Expert Perspectives on Hyperphosphatemia Management in CKD: A Focus on Sucroferric Oxyhydroxide and Phosphate Binders

Umesh B Khanna¹, Prem Prakash Varma², Tarun K Jeloka³, A K Bhalla⁴, Deodatta S Chafekar⁵, Umapati N Hegde⁶, Manoj K Singhal⁷, Sunil Prakash⁸, Sanjeev Gulati⁹, Manju Aggarwal¹⁰, Raj Kumar Sharma¹¹, Rajasekara Chakravarthi¹², Rajan Ravichandran¹³, Sanjeev Kumar Hiremath¹⁴, Anupam Roy¹⁵, Rajesh R Nair¹⁶, Sanjay Srinivasa¹⁷, Apoorva Jain¹⁸, Umang Kasturi¹⁹

¹Consultant Nephrologist, Founder & Director of Kidney Associates, Mumbai, Maharashtra.

²Chairman, Dept of Nephrology, Primus Hospital, New Delhi

³HOD, Manipal Hospitals, Baner, Pune, Maharashtra

⁴Chairman & HOD, Department of Nephrology, Sir Ganga Ram Hospital, New Delhi

⁵Supreme Kidney Care, Nashik

⁶Muljibhai Patel Urological Hospital, Nadiad, Gujarat

⁷Principal Director - Nephrology and Kidney Transplantation, Max Super Speciality Hospital New Delhi

⁸Principal Director & HOD, Department of Nephrology & Transplant Service, BLK - Max Super Speciality Hospital, New Delhi

⁹Executive Director and Head, Nephrology at Fortis Hospitals, Vasant Kunj, New Delhi.

¹⁰Chairperson, Department of Nephrology and Kidney Transplantation, Artemis Health Institute, Sector 51, Gurgaon.

¹¹Director & Head Department of Nephrology & Kidney Transplant Medicine, Medanta Kidney & Urology Institute, Lucknow.

¹²Clinical Director & HOD Nephrology & Transplant services, Yashoda Hospitals, Hitec City, Hyderabad, Telangana

¹³Director nephrology, MIOT International, Chennai

¹⁴Consultant Nephrologist, Sagar Hospitals, Bengaluru

¹⁵Associate Director, Department of Nephrology & Renal Transplant, Venkateshwar Hospital, New Delhi

¹⁶Professor and HOD of Nephrology Amrita Institute of Medical Sciences and Research Centre Amrita School of Medicine Kochi.

¹⁷Consultant Nephrologist, Dr Sanjay"S Center For Kidney and Diabetes, Bengaluru

¹⁸Professor and Head, Dept. of Nephrology, Sarojini Naidu Medical College, Agra, UP

¹⁹Nephrologist at Sir Ganga Ram Hospital, New Delhi

---

Abstract

Calcium and phosphorus homeostasis is crucially regulated by interactions between the kidneys, intestines, and bones, with key hormones like vitamin D, parathyroid hormone (PTH), and fibroblast growth factor 23 playing central roles. As chronic kidney disease (CKD) advances, especially to end-stage renal disease (ESRD), this balance is disrupted, leading to hyperphosphatemia, characterized by serum phosphorus levels >4.5 mg/dL. Hyperphosphatemia is a significant risk factor for cardiovascular complications and mortality in CKD patients, with prevalence ranging from 21% to 40% in those on dialysis, varying by region due to dietary patterns and dialysis practices.

Effective management includes dietary phosphorus restriction and phosphate binders(PBs). Sucroferric oxyhydroxide (SO), an iron-based PB, has shown promise due to its ability to reduce serum phosphorus with a lower pill burden compared to alternatives like sevelamer. This expert opinion aimed to guide SO use in CKD patients with hyperphosphatemia. The experts from various regions of India convened for a structured discussion moderated through live polling. Key insights emphasized that SO is effective, well-tolerated, and cost-effective, offering improved patient adherence due to reduced pill burden.

This guidance is intended to enhance treatment strategies, optimize patient outcomes, and address gaps in current clinical practice for managing hyperphosphatemia in CKD.

---

Introduction

Calcium and phosphorus homeostasis is regulated through interactions between the kidneys, intestines, and bones, with several hormones playing key roles, including active or analog forms of vitamin D, parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF23). As kidney function worsens and progresses to advanced stages of chronic kidney disease (CKD), eventually reaching end-stage renal disease (ESRD) that requires dialysis, this regulatory balance becomes increasingly disrupted.¹ Elevated serum phosphorus (sP) levels have been linked to a higher risk of mortality in both the general population and patients with CKD-MBD (chronic kidney disease-mineral and bone disorder).² Hyperphosphatemia is characterised by serum phosphorus levels exceeding 4.5 mg/dL or 1.78 mmol/L.³ The primary cause of elevated serum phosphate is kidney failure. Specifically, phosphate excretion decreases when the glomerular filtration rate drops below 30 mL/min. In the earlier stages of CKD, compensatory mechanisms, such as increased expression of FGF-23 and PTH, help prevent the development of hyperphosphatemia.⁴

In the general population, the incidence of hyperphosphatemia is around 12%.⁵ In patients with ESRD, it ranges between 50% and 74%.⁶ A recent meta-analysis reported that about 21% of critically ill patients experience elevated serum phosphate levels.⁷ In an Indian observational study by Vikrant et al., the prevalence of hyperphosphatemia progressively increased with advancing stages of CKD, ranging from 32.8% to 83.6%.⁸ Cardiovascular disease is the leading cause of death in individuals with ESRD, and hyperphosphatemia is a non-traditional CKD-related risk factor. It contributes to left ventricular hypertrophy, heart failure, vascular calcification, and arteriosclerosis.⁹

Proteins are high in phosphorus, and most scientific societies recommend reducing protein intake to retard the progression of CKD, which also limits the phosphorus intake. In hemodialysis (HD), the net phosphorus surplus over 48 hours is 1200–1400 mg daily, while dialysis only removes 500–600 mg per session.¹⁰ The Institute of Medicine's Food and Nutrition Board recommends a daily phosphorus intake of 700 mg for healthy adults and 1250 mg for children and pregnant women.¹¹ A diet that is too low in protein can lead to malnutrition and raise the risk of morbidity and mortality.¹² However, a low-protein diet may help slow the progression of kidney disease, whereas a normal or high-protein diet may worsen uremic symptoms and hyperphosphatemia. Achieving the right balance is essential.¹³

An often-overlooked health risk stems from the growing use of phosphate as a food additive and preservative. This "free" phosphate (not organically bound) is highly absorbable in the gastrointestinal tract. Foods commonly containing high levels of added phosphate include processed meats, ham, sausages, canned fish, baked goods, cola, and other soft drinks. Providing dietary guidance is particularly challenging because food packaging does not indicate the total phosphate content, especially the added phosphate.¹⁴ The treatment of hyperphosphatemia in dialysis-dependent CKD primarily involves dietary phosphorus restriction and phosphate binders. Initially, aluminium-based binders were used but were replaced by calcium-based binders due to safety concerns. Although calcium binders are effective and affordable, they raise concerns about vascular calcification, leading to the development of non-calcium binders like sevelamer and lanthanum carbonate and, more recently, iron-based binders such as ferric citrate and sucroferric oxyhydroxide.¹⁵ Sucroferric oxyhydroxide is well tolerated, associated with low systemic iron absorption, minimizes iron overload and reduces fibroblast growth factor-23-lowering effect, rendering it an attractive non-calcium-containing phosphate binder.¹⁶

Sucroferric oxyhydroxide is a potent, iron-based PB with a low daily pill burden, approved for controlling serum phosphorus concentrations in patients with CKD undergoing dialysis.¹⁷ This expert opinion will offer valuable guidance on the effective use of sucroferric oxyhydroxide in managing hyperphosphatemia, helping to bridge gaps in current clinical practice. By integrating expert insights, we can enhance treatment strategies and improve outcomes for CKD patients with elevated phosphorus levels.

Need for Expert Opinion

Despite significant advances in understanding hyperphosphatemia management in CKD, especially with the use of phosphate binders like sucroferric oxyhydroxide, there remains a notable gap in high-quality evidence. Most studies on phosphorus control and its impact on outcomes, including mortality, are observational, limiting the strength of the conclusions drawn. This highlights the need for expert perspectives to address the real-world challenges in managing hyperphosphatemia, particularly in balancing efficacy, safety, and patient adherence. Expert insights can provide valuable guidance where clinical evidence is sparse, helping to refine treatment approaches and optimise patient outcomes.

Methodology

A structured expert opinion exercise was conducted to evaluate the role of SO in managing hyperphosphatemia in CKD. As part of this initiative, two physical meetings were held, bringing together experts from various regions of India for in-person discussions. A moderator facilitated the sessions and guided the deliberations on key questions and perspectives using SO in hyperphosphatemia management. During these meetings, a live polling process was conducted, wherein each expert provided their opinions on nine pre-defined questions. The results of the polling, combined with the consensus insights gathered from the discussions, were subsequently used to formulate expert recommendations.

Expert Opinion

Burden of Hyperphosphatemia in CKD

Discussion: The prevalence of hyperphosphatemia varies globally due to differences in dietary patterns, particularly the type of protein and phosphorus intake, with preserved and canned foods high in phosphorus. Experts emphasized the need for dietary counselling and monitoring of phosphate intake to manage this condition effectively.

Evidence: The dietary source of phosphorus significantly impacts phosphatemia in CKD patients. Organic phosphorus from natural sources has approximately 60% bioavailability in a mixed diet, with lower levels in plant-based foods like legumes and nuts and higher levels in animal-based foods like meat and dairy. In contrast, inorganic phosphorus, added during food processing to enhance shelf life, flavour, and colour, is almost completely absorbed in the intestine, making a substantial contribution to phosphatemia in these patients.¹⁸ Dietitians and nephrologists generally advise dialysis patients to follow a diet low in phosphate, potassium, sodium, and fluids to prevent complications related to electrolyte overload. The challenge of continuous dietary management is intensified by the widespread presence of hidden phosphate additives in modern processed foods and medications. These dietary phosphates are often hidden because manufacturers are not obligated to list phosphate amounts from additives on product labels.¹⁹ Approximately 30% of dialysis patients are estimated to take at least one phosphorus-containing medication.²⁰

Statement 2: The Prevalence of hyperphosphatemia in CKD patients on dialysis is 30-50%. However, the prevalence of hyperphosphatemia in India is lower than in the Western population.

Discussion: Dialysis modalities, such as high-flux dialysis, hemodiafiltration, and dialysis adequacy, influence phosphorus levels. Notably, the prevalence of hyperphosphatemia in India is lower to that of the Western population, likely due to regional factors.

Evidence: Hyperphosphatemia affects up to 40% of patients on dialysis.²¹ According to the US Renal Data System (USRDS), 40% of patients undergoing HD have serum phosphate levels exceeding 5.5 mg/dL.²² Hyperphosphatemia is observed in less than 5% of individuals with normal kidney function or those in CKD stages 1 and 2. However, its prevalence increases with the progression of CKD, becoming more common in stage 3b (estimated glomerular filtration rate [eGFR] ≤ 44 mL/min/1.73 m²) and rising further in stages 4 (eGFR 15-29 mL/min/1.73 m²) at 20%, and stage 5 (eGFR < 15 mL/min/1.73 m²) at 40%.²³ In patients with ESRD, its prevalence ranges from 50% to 74%.⁶

Diagnosis of Hyperphosphatemia

Statement 3: Serum Phosphorus >4.5 mg/dl on more than one occasion (in adults >18 years) is termed hyperphosphatemia.

Discussion: The expert panel recommends diagnosing hyperphosphatemia when serum phosphorus levels exceed 4.5 mg/dL on more than one occasion. Treatment intervention is advised when serum phosphorus levels exceed 5.0–5.5 mg/dL. The initial management strategy should prioritise dietary counselling as a fundamental approach to controlling elevated phosphorus levels.

Evidence: Hyperphosphatemia is a serum phosphorus level exceeding 4.5 mg/dL (1.78 mmol/L). The primary methods to prevent hyperphosphatemia include dietary modifications, phosphate-lowering medications, and intensified dialysis regimens for patients with CKD G5D (GFR < 15ml/min/ 1.73 m²). The 2017 KDIGO guidelines suggested maintaining serum phosphate levels within the normal range for predialysis patients and reducing serum phosphate toward the normal range for those on dialysis.³ The Current Management of Secondary Hyperparathyroidism: A Multicentre Observational Study (COSMOS) of HD patients found that optimal patient survival was associated with serum phosphate levels around 4.4 mg/dL (1.42 mmol/L).²⁴

Statement 4: When serum phosphorous levels of more than 5.5 mg/dl, initiate phosphate-binder therapy

Discussion: In HD-CKD patients, phosphate binders remain the only pharmacological option for managing elevated phosphorus levels. After dietary modifications, if serum phosphorous is still more than 5.5 mg/dL, experts advised phosphate binders as the treatment choice.

Evidence: The National Kidney Foundation's Kidney Disease Outcomes Quality Initiative (KDOQI) Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease (2003) recommend maintaining stricter control of serum phosphorus levels, aiming for a range of 3.5 to 5.5 mg/dL.²⁵ Dietary phosphate restriction and dialysis alone are insufficient or unreliable in reducing phosphate levels to below 5.5 mg/dL. Phosphate binders, which function by binding dietary phosphate in the gut to form insoluble complexes which is excreted in the stool, are currently the only pharmacological option indicated for treating hyperphosphatemia.²⁶

Management of Hyperphosphatemia

Statement 5: Hyperphosphatemia treatment is based on serum phosphorus levels & not on CKD stages.

Discussion: Experts emphasized that hyperphosphatemia treatment should focus on serum phosphorus levels rather than CKD stages, highlighting the importance of individualized management based on biochemical parameters rather than disease progression alone.

Evidence: The 2009 KDIGO CKD-MBD guidelines provided treatment recommendations tailored to managing serum phosphate levels across various CKD stages based on GFR categories.²⁷ According to KDIGO 2017, serum phosphate, calcium, and PTH levels are regularly monitored in CKD patients, and these measurements frequently guide clinical decisions. The guideline Work Group deemed it appropriate to consider the context of therapeutic interventions when evaluating phosphate, calcium, and PTH levels. They emphasized the importance of recognizing the interdependence of these biochemical parameters in guiding clinical treatment decisions. Strategies to prevent hyperphosphatemia primarily involve dietary modifications, phosphate-lowering therapies, and more intensive dialysis schedules for CKD G5D patients.³ The 2009 KDIGO Guideline recommended maintaining serum phosphate levels within the normal range for predialysis patients and reducing them toward the normal range in dialysis patients.²⁷

Statement 6: Sucroferric oxyhydroxide (SO) as a Monotherapy as first-line treatment in the management of Hyperphosphatemia in CKD can be the preferred treatment option due to higher potency and decreased pill burden

Discussion: Studies have shown a higher percentage of patients achieve serum phosphorus levels with SO as first line than other PBs. SO is favoured due to its lower pill burden, better adherence, and cost-effectiveness, as well as its higher potency compared to sevelamer.

Evidence: The selection of phosphate binders should be tailored to each patient's needs, considering their metabolic profile (e.g., iron and calcium levels), safety, pill burden, and cost.²⁸ The SOLO-CKD study was an open-label, multicenter, non-comparative clinical trial assessing SO's efficacy, safety, and tolerability in CKD patients on dialysis. Of the 161 patients screened, 114 met the inclusion criteria, and 94 completed the study. At Week 12, 65.96% of patients achieved a sP level < 5.5 mg/dl, and 28.9% reached < 4.5 mg/dl. Safety analysis showed no significant changes in biochemistry, glucose profile, or clinical parameters, and no serious or treatment-related adverse events were observed. The most frequent side effects were pyrexia, nasopharyngitis and headache, and no patients discontinued the study due to a treatment-emergent adverse event. The study concluded that SO monotherapy is effective and well-tolerated for managing hyperphosphatemia in Indian CKD patients on HD, offering a safe and sustained phosphorus-lowering effect.²⁹ In another study, 596 adults undergoing in-centre HD were prescribed SO monotherapy within their first year of treatment. Among these, 286 patients had a dialysis vintage of ≤3 months. Following SO treatment, there were significant reductions in quarterly sP levels (mean decreases of 0.26–0.36 mg/dL; p < 0.0001 for each quarter and overall). During SO therapy, 55–60% of patients achieved sP levels ≤5.5 mg/dL, while 21–24% reached levels ≤4.5 mg/dL (p < 0.0001 for each quarter and overall compared to baseline). The daily PB pill burden was approximately four pills. Initiating SO as a first-line PB in HD patients significantly reduced sP while keeping the PB pill burden relatively low.³⁰ In the VELREAL study, SO was initiated in 70% of patients due to inadequate sP control and in 24.5% to reduce tablet burden. Monotherapy with SO increased from 44% to 74.1%, reducing the average daily tablet count from six to two. Serum phosphorous levels decreased by 20% (4.6 ± 1.2 vs. 5.8 ± 1.3 mg/dL; P < 0.001), with a 45.4% and 35.9% rise in patients achieving target sP levels of 5 and 4.5 mg/dL, respectively. SO improved sP control, reduced tablet burden, and enhanced therapeutic adherence in real-life settings.³¹ The SO 24-week Phase 3 clinical trial, involving 1,055 patients undergoing HD, found that SO was non-inferior to sevelamer carbonate in reducing sP levels after 12 weeks. It also had a lower daily pill burden (2.8 pills/day compared to 7.6 pills/day) and improved treatment adherence (86.2% vs. 76.9% at Week 24).³² These reductions in serum phosphorus with SO were maintained throughout a subsequent 28-week extension study.³³

The prospective, observational, multicentre FOSFASTUR study included 85 patients: 25 with advanced CKD not on dialysis, 25 on peritoneal dialysis, and 35 on HD. In 66 patients (78%), SO was the initial PB, while in 19, it replaced a previous binder due to poor efficacy or tolerance. After three months of treatment, sP levels significantly decreased by 19.6% (P<.001). These findings support SO as an effective option for managing hyperphosphataemia in advanced CKD and dialysis patients.³⁴

Statement 7: Serum Phosphate level testing to be done once a month in patients on phosphate binders

Discussion: 56% of Experts recommend that when initiating SO / any other PB, serum phosphate testing should be conducted monthly for the first three months to monitor the treatment's effectiveness closely. Following this initial period, if the response is satisfactory, testing can continue every three months to ensure sustained control of serum phosphorus levels.

Evidence: The KDIGO 2017 guidelines recommend serum phosphorus monitoring based on the stage of CKD.³ (Table 1)

Table 1: KDIGO 2017 recommendations for monitoring serum phosphorous as per CKD staging

Stage of CKD	Monitoring
Stage 3	Every 6-12 months
Stage 4	Every 3-6 months
Stage 5	Every 1-3 months

Statement 8: Sucroferric Oxyhydroxide has shown good effectiveness in patients with Hyperphosphatemia.

Discussion: Over 50% of experts emphasized the effectiveness of Sucroferric Oxyhydroxide in managing hyperphosphatemia, highlighting its potential as a reliable phosphate binder for patients with chronic kidney disease (CKD).

Evidence: In a real-world analysis, in adult in-center HD patients who transitioned from another PB to SO monotherapy, SO prescription was linked to a 62% increase in the proportion of patients achieving sP levels ≤ 5.5 mg/dL and a 42% reduction in daily pill burden. The increase in patients reaching sP ≤ 5.5 mg/dL after switching to SO varied by age: 113% in those aged 19–29, 96% in 30–39, 68% in 40–49, 77% in 50–59, 61% in 60–69, 37% in 70–79, and 40% in those ≥ 80 years. Overall, SO prescription improved sP control and reduced pill burden across all age groups.³⁵ A study examined data from 1,029 adult HD patients treated with SO monotherapy for up to 6 months. The majority of these patients initially had poor phosphorus control. Among them, 424 patients received SO prescriptions for more than three consecutive months. Within this group, the proportion achieving target sP levels (≤ 5.5 mg/dL) nearly doubled over the 6-month follow-up period, increasing from 15.6% at baseline to 30.4% (p < 0.0001). Additionally, the daily pill burden of phosphate binders decreased from 9.7 to 4.0 pills/day (p < 0.0001).³⁶ Also, Clinical studies in adults have shown that SO is well tolerated and effectively manages long-term sP levels.^32,33,37

Effectiveness and Benefits of Sucroferric Oxyhydroxide

Statement 9: Efficacy, safety, low pill burden & patient compliance are the important factors that gives a competitive advantage to Sucroferric Oxyhydroxide over other phosphate binders

Discussion: Experts note that the preference for PBs varies across countries, influenced by local practices and availability. Experts advise that SO is an effective option for managing hyperphosphatemia in patients with CKD. It provides reliable control of sP levels and offers the advantages of good tolerability and a significantly lower pill burden compared to other PBs, which can improve patient adherence to therapy.

Evidence: A systematic review analysed seven randomised controlled trials (RCTs), encompassing 11 records and 2,031 adult dialysis patients with hyperphosphatemia. The typical dosage of SO ranges from 750 mg to 3,000 mg per day. SO effectively reduces sP levels, comparable to sevelamer (mean difference [MD] = −0.03 mmol/L, 95% CI −0.10 to 0.03, I² = 49%) and lanthanum (MD = −0.02 mmol/L, 95% CI −0.36 to 0.33, I² = 0%). The decrease in serum phosphorus from baseline is similar to sevelamer (MD = −0.06 mmol/L, 95% CI −0.13 to 0.00, I² = 59%). Importantly, SO significantly reduces the daily pill intake (MD = −7.09 tablets/day, 95% CI −10.45 to −3.73, p < 0.0001, I² = 99%) compared to sevelamer. SO is comparable to sevelamer and lanthanum in reducing sP levels and reducing pill burden, potentially enhancing patient adherence.³⁸ A study compared adult in-center HD patients on two years of uninterrupted SO therapy (maintenance SO; n = 222) with those who discontinued SO within 90 days of the first prescription and switched to other PBs (discontinued SO; n = 596). At quarter 8, 100 patients on maintenance SO reached target phosphorus levels with a reduction in daily pill burden from 7.5 to 4.4 pills (P < 0.001), whereas 190 patients in the discontinued SO group achieved similar levels but without a significant change in pill burden (P = 0.3). Over two years, mean sP levels decreased more in the maintenance SO group (−0.66 mg/dL) compared to the discontinued group (P = 0.014). Additionally, mean daily pill burden decreased in the maintenance SO group (8.5 to 5.1 pills; P < 0.001) but not in the discontinued group (11.6 to 10.9 pills; P = 0.2). Patients on SO therapy were more likely to reach target sP levels, required 50% fewer PB pills daily, and experienced fewer hospital admissions compared to those switched to other binders.³⁹ In terms of safety, Experts support the use of SO based on evidence from clinical trials and real-world studies, which consistently demonstrate its favourable safety and tolerability profile. The most reported side effects are gastrointestinal in nature, primarily black discolouration of stools and mild to moderate, transient diarrhoea, both of which are generally manageable. Importantly, SO exhibits minimal systemic iron absorption, resulting in a low risk of iron overload. Taken together, these attributes make SO an effective and well-tolerated option for the treatment of hyperphosphatemia.⁴⁰

Figure 1: Algorithm for management of Hyperphosphatemia in CKD

Table 2: Expert Opinion

Sr. No.	Expert Opinion
1	Prevalence of hyperphosphatemia varies from one region to another because of diet pattern and type of protein/phosphorus intake – preserved & canned food has high phosphorus content.
2	The prevalence of hyperphosphatemia in CKD patients on dialysis is 30-50%. However, prevalence of hyperphosphatemia in India is lower than Western population.
3	Serum Phosphorus >4.5 mg/dl on more than one occasion (in adults >18 years) is termed hyperphosphatemia.
4	When serum phosphorous levels of more than 5.5 mg/dl, initiate phosphate-binder therapy.
5	Hyperphosphatemia treatment is based on serum phosphorus levels & not on CKD stages.
6	Sucroferric oxyhydroxide (SO) as a Monotherapy as first line treatment in management of Hyperphosphatemia in CKD can be preferred treatment option due to higher potency and decrease pill burden.
7	Serum Phosphate level testing to be done once a month in patients on phosphate binders.
8	Sucroferric Oxyhydroxide has shown good effectiveness in patients with Hyperphosphatemia.
9	Efficacy, safety, low pill burden & patient compliance are the important factors that gives a competitive advantage to Sucroferric Oxyhydroxide over other phosphate binders

Conclusion

The management of hyperphosphatemia in CKD patients requires individualized approaches, focusing on dietary modifications and the appropriate use of PBs. The prevalence of hyperphosphatemia is significantly higher in dialysis patients than in non-dialysis CKD patients, necessitating targeted monitoring. SO has emerged as an effective PB, offering superior sP control, reduced pill burden, and improved adherence compared to other PBs. Experts recommend a preference for SO, especially for HD-CKD patients, while acknowledging a need for more evidence regarding its use in non-dialysis CKD patients.

Acknowledgement

We acknowledge Dr. Sachin Suryawanshi & Dr. Priti Gajbe from Medical services, Emcure Pharmaceuticals, for their support in the development of final manuscript. We also thank IntelliMed Healthcare Solutions Pvt. Ltd, Mumbai, for medical writing assistance and support.

Conflict of Interest

Emcure Pharmaceuticals funded the advisory board meeting related to this expert opinion. However, the sponsor had no role in the conceptualization, methodology, data analysis, or manuscript drafting. The views expressed in this manuscript solely represent the expert panel's opinion.

References

1. Rastogi A, Bhatt N, Rossetti S, et al. Management of Hyperphosphatemia in End-Stage Renal Disease: A New Paradigm. J Ren Nutr. 2021 Jan 1; 31(1): 21–34.
2. Hou Y, Li X, Sun L, et al. Phosphorus and mortality risk in end-stage renal disease: A meta-analysis. Clin Chim Acta. 2017 Nov 1; 474: 108–13.
3. Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Update Work Group. KDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). Kidney Int Suppl. 2017 Jul; 7(1): 1–59.
4. Cernaro V, Santoro D, Lucisano S, et al. The future of phosphate binders: a perspective on novel therapeutics. Expert Opin Investig Drugs. 2014 Nov 1; 23(11): 1459–63.
5. Thongprayoon C, Cheungpasitporn W, Mao MA, et al. Admission hyperphosphatemia increases the risk of acute kidney injury in hospitalized patients. J Nephrol. 2018 Apr 1; 31(2): 241–7.
6. Leaf DE, Wolf M. A Physiologic–Based Approach to the Evaluation of a Patient With Hyperphosphatemia. Am J Kidney Dis Off J Natl Kidney Found. 2013 Feb; 61(2): 330–6.
7. Zheng WH, Yao Y, Zhou H, et al. Hyperphosphatemia and Outcomes in Critically Ill Patients: A Systematic Review and Meta-Analysis. Front Med. 2022 May 17; 9: 870637.
8. Vikrant S, Parashar A. Prevalence and severity of disordered mineral metabolism in patients with chronic kidney disease: A study from a tertiary care hospital in India. Indian J Endocrinol Metab. 2016; 20(4): 460–7.
9. Ogata H, Sugawara H, Yamamoto M, et al. Phosphate and Coronary Artery Disease in Patients with Chronic Kidney Disease. J Atheroscler Thromb. 2024; 31(1): 1–14.
10. Levey AS, Greene T, Beck GJ, et al. Dietary Protein Restriction and the Progression of Chronic Renal Disease: What Have All of the Results of the MDRD Study Shown? J Am Soc Nephrol. 1999 Nov; 10(11): 2426.
11. Medicine I of, Board F and N, Intakes SC on the SE of DR. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. National Academies Press; 1999. 449 p.
12. Fouque D, Pelletier S, Mafra D, et al. Nutrition and chronic kidney disease. Kidney Int. 2011 Aug 2; 80(4): 348–57.
13. Shinaberger CS, Greenland S, Kopple JD, et al. Is Controlling Phosphorus by Decreasing Dietary Protein Intake Beneficial or Harmful in Individuals with Chronic Kidney Disease? Am J Clin Nutr. 2008 Dec; 88(6): 1511–8.
14. Ritz E, Hahn K, Ketteler M, et al. Phosphate Additives in Food—a Health Risk. Dtsch Ärztebl Int. 2012 Jan; 109(4): 49–55.
15. Berner T, Ferro C, Dieguez G, et al. Real-World Phosphate Binder Use among Dialysis-Dependent Patients with CKD. Nephron. 2023 Mar 30; 147(10): 583–90.
16. Sprague SM, and Floege J. Sucroferric oxyhydroxide for the treatment of hyperphosphatemia. Expert Opin Pharmacother. 2018 Jul 3; 19(10): 1137–48.
17. Sucroferric Oxyhydroxide Prescribing Information 2018 [Internet]. [cited 2024 Sep 18]. Available from: https://www.accessdata.fda.gov/drugsatfda_docs/label/2018/205109s006lbl.pdf
18. Uribarri J, Calvo MS. Hidden sources of phosphorus in the typical American diet: does it matter in nephrology? Semin Dial. 2003; 16(3): 186–8.
19. Kalantar-Zadeh K, Brown A, Chen JLT, et al. Dietary Restrictions in Dialysis Patients: Is There Anything Left to Eat? Semin Dial. 2015 Mar; 28(2): 159–68.
20. Nelson SML, Sarabia SRS, Christilaw E, et al. Phosphate-Containing Prescription Medications Contribute to the Daily Phosphate Intake in a Third of Hemodialysis Patients. J Ren Nutr. 2017 Mar 1; 27(2): 91–6.
21. Huang N, Li H, Fan L, et al. Serum Phosphorus and Albumin in Patients Undergoing Peritoneal Dialysis: Interaction and Association With Mortality. Front Med. 2021 Dec 1; 8: 760394.
22. Johansen KL, Chertow GM, Foley RN, et al. US Renal Data System 2020 Annual Data Report: Epidemiology of Kidney Disease in the United States. Am J Kidney Dis Off J Natl Kidney Found. 2021 Apr; 77(4 Suppl 1): A7–8.
23. Rastogi A, Bhatt N, Rossetti S, et al. Management of Hyperphosphatemia in End-Stage Renal Disease: A New Paradigm. J Ren Nutr. 2021 Jan 1; 31(1): 21–34.
24. Fernández-Martín JL, Martínez-Camblor P, Dionisi MP, et al. Improvement of mineral and bone metabolism markers is associated with better survival in haemodialysis patients: the COSMOS study. Nephrol Dial Transplant Off Publ Eur Dial Transpl Assoc - Eur Ren Assoc. 2015 Sep; 30(9): 1542–51.
25. Qunibi WY, Nolan CR. Treatment of hyperphosphatemia in patients with chronic kidney disease on maintenance hemodialysis: Results of the CARE study. Kidney Int. 2004 Sep 1; 66: S33–8.
26. McCullough PA. Phosphate Control: The Next Frontier in Dialysis Cardiovascular Mortality. Cardiorenal Med. 2021 Jun 11; 11(3): 123–32.
27. KDIGO 2009 Clinical Practice Guideline for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease–Mineral and Bone Disorder (CKD–MBD). Kidney Int Suppl. 2009 Aug; 76.
28. Sekar A, Kaur T, Nally JV, et al. Phosphorus binders: The new and the old, and how to choose. Cleve Clin J Med. 2018 Aug; 85(8): 629–38.
29. Niranjan MR, Srinivasa S, Gupta V, et al. Sucroferric oxyhydroxide monotherapy for hyperphosphatemia in Indian chronic kidney disease patients undergoing hemodialysis: A phase IV, single-arm, open-label study. World J Nephrol. 2025 Jun 25; 14(2): 100117.
30. Medaura JA, Zhou M, Ficociello LH, et al. Serum Phosphorus Management with Sucroferric Oxyhydroxide as a First-Line Phosphate Binder within the First Year of Hemodialysis. Am J Nephrol. 2024 Mar; 55(2): 127–35.
31. Navarro-González JF, Arenas MD, Henríquez-Palop F, et al. Real-world management of hyperphosphataemia with sucroferric oxyhydroxide: the VELREAL multicentre study. Clin Kidney J. 2021 Feb 1; 14(2): 681–7.
32. Floege J, Covic AC, Ketteler M, et al. A phase III study of the efficacy and safety of a novel iron-based phosphate binder in dialysis patients. Kidney Int. 2014 Sep; 86(3): 638–47.
33. Floege J, Covic AC, Ketteler M, et al. Long-term effects of the iron-based phosphate binder, sucroferric oxyhydroxide, in dialysis patients. Nephrol Dial Transplant. 2015 Jun; 30(6): 1037–46.
34. Sanchez-Alvarez JE, Astudillo Cortés E, Seras Mozas M, et al. Efficacy and safety of sucroferric oxyhydroxide in the treatment of hyperphosphataemia in chronic kidney disease in Asturias. FOSFASTUR study. Nefrologia. 2021; 41(1): 45–52.
35. Rhee CM, Zhou M, Woznick R, et al. A real-world analysis of the influence of age on maintenance hemodialysis patients: managing serum phosphorus with sucroferric oxyhydroxide as part of routine clinical care. Int Urol Nephrol. 2023; 55(2): 377.
36. Coyne DW, Ficociello LH, Parameswaran V, et al. Real-world effectiveness of sucroferric oxyhydroxide in patients on chronic hemodialysis: A retrospective analysis of pharmacy data. Clin Nephrol. 2017 Aug; 88(2): 59–67.
37. Wüthrich RP, Chonchol M, Covic A, et al. Randomized Clinical Trial of the Iron-Based Phosphate Binder PA21 in Hemodialysis Patients. Clin J Am Soc Nephrol CJASN. 2012 Nov 2; 8(2): 280.
38. Oracion-Relato KR, Flores GP. The effectiveness and safety of sucroferric oxyhydroxide in the treatment of hyperphosphatemia in dialysis patients: a systematic review. Nephrol Dial Transplant. 2024 May 1; 39(Supplement_1): gfae069-0852–1579.
39. Coyne DW, Ficociello LH, Parameswaran V, et al. Sucroferric Oxyhydroxide in Maintenance Hemodialysis: A Retrospective, Comparative Cohort Study. Kidney Med. 2020 Jun; 2(3): 307.
40. Sprague SM, Ketteler M. A safety evaluation of sucroferric oxyhydroxide for the treatment of hyperphosphatemia. Expert Opin Drug Saf. 2021 Dec; 20(12): 1463–72.