Patiromer: The Gut Potassium Binder for High Blood Potassium

Table of Contents

1. What High Blood Potassium Is
2. How Patiromer Works in the Colon
3. OPAL-HK: The Main Trial
4. AMETHYST-DN: One Year in Diabetic Kidney Disease
5. DIAMOND and AMBER: Keeping Heart and Kidney Medicines Going
6. How Fast It Works, and the Emergency Room Studies
7. What the US Label States
8. Side Effects: Constipation, Magnesium and Other Minerals
9. The Older and the Newer Binders
10. What Is Not Known
11. Key Research Papers
12. Connections
13. Featured Videos

What High Blood Potassium Is

Potassium is a mineral that carries an electrical charge in body fluids, and the heart depends on the blood level staying inside a narrow range. Several of the trials on this page define hyperkalemia as a blood (serum) potassium level above 5.0 mmol per liter. Doctors write potassium in either mmol per liter or mEq per liter; for potassium the two give the same number. Healthy kidneys remove extra potassium in the urine, so the condition is most common in people with chronic kidney disease, diabetes or heart failure, and in people taking medicines that block the renin-angiotensin-aldosterone system (RAAS), the hormone chain that controls salt, water and blood pressure. RAAS inhibitors include the ACE inhibitors, the angiotensin receptor blockers and the mineralocorticoid receptor blockers such as spironolactone. High potassium is often silent and is usually found on a blood test; the danger lies in its effect on the heart rhythm. The hyperkalemia hub covers the causes, the blood-test bands and the hospital treatment, and the deep-dive pages on heart palpitations and arrhythmia and nausea describe the symptoms.

Patiromer belongs to a group of medicines called potassium binders. They do not stabilise the heart and do not move potassium into cells the way hospital emergency treatments do. They remove potassium from the body over hours to days by trapping it in the gut.

How Patiromer Works in the Colon

Patiromer is a man-made polymer: tiny spherical beads of a cross-linked plastic-like material that does not dissolve in water. The US label names the active ingredient patiromer sorbitex calcium. The beads carry calcium, with sorbitol as part of the counter-ion. As the beads pass through the bowel, they let go of calcium and take up potassium in its place. This trade is called cation exchange. The potassium stays locked in the beads, and the beads leave the body in the stool.

Most of the binding happens in the colon, the last part of the large bowel. A 2016 report from the drug's developers describes patiromer as designed to bind and remove potassium “primarily in the colon”. In laboratory tests at a pH like that of the colon, it bound 8.5 to 8.8 mEq of potassium per gram of polymer, a higher capacity in that test than the older polystyrene sulfonate resins. Studies with radioactively labelled drug in rats and dogs found that patiromer was not absorbed into the circulation. A 2026 review sums up the difference from its newest rival: patiromer “exchanges potassium for calcium in the colon and has a slower onset of action”, while sodium zirconium cyclosilicate binds potassium in exchange for sodium and hydrogen throughout the gut.

The same 2016 report explains why the colon matters. When kidney function falls, the colon steps up its own potassium secretion to compensate, but this adaptation is not enough to stop the blood level rising. In healthy volunteers, patiromer raised the potassium lost in the stool and lowered the potassium lost in the urine, so more of the body’s potassium left through the bowel instead of the kidneys.

The binding is not perfectly selective. In a study of healthy adults, a daily 25.2-gram dose lowered urine potassium by 1,140 mg a day, and also lowered urine magnesium by 45 mg a day and urine sodium by 225 mg a day, while urine calcium rose by 73 mg a day. The authors explain that binding is not specific for potassium, so patiromer can bind other positively charged minerals, and that urine levels reflect what was absorbed from the gut. This is the background to the low-magnesium warning on the label, covered below.

OPAL-HK: The Main Trial

OPAL-HK, published in the New England Journal of Medicine in 2015, is the trial the US label describes as demonstrating the drug’s effect. It enrolled people with chronic kidney disease who were taking at least one RAAS inhibitor and whose potassium was between 5.1 and just under 6.5 mmol per liter. It had two parts.

• Part A, four weeks on the drug for everyone. The trial gave patiromer at a starting dose of 4.2 g or 8.4 g twice a day, depending on how high the potassium was. Among the 237 patients with a usable measurement, the blood potassium fell by an average of 1.01 mmol per liter. At week 4, 76% had reached the target range of 3.8 to just under 5.1 mmol per liter. The US label breaks this down: a fall of 0.65 in those who started between 5.1 and 5.5, and 1.23 in those who started between 5.5 and 6.5.
• Part B, the withdrawal test. 107 people whose starting potassium had been 5.5 or higher and whose level had come into range were randomly assigned to stay on patiromer (55) or switch to a dummy powder (52) for eight weeks. Potassium climbed back to 5.5 or more in 60% of the placebo group against 15% of the patiromer group. The label adds that the median potassium rose by 0.72 mEq per liter on placebo and did not change on patiromer.

Mild-to-moderate constipation was the most common side effect, in 11% of patients, and potassium fell too low (hypokalemia) in 3%.

Two planned sub-group reports from the same trial looked at people with heart failure and at older people. Of the 243 patients treated, 102 (42%) had heart failure; in them, potassium fell by an average of 1.06 mEq per liter over four weeks, and in the withdrawal phase high potassium returned in 52% of the placebo group and 8% of the patiromer group. In patients aged 65 and over, potassium fell by an average of 1.01 mEq per liter. Using a lower cut-off of 5.1, high potassium came back in 92% of the older patients switched to placebo against 30% of those kept on patiromer. Constipation was reported in 15% of the older patients in Part A and 7% in Part B, and potassium below 3.5 and magnesium below 1.4 mg/dL each occurred in 4% of them in Part A.

OPAL-HK was funded by the company developing the drug, and several authors worked for it. It was short and measured blood potassium; it was not built to show whether patiromer prevents heart rhythm problems, hospital stays or deaths.

AMETHYST-DN: One Year in Diabetic Kidney Disease

AMETHYST-DN, published in JAMA in 2015, was an open-label phase 2 trial at 48 sites in Europe between June 2011 and June 2013. It enrolled 306 outpatients with type 2 diabetes, reduced kidney function (an estimated filtration rate of 15 to under 60) and potassium above 5.0 mEq per liter. Every patient was taking a RAAS inhibitor before and during the trial. Its purpose was to pick starting doses and to watch safety over a full year.

Patients were split into a mild and a moderate group by their starting potassium, and the trial gave each person one of three randomly assigned starting doses, which were then adjusted to keep potassium at 5.0 or lower.

• Mild high potassium: at four weeks the potassium fell by 0.35, 0.51 and 0.55 mEq per liter on starting doses of 4.2 g, 8.4 g and 12.6 g twice daily.
• Moderate high potassium: the falls were 0.87, 0.97 and 0.92 mEq per liter on starting doses of 8.4 g, 12.6 g and 16.8 g twice daily.

The lower potassium held at every monthly check from week 4 through week 52. Over the year, low magnesium (hypomagnesemia, 7.2%) was the most common side effect judged to be caused by the drug, mild-to-moderate constipation (6.3%) was the most common gut complaint, and potassium fell below 3.5 mEq per liter in 5.6% of patients. The journal later published a correction for a dosage error in the article text. The trial had no placebo group, so it shows how potassium behaved on the drug over a year rather than proving the drug alone caused every change.

DIAMOND and AMBER: Keeping Heart and Kidney Medicines Going

The RAAS inhibitors protect the heart in heart failure and slow kidney damage in many people with chronic kidney disease, but they raise potassium. A common response to high potassium is to lower the dose or stop the medicine. Two later trials asked whether patiromer lets people stay on these medicines.

DIAMOND (heart failure, 2022)

DIAMOND, published in the European Heart Journal, studied people with heart failure with reduced ejection fraction (a weak pumping heart) who had high potassium on these medicines, or had had it in the past. Of 1,642 people screened, 1,195 entered a run-in phase on patiromer while their doctors raised their medicines to at least half the target dose of an ACE inhibitor, angiotensin receptor blocker or angiotensin receptor-neprilysin inhibitor, plus 50 mg of spironolactone or eplerenone. 878 people (84.6%) reached those doses and were then randomly assigned to keep taking patiromer (439) or switch to placebo (439), with neither patients nor doctors knowing which.

Over a median of 27 weeks, potassium rose by an adjusted 0.03 mmol per liter on patiromer and 0.13 on placebo, a difference of 0.10. Patiromer lowered the risk of potassium going above 5.5 (hazard ratio 0.63) and of the spironolactone or eplerenone dose having to be cut (hazard ratio 0.62). Total high-potassium events were 77.7 per 100 person-years on patiromer against 118.2 on placebo. Adverse events were similar between the groups. DIAMOND measured potassium and medicine use; it did not test whether patiromer reduces heart failure deaths or hospital stays.

AMBER (resistant high blood pressure and kidney disease, 2019)

AMBER, a phase 2 trial in The Lancet, enrolled 295 people with chronic kidney disease (filtration rate 25 to 45) and high blood pressure that had not come under control on other drugs. Everyone was started on spironolactone at 25 mg a day; the trial added either patiromer, starting at 8.4 g once daily, or placebo, without telling patients which. At week 12, 86% (126 of 147) of the patiromer group were still taking spironolactone against 66% (98 of 148) of the placebo group, a difference of 19.5 percentage points. Adverse events, mostly mild or moderate, occurred in 56% and 53%.

How Fast It Works, and the Emergency Room Studies

Patiromer is slow compared with hospital emergency treatment. In a 2015 study, 25 patients with kidney disease and potassium between 5.5 and 6.5 were kept on a fixed diet in a research unit and given 8.4 g with morning and evening meals. Their average starting potassium of 5.93 mEq per liter was measurably lower by 7 hours after the first dose, fell below 5.5 within 20 hours, and was 0.75 lower at 48 hours. The US label reports the same study as a fall of 0.2 at 7 hours and 0.8 at 48 hours, with levels rising again during the days after the drug was stopped.

Two trials have tested the drug in the emergency department:

• A 2020 single-centre pilot randomised 30 dialysis patients with potassium of 6.0 or higher to usual care alone or usual care plus one 25.2 g dose. Potassium was lower in the patiromer group at 2 hours (5.90 against 6.51), but there was no difference at 6 hours, which was the main outcome. The authors described it as a first signal needing more rigorous study.
• PLATINUM, a 2026 double-blind trial at 16 US emergency departments, compared patiromer with placebo on top of usual combination treatment in patients with potassium of 5.8 or higher. It was stopped early, and 111 patients were analysed. Potassium at 2, 4 and 6 hours and the number of extra potassium-lowering treatments needed were similar in both groups. The authors noted that the trial was too small to detect a difference.

The US label carries a matching limitation: patiromer is not for emergency treatment of life-threatening high potassium, because its effect is delayed.

What the US Label States

The US prescribing information lists an initial approval in 2015. Its points, as written in the current label:

• Approved use: treatment of high potassium in adults and in children aged 12 and older. It is not approved as emergency treatment for life-threatening high potassium, because its onset is delayed.
• Dose for adults: the label gives a starting dose of 8.4 g once a day, adjusted by 8.4 g at intervals of one week or longer according to the blood potassium, up to 25.2 g once a day.
• Dose for ages 12 to 17: the label gives a starting dose of 4 g once a day, adjusted in 4 g steps at intervals of one week or longer. In a study that included 9 children aged 6 to under 12, the regimen tested did not appear to lower potassium (an average change of −0.1 mEq per liter after two weeks), and the label gives no dose for that age group.
• The 3-hour rule: patiromer can bind other medicines taken by mouth in the gut and reduce how much is absorbed. The label states that other oral medicines are taken at least 3 hours before or 3 hours after patiromer, except those tested and shown not to interact. Its list of drugs with a clinically important interaction includes telmisartan, bisoprolol, carvedilol, nebivolol, ciprofloxacin, levothyroxine, metformin, mycophenolate mofetil, quinidine and thiamine. Its list with no important interaction includes many common heart and kidney drugs, among them several ACE inhibitors and angiotensin receptor blockers, spironolactone, eplerenone, finerenone, furosemide, metoprolol, warfarin, apixaban and the SGLT2 inhibitors.
• Preparation: the powder is not taken dry and not heated. The label describes stirring it into about a third of a cup of water, or into soft foods such as apple sauce or yogurt; it does not dissolve and the mixture looks cloudy. It can be taken with or without food.
• Warnings: worsening of bowel movement problems, and low magnesium. People with severe constipation, bowel blockage or impaction, abnormal bowel movement after surgery, a history of bowel obstruction or major bowel surgery, severe gut disorders or swallowing disorders were not included in the trials, and the label states that the drug may not work and may worsen the bowel problem in severe constipation, blockage or impaction.
• Only contraindication: a past allergic reaction to the drug or its ingredients.
• Pregnancy and breastfeeding: because it is not absorbed, the label states that use is not expected to put the unborn baby or a breastfed infant at risk.
• Overdose: doses above 50.4 g a day have not been tested; too much can drive potassium too low.

The 3-hour rule comes from a set of twelve studies in healthy volunteers. Taken at the same time as patiromer, nine of the twelve test drugs were absorbed normally. Ciprofloxacin was absorbed less (its total exposure fell to 71.5% of normal), and levothyroxine and metformin showed smaller reductions. When patiromer was taken 3 hours after each drug, all twelve were absorbed within the normal range.

Side Effects: Constipation, Magnesium and Other Minerals

The US label pools 666 adults who took patiromer in the trials. The side effects reported in 2% or more were:

• Constipation: 7.2% (it generally settled during treatment, according to the label)
• Low magnesium (hypomagnesemia): 5.3%
• Diarrhea: 4.8%
• Nausea: 2.3%
• Abdominal discomfort: 2.0%
• Flatulence: 2.0%

Gut side effects led 2.7% of patients to stop the drug. Mild-to-moderate allergic reactions, including swelling of the lips, were reported in 0.3%. On blood tests, about 4.7% of adults had a potassium below 3.5 mEq per liter and about 9% had a magnesium below 1.4 mg/dL. The label explains the magnesium effect directly: the drug binds magnesium in the colon. Its warning section calls for blood magnesium to be monitored. Patients aged 65 and over, who made up 60% of the trial population, reported more gut side effects than younger patients.

A pooled analysis of the four-week phases of three trials (AMETHYST-DN, OPAL-HK and TOURMALINE), covering 626 people with kidney disease, found potassium falls of 0.84 mEq per liter in those with more advanced kidney disease (filtration rate under 45) and 0.60 in those with milder disease. Constipation was reported in 8% and 3% of these two groups, diarrhea in 4% and 2%, and side effects led 6% and 2% to stop the drug.

Because patiromer releases calcium as it binds potassium, researchers have also looked at bone and mineral markers. In the four-week TOURMALINE study, blood calcium did not change (an average change of 0.0 mg/dL), blood magnesium fell by an average of 0.2 mg/dL, and parathyroid hormone fell by a median of 13 pg/mL. Urine phosphate fell, and in the small group of patients who started with high phosphate, blood phosphate also fell. The authors report this in a small subset of patients; phosphate lowering is not an approved use.

The Older and the Newer Binders

Patiromer is one of three potassium binders whose US labels were read for this page. No randomised trial comparing their potassium-lowering effect head to head has been published in full; a 2026 review states that “no head-to-head randomised trials are available”, and a four-arm trial comparing all three in hospital patients (KBindER) appears in PubMed only as a design paper so far. What follows sets the three side by side from their own labels and trials, which used different patients and different measures and cannot be compared directly.

Sodium polystyrene sulfonate (the older resin)

Sodium polystyrene sulfonate is a resin first approved in the United States in 1958. It swaps sodium for potassium, and its label states that each 15 g dose contains 1,500 mg (60 mEq) of sodium and that people sensitive to sodium, such as those with heart failure, high blood pressure or swelling, are watched for fluid overload. Its label warns of intestinal necrosis (death of bowel tissue), some cases fatal, and of other serious bowel injuries such as bleeding, ischemic colitis and perforation; most reported cases involved sorbitol given at the same time. Like patiromer, its label sets a 3-hour separation from other oral medicines (6 hours in people with gastroparesis) and states it is not an emergency treatment. For a long time there was little trial evidence for it; a 2015 randomised trial in 33 outpatients with kidney disease and mild high potassium found that 30 g once daily for seven days lowered potassium by 1.04 mEq per liter more than placebo, with a trend toward more electrolyte disturbances and gut side effects.

Sodium zirconium cyclosilicate (the newer crystal)

Sodium zirconium cyclosilicate is a non-absorbed crystal approved in the United States in 2018. Its label states that it captures potassium in exchange for hydrogen and sodium and that potassium falls were seen one hour after the first dose. In the HARMONIZE trial, 84% of 258 outpatients reached a normal potassium within 24 hours on the starting regimen and 98% within 48 hours. Its label notes that each 5 g dose contains about 400 mg of sodium; swelling (edema) was reported in 4.4%, 5.9% and 16.1% of patients on 5 g, 10 g and 15 g a day against 2.4% on placebo. Its label separates other oral medicines by 2 hours, and it too states it is not an emergency treatment.

Patiromer

Patiromer contains no sodium; it uses calcium as its exchange ion. The trade-offs described in the 2026 review are that patiromer is associated with low magnesium while sodium zirconium cyclosilicate delivers a sodium load that may predispose to fluid retention, and that patiromer has the slower onset.

One randomised study did compare the three directly, but on taste rather than effect. In the APPETIZE study, 144 people with kidney disease and high potassium tasted each binder, blinded, and spat it out. In every region studied, sodium zirconium cyclosilicate and patiromer scored higher than the polystyrene sulfonate resins on overall palatability, and a numerically larger share ranked sodium zirconium cyclosilicate as their first choice.

What Is Not Known

• Hard outcomes. The trials measured blood potassium and whether people stayed on their RAAS inhibitors. None of those on this page was designed to show that patiromer prevents heart rhythm emergencies, hospital admissions, kidney failure or death. The 2026 review describes the evidence for improvement in heart failure illness or death as limited.
• Comparison with the other binders. No published randomised trial compares patiromer’s potassium-lowering effect with that of sodium polystyrene sulfonate or sodium zirconium cyclosilicate.
• Emergencies. The two emergency-department trials were small, and the larger one was stopped early. Whether patiromer adds anything to standard emergency treatment remains unsettled.
• Children under 12. The label gives no dose for this age group because the regimen studied did not appear to work.
• Long-term mineral effects. The falls in magnesium and parathyroid hormone and the shifts in urine calcium and phosphate are documented over weeks to a year; their meaning for bone and heart health over many years has not been studied in long trials.
• Who produced the evidence. OPAL-HK and AMBER were funded by the drug’s developer; AMETHYST-DN and DIAMOND included authors employed by the developer or the company that later sold the drug; and the 2016 mechanism report was written by the developer’s scientists.

Decisions about potassium-lowering medicines belong with the clinician who is following a person’s blood tests.

Key Research Papers

1. Weir MR, Bakris GL, Bushinsky DA, Mayo MR, Garza D, Stasiv Y, et al. Patiromer in patients with kidney disease and hyperkalemia receiving RAAS inhibitors. N Engl J Med. 2015;372(3):211-21. PubMed PMID: 25415805
2. Pitt B, Bakris GL, Bushinsky DA, Garza D, Mayo MR, Stasiv Y, et al. Effect of patiromer on reducing serum potassium and preventing recurrent hyperkalaemia in patients with heart failure and chronic kidney disease on RAAS inhibitors. Eur J Heart Fail. 2015;17(10):1057-65. PubMed PMID: 26459796
3. Weir MR, Bushinsky DA, Benton WW, Woods SD, Mayo MR, Arthur SP, et al. Effect of Patiromer on Hyperkalemia Recurrence in Older Chronic Kidney Disease Patients Taking RAAS Inhibitors. Am J Med. 2018;131(5):555-564.e3. PubMed PMID: 29180023
4. Bakris GL, Pitt B, Weir MR, Freeman MW, Mayo MR, Garza D, et al. Effect of Patiromer on Serum Potassium Level in Patients With Hyperkalemia and Diabetic Kidney Disease: The AMETHYST-DN Randomized Clinical Trial. JAMA. 2015;314(2):151-61. PubMed PMID: 26172895
5. Butler J, Anker SD, Lund LH, Coats AJS, Filippatos G, Siddiqi TJ, et al. Patiromer for the management of hyperkalemia in heart failure with reduced ejection fraction: the DIAMOND trial. Eur Heart J. 2022;43(41):4362-4373. PubMed PMID: 35900838
6. Agarwal R, Rossignol P, Romero A, Garza D, Mayo MR, Warren S, et al. Patiromer versus placebo to enable spironolactone use in patients with resistant hypertension and chronic kidney disease (AMBER): a phase 2, randomised, double-blind, placebo-controlled trial. Lancet. 2019;394(10208):1540-1550. PubMed PMID: 31533906
7. Haller H, Bianchi S, McCafferty K, Arthur S, Quinn CM, Budden J, et al. Safety and Efficacy of Patiromer in Hyperkalemic Patients with CKD: A Pooled Analysis of Three Randomized Trials. Kidney360. 2022;3(12):2019-2026. PubMed PMID: 36591361
8. Li L, Harrison SD, Cope MJ, Park C, Lee L, Salaymeh F, et al. Mechanism of Action and Pharmacology of Patiromer, a Nonabsorbed Cross-Linked Polymer That Lowers Serum Potassium Concentration in Patients With Hyperkalemia. J Cardiovasc Pharmacol Ther. 2016;21(5):456-65. PubMed PMID: 26856345
9. Bushinsky DA, Spiegel DM, Gross C, Benton WW, Fogli J, Hill Gallant KM, et al. Effect of Patiromer on Urinary Ion Excretion in Healthy Adults. Clin J Am Soc Nephrol. 2016;11(10):1769-1776. PubMed PMID: 27679518
10. Bushinsky DA, Spiegel DM, Yuan J, Warren S, Fogli J, Pergola PE. Effects of the Potassium-Binding Polymer Patiromer on Markers of Mineral Metabolism. Clin J Am Soc Nephrol. 2019;14(1):103-110. PubMed PMID: 30381412
11. Lesko LJ, Offman E, Brew CT, Garza D, Benton W, Mayo MR, et al. Evaluation of the Potential for Drug Interactions With Patiromer in Healthy Volunteers. J Cardiovasc Pharmacol Ther. 2017;22(5):434-446. PubMed PMID: 28585859
12. Bushinsky DA, Williams GH, Pitt B, Weir MR, Freeman MW, Garza D, et al. Patiromer induces rapid and sustained potassium lowering in patients with chronic kidney disease and hyperkalemia. Kidney Int. 2015;88(6):1427-1433. PubMed PMID: 26376130
13. Rafique Z, Safdar B, Duanmu Y, Boone S, Meltzer A, Bischof JJ, et al. Patiromer utility as an adjunct treatment in patients needing urgent hyperkalaemia management (PLATINUM): a randomised controlled trial in the emergency department. BMJ Open. 2026;16(2):e105103. PubMed PMID: 41730555
14. Lepage L, Dufour AC, Doiron J, Handfield K, Desforges K, Bell R, et al. Randomized Clinical Trial of Sodium Polystyrene Sulfonate for the Treatment of Mild Hyperkalemia in CKD. Clin J Am Soc Nephrol. 2015;10(12):2136-42. PubMed PMID: 26576619
15. Packham DK, Rasmussen HS, Lavin PT, El-Shahawy MA, Roger SD, Block G, et al. Sodium zirconium cyclosilicate in hyperkalemia. N Engl J Med. 2015;372(3):222-31. PubMed PMID: 25415807
16. Kosiborod M, Rasmussen HS, Lavin P, Qunibi WY, Spinowitz B, Packham D, et al. Effect of sodium zirconium cyclosilicate on potassium lowering for 28 days among outpatients with hyperkalemia: the HARMONIZE randomized clinical trial. JAMA. 2014;312(21):2223-33. PubMed PMID: 25402495
17. Wheeler DC, Søndergaard H, Gwynn C, Hedman K, Hedberg J, Allum A, et al. Randomised, blinded, cross-over evaluation of the palatability of and preference for different potassium binders in participants with chronic hyperkalaemia in the USA, Canada and Europe: the APPETIZE study. BMJ Open. 2024;14(2):e074954. PubMed PMID: 38387989
18. Prajapathi S, Pradhan A, Mahajan K, Agarwala R, Alfonso Perrone M. Overcoming Hyperkalaemia to Optimise Heart Failure Therapy: The Emerging Role of Novel Potassium Binders. Card Fail Rev. 2026;12:e32. PubMed PMID: 42866084

The US prescribing information for patiromer, sodium polystyrene sulfonate and sodium zirconium cyclosilicate was read on DailyMed (National Library of Medicine). The 2020 emergency-department pilot study is described from its abstract (Acad Emerg Med. 2020;27(1); PubMed PMID: 31599043) and the KBindER design from its protocol paper (PubMed PMID: 37016309).

PubMed Topic Searches

1. PubMed: Patiromer randomized trials in hyperkalemia
2. PubMed: Patiromer, heart failure and RAAS inhibitors
3. PubMed: Patiromer and low magnesium
4. PubMed: Potassium binders compared

Connections

• Drugs — every drug page on the site
• Hyperkalemia (High Potassium) — causes, blood-test bands and hospital treatment
• Hyperkalemia and Heart Palpitations — why high potassium endangers the heart rhythm
• Hyperkalemia and Nausea — the gut symptoms and their usual causes
• Potassium — the mineral itself
• Hypomagnesemia (Low Magnesium) — the mineral patiromer can lower
• Kidney Disease — the condition behind most high potassium
• Diabetic Nephropathy — the kidney disease studied in AMETHYST-DN
• Heart Failure — the condition studied in DIAMOND
• Finerenone — a kidney-and-heart drug whose labelled potassium rules matter here

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