloux B, Guize L, Ducimetiere P, Benetos A. Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in hypertensive patients. Hypertension. 2001 May;37(5):1236-41. doi: 10.1161/01.hyp.37.5.1236.
• Willum-Hansen T, Staessen JA, Torp-Pedersen C, Rasmussen S, Thijs L, Ibsen H, Jeppesen J. Prognostic value of aortic pulse wave velocity as index of arterial stiffness in the general population. Circulation. 2006 Feb 7;113(5):664-70. doi: 10.1161/CIRCULATIONAHA.105.579342.
• Solomon SD, McMurray JJV, Claggett B, de Boer RA, DeMets D, Hernandez AF, Inzucchi SE, Kosiborod MN, Lam CSP, Martinez F, Shah SJ, Desai AS, Jhund PS, Belohlavek J, Chiang CE, Borleffs CJW, Comin-Colet J, Dobreanu D, Drozdz J, Fang JC, Alcocer-Gamba MA, Al Habeeb W, Han Y, Cabrera Honorio JW, Janssens SP, Katova T, Kitakaze M, Merkely B, O'Meara E, Saraiva JFK, Tereshchenko SN, Thierer J, Vaduganathan M, Vardeny O, Verma S, Pham VN, Wilderang U, Zaozerska N, Bachus E, Lindholm D, Petersson M, Langkilde AM; DELIVER Trial Committees and Investigators. Dapagliflozin in Heart Failure with Mildly Reduced or Preserved Ejection Fraction. N Engl J Med. 2022 Sep 22;387(12):1089-1098. doi: 10.1056/NEJMoa2206286. Epub 2022 Aug 27.
• The EMPA-KIDNEY Collaborative Group; Herrington WG, Staplin N, Wanner C, Green JB, Hauske SJ, Emberson JR, Preiss D, Judge P, Mayne KJ, Ng SYA, Sammons E, Zhu D, Hill M, Stevens W, Wallendszus K, Brenner S, Cheung AK, Liu ZH, Li J, Hooi LS, Liu W, Kadowaki T, Nangaku M, Levin A, Cherney D, Maggioni AP, Pontremoli R, Deo R, Goto S, Rossello X, Tuttle KR, Steubl D, Petrini M, Massey D, Eilbracht J, Brueckmann M, Landray MJ, Baigent C, Haynes R. Empagliflozin in Patients with Chronic Kidney Disease. N Engl J Med. 2023 Jan 12;388(2):117-127. doi: 10.1056/NEJMoa2204233. Epub 2022 Nov 4.
• Schillaci G, Pucci G, Pirro M, Monacelli M, Scarponi AM, Manfredelli MR, Rondelli F, Avenia N, Mannarino E. Large-artery stiffness: a reversible marker of cardiovascular risk in primary hyperparathyroidism. Atherosclerosis. 2011 Sep;218(1):96-101. doi: 10.1016/j.atherosclerosis.2011.05.010. Epub 2011 May 18.
• Fares J, El Fadel O, Zhao J, Li M, Sun J, Roman J, Loizidis G, Summer R. Mortality and Health Outcomes Among Patients With Sarcoidosis Treated With Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers. Chest. 2025 Mar;167(3):772-780. doi: 10.1016/j.chest.2024.09.009. Epub 2024 Sep 21.
• Crouser ED, Julian MW, Locke LW, Bicer S, Mitchell JR, Singha A, Kramer PJ, Rajaram MVS, Raman SV. The Renin-Angiotensin-Aldosterone System Regulates Sarcoidosis Granulomatous Inflammation. Am J Respir Crit Care Med. 2024 Aug 15;210(4):497-507. doi: 10.1164/rccm.202402-0265OC.
• Yahyavi SK, Theilade S, Hansen D, Berg JO, Andreassen CH, Lorenzen M, Jorgensen A, Juul A, Faber J, Eldrup E, Blomberg Jensen M. Treatment options for hypercalcemia after cosmetic oil injections: Lessons from human tissue cultures and a pilot intervention study. Bone. 2022 Jan;154:116244. doi: 10.1016/j.bone.2021.116244. Epub 2021 Oct 29.
• Yahyavi SK, Wall-Gremstrup G, Makki A, Juel J, Theilade S, Berg JO, Juul A, Momsen O, Eldrup E, Blomberg Jensen M. Debulking Surgery After Muscular Paraffin Oil Injections: Effects on Calcium Homeostasis and Patient Satisfaction. J Clin Endocrinol Metab. 2025 Feb 18;110(3):649-657. doi: 10.1210/clinem/dgae606.
• Eldrup E, Theilade S, Lorenzen M, Andreassen CH, Poulsen KH, Nielsen JE, Hansen D, El Fassi D, Berg JO, Bagi P, Jorgensen A, Blomberg Jensen M. Hypercalcemia After Cosmetic Oil Injections: Unraveling Etiology, Pathogenesis, and Severity. J Bone Miner Res. 2021 Feb;36(2):322-333. doi: 10.1002/jbmr.4179. Epub 2020 Oct 13.
• Alexander RT, McArthur E, Jandoc R, Welk B, Hayward JS, Jain AK, Braam B, Flockerzi V, Garg AX, Quinn RR. Antihypertensive medications and the risk of kidney stones in older adults: a retrospective cohort study. Hypertens Res. 2017 Sep;40(9):837-842. doi: 10.1038/hr.2017.42. Epub 2017 Mar 23.
• Xie X, Liu Y, Perkovic V, Li X, Ninomiya T, Hou W, Zhao N, Liu L, Lv J, Zhang H, Wang H. Renin-Angiotensin System Inhibitors and Kidney and Cardiovascular Outcomes in Patients With CKD: A Bayesian Network Meta-analysis of Randomized Clinical Trials. Am J Kidney Dis. 2016 May;67(5):728-41. doi: 10.1053/j.ajkd.2015.10.011. Epub 2015 Nov 18.
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• Moraitis AG, Hewison M, Collins M, Anaya C, Holick MF. Hypercalcemia associated with mineral oil-induced sclerosing paraffinomas. Endocr Pract. 2013 Mar-Apr;19(2):e50-6. doi: 10.4158/EP12092.CR.
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• Gyldenlove M, Rorvig S, Skov L, Hansen D. Severe hypercalcaemia, nephrocalcinosis, and multiple paraffinomas caused by paraffin oil injections in a young bodybuilder. Lancet. 2014 Jun 14;383(9934):2098. doi: 10.1016/S0140-6736(14)60806-0. No abstract available.
• Solling ASK, Tougaard BG, Harslof T, Langdahl B, Brockstedt HK, Byg KE, Ivarsen P, Ystrom IK, Mose FH, Isaksson GL, Hansen MSS, Nagarajah S, Ejersted C, Bendstrup E, Rejnmark L. Non-parathyroid hypercalcemia associated with paraffin oil injection in 12 younger male bodybuilders: a case series. Eur J Endocrinol. 2018 Jun;178(6):K29-K37. doi: 10.1530/EJE-18-0051. Epub 2018 Mar 29.
• Nerild HH, Theilade KS, Eldrup E. [Paraffin oil injecions due to bigorexia may cause hypercalcaemia]. Ugeskr Laeger. 2018 Nov 26;180(48):V04180256. Danish.
• Tachamo N, Donato A, Timilsina B, Nazir S, Lohani S, Dhital R, Basnet S. Hypercalcemia associated with cosmetic injections: a systematic review. Eur J Endocrinol. 2018 Apr;178(4):425-430. doi: 10.1530/EJE-17-0938. Epub 2018 Feb 16.
• Levy LL, Emer JJ. Complications of minimally invasive cosmetic procedures: prevention and management. J Cutan Aesthet Surg. 2012 Apr;5(2):121-32. doi: 10.4103/0974-2077.99451.

Study record dates

Study Major Dates

• Study Start (Estimated): September 1, 2026
• Primary Completion (Estimated): March 1, 2029
• Study Completion (Estimated): April 1, 2029

Study Registration Dates

• First Submitted: September 11, 2026
• First Submitted That Met QC Criteria: September 17, 2026
• First Posted (Actual): September 18, 2026

Study Record Updates

• Last Update Posted (Actual): September 18, 2026
• Last Update Submitted That Met QC Criteria: September 17, 2026
• Last Verified: September 1, 2026

More Information

Terms related to this study

• Keywords: Vitamin D; Hypercalcemia; Nephrocalcinosis; Nephrolithiasis; Paraffin Oil; Foreign-Body Granuloma; Intra-Muscular Oil Injection; Paraffinoma
• Additional Relevant MeSH Terms: Urogenital Diseases; Wounds and Injuries; Pathologic Processes; Male Urogenital Diseases; Kidney Diseases; Urologic Diseases; Female Urogenital Diseases; Female Urogenital Diseases and Pregnancy Complications; Urolithiasis; Metabolic Diseases; Water-Electrolyte Imbalance; Granuloma; Calcium Metabolism Disorders; Calcinosis; Pathological Conditions, Signs and Symptoms; Nutritional and Metabolic Diseases; Foreign Bodies; Foreign-Body Reaction; Nephrolithiasis; Hypercalcemia; Nephrocalcinosis; Granuloma, Foreign-Body; Organic Chemicals; Heterocyclic Compounds, 1-Ring; Heterocyclic Compounds; Azoles; Hydrocarbons; Hydrocarbons, Cyclic; Hydrocarbons, Aromatic; Imidazoles; Benzene Derivatives; Tetrazoles; Biphenyl Compounds; Losartan; empagliflozin
• Other Study ID Numbers: 2026-525608-85-00 (Ctis)

Plan for Individual participant data (IPD)

• Plan to Share Individual Participant Data (IPD)?: NO

Drug and device information, study documents

• Studies a U.S. FDA-regulated drug product: No
• Studies a U.S. FDA-regulated device product: No