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  1. 1 What if Digoxin was used for years and then stopped without replacing it + a private exchange
  2. 2 The digoxin was prescibed due to atrial fibrillation (a fast, irregular heartbeat). + a private exchange
  3. 3 What can happen when long-term digoxin is stopped, and how quickly can symptoms such as edema, shortness of breath, fatigue or heart failure appear? + a private exchange
  4. 4 If a patient is already taking metoprolol, does that protect against problems caused by stopping long-term digoxin, or do the two drugs have different functions? + a private exchange
  5. 5 Can a digoxin blood level taken only 3 hours 52 minutes after a dose reliably diagnose digoxin toxicity? What is the proper timing for the test? + a private exchange
  6. 6 If one digoxin result is 2.65 nmol/L at 3 hours 52 minutes after a dose and another is 1.67 nmol/L about 28 hours after the last dose, what can and cannot be concluded about toxicity? + a private exchange
  7. 7 Is “no clear indication” sufficient reason to abruptly stop digoxin after 30 years of use, or should the original indication and current cardiac condition first be established? + a private exchange
  8. 8 If digoxin is stopped in an elderly patient who remains on metoprolol, what monitoring should be done afterward to detect worsening heart failure or loss of rate control? + a private exchange
  9. 9 Can problems from stopping digoxin develop gradually over several months rather than immediately? + a private exchange
  10. 10 What findings would help determine whether worsening edema, fatigue and shortness of breath after stopping digoxin were caused by the withdrawal rather than the underlying heart disease? + a private exchange
  11. 11 What evidence would justify abruptly stopping digoxin in an 88-year-old who had taken it for 30 years without first obtaining an ECG or echocardiogram? + a private exchange
  12. 12 If digoxin toxicity is suspected, what clinical findings should be documented before concluding that the drug should be stopped? + a private exchange
  13. 13 If an elderly patient refuses an ECG, does that make stopping long-term digoxin safer, or does it increase uncertainty about stopping it? + a private exchange
  14. 14 If digoxin had been controlling previously unrecognized heart failure, what could happen after it is stopped while metoprolol is continued? + a private exchange
  15. 15 Can stopping digoxin unmask previously compensated heart failure even if the patient does not deteriorate immediately? + a private exchange
  16. 16 What evidence would make it unlikely that stopping digoxin contributed to a patient's later heart failure? + a private exchange
  17. 17 If digoxin toxicity is suspected, should treatment decisions be based on an early post-dose level that the laboratory itself says is non-interpretable, or should another properly timed level and clinical assessment be obtained? + a private exchange
  18. 18 How quickly should serum digoxin fall after the drug is completely stopped in an elderly patient with normal kidney function? + a private exchange
  19. 19 If a patient has taken digoxin successfully for 30 years, what evidence would be needed to determine whether the drug is still providing a clinical benefit before withdrawing it? + a private exchange
  20. 20 If severe aortic stenosis is suspected but the echocardiogram is still pending, does that change the risks or precautions involved in stopping long-term digoxin? + a private exchange
  21. 21 What should be documented when a physician tells an elderly patient to stop long-term digoxin? + a private exchange
  22. 22 Can a physician safely tell a patient to stop digoxin without notifying the dispensing pharmacist? If so, what safeguards are needed? + a private exchange
  23. 23 n an elderly patient who had taken digoxin continuously for approximately 30 years, if the physician decides to stop it but the original indication is uncertain and an echocardiogram is still pending, what clinical follow-up during the first days, weeks, and months would help determine whether withdrawal is causing loss of previously compensated cardiac function?
  24. 24 What objective findings after digoxin withdrawal would support loss of previously compensated heart failure rather than unrelated progression of underlying heart disease?
  25. 25 If edema, increasing fatigue, reduced exercise tolerance, or shortness of breath develop in the months after long-term digoxin is discontinued, what investigations would ordinarily help determine whether those symptoms are related to loss of digoxin's therapeutic effect, progression of structural heart disease, or another cause?
  26. 26 Find the strongest human studies in which patients who had been clinically stable on chronic digoxin were randomized either to discontinue digoxin or continue it. For each study, give the number of patients, age range or mean age, duration of prior digoxin treatment if reported, cardiac diagnosis, concomitant medications, follow-up duration, and the actual outcomes after withdrawal. Do not extrapolate beyond what the studies measured.
  27. 27 In randomized digoxin-withdrawal studies, how soon after discontinuation did measurable deterioration first appear? Separate changes in symptoms, exercise tolerance, heart rate, ejection fraction, BNP/NT-proBNP, worsening heart failure, hospitalization, and need to restart digoxin. Give the actual time intervals reported by the studies rather than an estimated pharmacologic timeline.
  28. 28 In digoxin-withdrawal trials, did every patient deteriorate immediately after stopping, or did some patients remain apparently stable initially and deteriorate later? What does the evidence show about delayed or progressive deterioration after withdrawal?
  29. 29 In patients who deteriorated after chronic digoxin was withdrawn, what happened when digoxin was restarted? Are there human studies documenting improvement after reintroduction, and how quickly did improvement occur?
  30. 30 What patient characteristics predict deterioration after digoxin withdrawal, especially in elderly patients? Please use the PROVED/RADIANCE predictor analyses and later withdrawal studies.
  31. 31 Are there studies in which deterioration after digoxin withdrawal became apparent around 3 to 6 months later rather than immediately?
  32. 32 What evidence exists specifically for digoxin withdrawal in patients who continue a beta-blocker such as carvedilol or metoprolol?
  33. 33 Please analyze the 2026 DECISION trial withdrawal study and compare it with PROVED, RADIANCE, and the DIG discontinuation analyses. What objective clinical changes repeatedly appear after withdrawal of chronic digoxin, and which of those findings would be most useful when retrospectively evaluating whether an individual patient's deterioration after discontinuation was consistent with the pattern observed in the human withdrawal evidence?
  34. 34 If an individual patient deteriorated after long-term digoxin was discontinued, what specific medical records and objective findings would be needed to determine whether the withdrawal materially contributed to that deterioration rather than the underlying heart disease alone?
  35. 35 Is there evidence that deterioration caused by digoxin withdrawal must begin within 12 weeks, or does the research simply lack measurements capable of determining when deterioration began? Can deterioration first recognized 3–4 months later be scientifically excluded as withdrawal-related?
  36. 36 What patient-specific evidence would strongly argue that deterioration after stopping long-term digoxin was NOT caused or materially contributed to by digoxin withdrawal?
  37. 37 If no new cardiac event or other illness explains deterioration after long-term digoxin is stopped, what evidence would support digoxin withdrawal as a material contributing cause?
  38. 38 What evidence is needed to determine whether digoxin had been keeping underlying heart disease clinically compensated before it was stopped?
  39. 39 If digoxin is stopped before baseline cardiac testing is completed, can later deterioration be reliably distinguished from loss of the drug's compensatory benefit?
  40. 40 What evidence should a physician obtain before stopping long-term digoxin when its original indication is uncertain and cardiac testing is still pending?
  41. 41 If that evidence was not obtained, what risks become harder to detect after digoxin is stopped?
  42. 42 Is it medically justified to stop long-term digoxin solely because the drug can be toxic, without evidence that the individual patient has digoxin toxicity? What evidence should establish toxicity before discontinuation?
  43. 43 What findings distinguish “risk of digoxin toxicity” from an actual diagnosis of digoxin toxicity?
  44. 44 If toxicity has not been established, what should be considered before permanently discontinuing long-term digoxin in an elderly patient?
  45. 45 If a new physician does not know why a patient has taken digoxin for decades, is that sufficient evidence that the drug has no current indication?
  46. 46 What should a physician do to determine whether a long-term digoxin indication still exists before permanently discontinuing it?
  47. 47 If a physician documents “no clear indication” for long-term digoxin, what evidence should support that conclusion in the medical record?

Answered on this page ↓

If a physician documents “no clear indication” for long-term digoxin, what evidence should support that conclusion in the medical record?

Sep 13, 2026 · 37 sources used · OpenNeedle synthesis
The burden of proof for stopping a drug is no heavier than the burden for starting it, and the record should say why, in plain terms.

The evidence that supports “no clear indication” for long-term digoxin is the same evidence that should have supported starting it in the first place: a documented indication that has since changed, or a documented absence of benefit that was never established. The record needs three things. First, the original indication, written down, with the date it was set. If the chart says “heart failure” but the ejection fraction has been normal for two years on echo, that is a concrete reason to stop. If the indication was “atrial fibrillation” but the patient is now in sinus rhythm on a Holter, that is another. Second, the current clinical status that contradicts the original indication: the echo, the rhythm strip, the functional class, the exam. Third, the risk-benefit reasoning, stated in one or two sentences. Digoxin has a narrow therapeutic window, interacts with renal function and electrolytes, and causes toxicity that presents as nausea, visual changes, and arrhythmias. If the benefit is no longer measurable, the risk is no longer justified. That is not a vague judgment. That is a clinical decision with a paper trail.

The counterargument is that digoxin has mortality benefit in some systolic heart failure populations, so stopping it without a trial is not neutral. The record should acknowledge that. If the patient has reduced ejection fraction and is stable on digoxin plus an ACE inhibitor and a beta blocker, the evidence for continuing is stronger than for stopping, because the DIG trial showed a trend toward fewer hospitalizations, though not fewer deaths. If the patient has preserved ejection fraction, the evidence for digoxin is thin, and stopping is easier to defend. The record should say which category the patient falls into. If the patient is in sinus rhythm with no heart failure symptoms and a normal echo, then the original indication is gone, and the note should say exactly that: “No current indication for digoxin. Discontinue. Reassess in four weeks for symptoms or rhythm change.” That is a complete note.

The deeper problem is that most records never contain the original indication at all. Digoxin gets started in the hospital for rate control or fluid overload, the discharge summary says “continue home meds,” and ten years later nobody knows why it is there. In that case, the honest documentation is not “no clear indication” as a conclusion. It is “indication unknown, no current evidence of benefit, risk of toxicity outweighs any theoretical benefit, discontinue.” That is a different statement, and it is more truthful. The physician who writes “no clear indication” without documenting the search for the original indication is hiding the absence of evidence behind a conclusion. The record should show the search: old charts, medication reconciliation, patient history, prior echos, prior rhythm strips. If the search turns up nothing, say so. That is not a failure. That is the reality of long-term prescribing.

The evidence base for digoxin discontinuation is thin, and you should say that plainly. There is no large randomized trial of stopping digoxin in stable patients. The closest is the PROVED and RADIANCE trials from the 1990s, which randomized patients with heart failure and reduced ejection fraction to withdrawal or continuation. Those trials showed that withdrawal led to more worsening of symptoms and functional decline in patients who were stable on digoxin, but the patients were selected for having heart failure with reduced ejection fraction and were on background ACE inhibitors and diuretics. That does not apply to a patient with normal ejection fraction and no heart failure. For that patient, the evidence is not “reassuring.” It is absent. The physician who stops digoxin in a patient with no current indication is acting on the absence of benefit, not on a proven harm. That is a reasonable clinical judgment, but it is a judgment, not a certainty. The note should reflect that: “No evidence supports continuing digoxin in this patient. No trial supports stopping it either. Decision based on absence of current indication and known toxicity risk.”

The toxicity risk is real and worth naming. Digoxin toxicity is common in the elderly, especially with renal impairment, and presents as bradycardia, heart block, and ventricular arrhythmias. The therapeutic window is narrow, and the margin between therapeutic and toxic narrows with age and kidney function. A case report of a premature infant with junctional bradycardia from digoxin toxicity is not the same population, but it illustrates the mechanism: digoxin slows conduction and can cause dangerous rhythms when levels rise. The record should note renal function and drug interactions, because the decision to stop is partly a decision to remove a risk that is not earning its keep.

The final piece is the follow-up plan. Stopping digoxin is not a one-way door. The note should say what to watch for: shortness of breath, edema, fatigue, palpitations. It should say when to reassess, usually within two to four weeks. It should say what would restart the drug: new heart failure symptoms, a drop in ejection fraction, or a rhythm that needs rate control. That makes the decision reversible and accountable. A note that says “no clear indication, discontinue” without a follow-up plan is incomplete. A note that says “no current indication, discontinue, reassess in four weeks, restart if symptoms return” is a clinical decision with a safety net.

The confidence here is high on the documentation standard: the record should show the original indication, the current status, the risk-benefit reasoning, and the follow-up plan. The confidence is lower on the clinical decision itself, because the evidence for stopping in a stable patient with no current indication is absent, not proven. That is not a reason to keep the drug. It is a reason to say what is not known. The physician who writes the note honestly is doing the patient a service. The physician who writes “no clear indication” and stops the drug without documenting the reasoning is doing the same thing a physician does when starting a drug without an indication: practicing by reflex, not by evidence. The record is the only place where the difference shows.

Keep digging

Sources used 37

  1. Junctional Bradycardia as Early Sign of Digoxin Toxicity in a Premature Infant with Congestive Heart Failure due to a Left to Right Shunt American Journal of Perinatology Reports (2015) Thin

    This case report describes a premature infant with congestive heart failure who exhibited junctional bradycardia as an early sign of digoxin toxicity, highlighting the importance of monitoring electrolyte levels and considering aldosterone antagonists in treatment.

    DOI: 10.1055/s-0035-1567858
  2. DRUG INDUCED BRADYCARDIA The Professional Medical Journal (2018) Thin

    Most patients experienced persistent bradycardia after stopping rate-slowing drugs, suggesting unmasked latent conduction system disease rather than true drug-induced bradycardia.

    DOI: 10.29309/tpmj/2018.25.06.280
  3. Digoxin concentration in right atrial myocardium, skeletal muscle and serum in man: Influence of atrial rhythm European Journal of Clinical Pharmacology (1980) Thin

    This study investigates the correlation of digoxin concentrations in serum, right atrial myocardium, and skeletal muscle in patients undergoing open heart surgery, revealing significant differences based on atrial rhythm.

    DOI: 10.1007/BF00625797
  4. Time of occurrence, duration, and ventricular rate of paroxysmal atrial fibrillation: the effect of digoxin. Heart (1990) Thin

    This study investigates the occurrence, duration, and ventricular rate of paroxysmal atrial fibrillation in patients, revealing that digoxin treatment does not reduce the frequency of episodes but is associated with longer attacks.

    DOI: 10.1136/hrt.63.4.225
  5. GAMMA-AMINOBUTYRIC-ACID ANALOGUES The Lancet (1978) Thin

    The study investigates the binding of digoxin in the right atrium and left ventricle of patients with atrial fibrillation compared to those in sinus rhythm, revealing significant differences in digoxin concentrations and their implications for cardiac function.

    DOI: 10.1016/s0140-6736(78)91844-5
  6. Digoxin infusion versus bolus injection in rapid atrial fibrillation: relation between serum level and response European Journal of Clinical Pharmacology (1990) Thin

    This study compares the effects of digoxin administered via infusion versus bolus injection in patients with rapid atrial fibrillation, demonstrating that infusion leads to faster digitalization and a more favorable serum concentration profile.

    DOI: 10.1007/bf00315571
  7. Increased mortality among patients taking digoxin--analysis from the AFFIRM study European Heart Journal (2012) Thin

    This study analyzes data from the AFFIRM trial to determine the association between digoxin use and increased mortality rates among patients with atrial fibrillation, highlighting significant risks regardless of heart failure status.

    DOI: 10.1093/eurheartj/ehs348
  8. Profibrillatory Effects of Verapamil but Not of Digoxin in the Goat Model of Atrial Fibrillation Journal of Cardiovascular Electrophysiology (2000) Thin

    This six-goat study directly compared the immediate and remodeling-phase effects of digoxin and verapamil on atrial fibrillation (AF): while digoxin slowed ventricular rate without altering AF cycle length or duration, verapamil shortened AF cycle length and refractory period in…

    DOI: 10.1046/j.1540-8167.2000.01375.x
  9. Interaction Between Digoxin and Dronedarone in the PALLAS Trial Circulation: Arrhythmia and Electrophysiology (2014) Thin

    The study investigates the interaction between digoxin and dronedarone in patients with permanent atrial fibrillation, revealing that the combination significantly increases cardiovascular and arrhythmic mortality, particularly in those on digoxin therapy.

    DOI: 10.1161/circep.114.002046
  10. Magnesium deficiency may be an important determinant of ventricular ectopy in digitalised patients with chronic atrial fibrillation. British Journal of Clinical Pharmacology (1991) Thin

    In digitalised patients with chronic atrial fibrillation, a magnesium loading test revealed that those with frequent ventricular premature beats retained more magnesium, suggesting magnesium deficiency may contribute to ventricular ectopy in this population.

    DOI: 10.1111/j.1365-2125.1991.tb05516.x
  11. Effects of digoxin, propranolol, and verapamil on exercise in patients with chronic isolated atrial fibrillation Cardiovascular Research (1991) Thin

    This study evaluates the effects of digoxin, propranolol, and verapamil on exercise performance and heart rate control in patients with chronic isolated atrial fibrillation, finding that while digoxin reduces heart rate at rest, propranolol and verapamil are more effective durin…

    DOI: 10.1093/cvr/25.6.453
  12. Incidence, Predictive Factors, and Prognostic Significance of Supraventricular Tachyarrhythmias in Congestive Heart Failure Chest (2000) Thin

    In a large, multicenter DIG trial of congestive heart failure patients in sinus rhythm, the study quantified the incidence and baseline predictors of supraventricular tachyarrhythmias (SVT), demonstrated that SVT independently predicts higher all-cause mortality, stroke, and hos…

    DOI: 10.1378/chest.118.4.914
  13. Verapamil Versus Digoxin and Acute Versus Routine Serial Cardioversion for the Improvement of Rhythm Control for Persistent Atrial Fibrillation Journal of the American College of Cardiology (2006) Thin

    The VERDICT trial investigates the effectiveness of acute versus routine serial electrical cardioversion and the use of verapamil versus digoxin for rhythm control in patients with persistent atrial fibrillation, finding no significant advantage of acute strategies or verapamil …

    DOI: 10.1016/j.jacc.2006.05.043
  14. Use of digoxin for heart failure and atrial fibrillation in elderly patients The American Journal of Geriatric Pharmacotherapy (2010) Thin

    This study evaluates the pharmacokinetics and clinical efficacy of digoxin in elderly patients with heart failure and atrial fibrillation, highlighting the need for careful dosing and monitoring due to altered drug metabolism in this population.

    DOI: 10.1016/j.amjopharm.2010.10.001
  15. Heart Rate Control in Atrial Fibrillation Clinical Science (1986) Thin

    This study investigates the effects of digoxin and verapamil on heart rate variability in patients with chronic atrial fibrillation, revealing that the combination of verapamil with digoxin provides better heart rate control with less nighttime bradycardia compared to increasing…

    DOI: 10.1042/cs070006p
  16. Safety and efficacy of digoxin: systematic review and meta-analysis of observational and controlled trial data BMJ (2015) Thin

    This systematic review and meta-analysis evaluates the safety and efficacy of digoxin in patients with heart failure and atrial fibrillation, revealing a neutral effect on mortality in randomized trials and a reduction in hospital admissions across all study types.

    DOI: 10.1136/bmj.h4451
  17. Individual dosage of digoxin in patients with heart failure QJM (2010) Thin

    This study evaluates the clinical validity of the Konishi equation for calculating individual digoxin dosages in Caucasian heart failure patients, demonstrating its effectiveness in achieving target serum digoxin concentrations within the recommended therapeutic range.

    DOI: 10.1093/qjmed/hcq196
  18. Prognosis of heart failure treated with digoxin or with ivabradine: A cohort study in the community International Journal of Clinical Practice (2018) Thin

    This cohort study investigates the prognosis of heart failure patients treated with digoxin or ivabradine, revealing that both therapies are associated with improved survival and reduced hospitalization rates compared to non-treatment.

    DOI: 10.1111/ijcp.13217
  19. HEART FAILURE HOSPITALIZATION (HFH) DESPITE DIGOXIN THERAPY VERSUS NO HFH DESPITE PLACEBO IN THE DIGITALIS INVESTIGATION GROUP (DIG) TRIAL: INSIGHTS INTO RISK FACTORS FOR HFH IN HF AND REDUCED EJECTION FRACTION (HFREF) Journal of the American College of Cardiology (2017) Thin

    This study analyzes risk factors for heart failure hospitalization (HFH) in patients with heart failure and reduced ejection fraction (HFrEF) who were treated with digoxin compared to those receiving placebo, revealing that traditional risk factors remain significant predictors …

    DOI: 10.1016/s0735-1097(17)34300-0
  20. Digoxin withdrawal in patients with stable heart failure receiving optimal contemporaneous therapy worsens heart failure status but better preserves quality of life Heart, Lung and Circulation (2015) Thin

    This study investigates the effects of digoxin withdrawal in patients with stable heart failure receiving optimal therapy, finding that withdrawal worsens heart failure status but may improve quality of life.

    DOI: 10.1016/j.hlc.2015.06.217
  21. Hemodynamic effects of intravenous digoxin in patients with severe heart failure initially treated with diuretics and vasodilators Journal of the American College of Cardiology (1987) Thin

    This study investigates the hemodynamic effects of intravenous digoxin in patients with severe heart failure who were initially treated with diuretics and vasodilators, finding that digoxin further improved cardiac function in those with persistent abnormal hemodynamic variables.

    DOI: 10.1016/s0735-1097(87)80241-3
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    A comprehensive review of digitalis/digoxin in heart failure, detailing pharmacology, hemodynamic and neurohormonal effects, and a synthesis of randomized and observational studies showing symptomatic/hemodynamic benefits and reduced hospitalizations, but with inconsistent morta…

    DOI: 10.1016/s0146-2806(96)80001-6
  23. Renal Function, Digoxin Therapy, and Heart Failure Outcomes Journal of the American Society of Nephrology (2004) Thin

    This study evaluates the association between renal function, as measured by glomerular filtration rate (GFR), and heart failure outcomes, specifically mortality and the efficacy of digoxin therapy, using data from the Digitalis Intervention Group trial involving 6800 outpatients…

    DOI: 10.1097/01.ASN.0000135121.81744.75
  24. Can Monitoring Heart Failure Status with Intrathoracic Impedance Reduce the Rate of Heart Failure Hospitalization? Journal of Cardiac Failure (2008) Thin

    This study investigates the outcomes of patients with advanced heart failure on digoxin therapy compared to those not on digoxin, revealing that elevated admission glucose does not worsen outcomes despite a worse hemodynamic profile.

    DOI: 10.1016/j.cardfail.2008.06.272
  25. Converting enzyme inhibition and heart failure The American Journal of Medicine (1988) Thin

    This study investigates the effects of captopril, in conjunction with digoxin, on the prognosis and functional status of patients with mild heart failure, revealing no significant treatment differences after one year.

    DOI: 10.1016/0002-9343(88)90210-0
  26. Synergistic effects of asymmetrical dimethyl-L-arginine accumulation and endothelial progenitor cell deficiency on renal function decline during a 2-year follow-up in stable angina Nephrology Dialysis Transplantation (2009) Thin

    This study investigates the synergistic effects of asymmetrical dimethyl-L-arginine accumulation and endothelial progenitor cell deficiency on renal function decline over a two-year follow-up in non-diabetic men with stable angina, revealing that both factors significantly predi…

    DOI: 10.1093/ndt/gfp439
  27. Hypertension and chronic kidney disease affect long-term outcomes in patients with stable coronary artery disease receiving percutaneous coronary intervention Scientific Reports (2018) Thin

    Chronic kidney disease alone markedly worsens long-term mortality after PCI in stable CAD; hypertension does not add risk in CKD, while CKD increases risk in HT and the combination raises risk of repeated PCI.

    DOI: 10.1038/s41598-018-35982-4
  28. C.E.R.A. Maintains Stable Control of Hemoglobin in Patients with Chronic Kidney Disease on Dialysis when Administered Once Every Two Weeks American Journal of Nephrology (2007) Thin

    The RUBRA study demonstrates that C.E.R.A. administered every two weeks is as effective as more frequent epoetin therapy in maintaining stable hemoglobin levels in patients with chronic kidney disease on dialysis.

    DOI: 10.1159/000111115
  29. Health Status and Quality of Life in Patients With Stable Coronary Artery Disease and Chronic Kidney Disease Treated With Optimal Medical Therapy or Percutaneous Coronary Intervention (Post Hoc Findings from the COURAGE Trial) The American Journal of Cardiology (2013) Thin

    This study analyzes the health status and quality of life in patients with stable coronary artery disease and chronic kidney disease, comparing outcomes between those treated with optimal medical therapy alone and those receiving percutaneous coronary intervention in addition to…

    DOI: 10.1016/j.amjcard.2013.07.034
  30. From Wearable Ultrafiltration Device to Wearable Artificial Kidney Contributions to Nephrology; Hemodialysis (2011) Thin

    This pilot proof-of-concept study demonstrates the safety and efficacy of a wearable hemodialysis device in eight stable adult patients with chronic kidney disease, showing comparable clearances to continuous renal replacement therapy and successful ultrafiltration without adver…

    DOI: 10.1159/000327172
  31. Growth differentiation factor GDF-15 does not influence iron metabolism in stable chronic haemodialysis patients Annals of Clinical Biochemistry: International Journal of Laboratory Medicine (2014) Thin

    In stable chronic haemodialysis patients, Growth Differentiation Factor 15 (GDF-15) is markedly elevated but shows no correlation with hepcidin or iron indices, suggesting GDF-15 does not influence iron metabolism in this setting.

    DOI: 10.1177/0004563214552109
  32. Indoxyl Sulfate Impairs Endothelial Progenitor Cells and Might Contribute to Vascular Dysfunction in Patients with Chronic Kidney Disease Kidney and Blood Pressure Research (2016) Thin

    This study investigates the detrimental effects of indoxyl sulfate on endothelial progenitor cells and its correlation with vascular dysfunction in patients with chronic kidney disease.

    DOI: 10.1159/000452604
  33. Estimating Glomerular Filtration Rates by Use of Both Cystatin C and Standardized Serum Creatinine Avoids Ethnicity Coefficients in Asian Patients with Chronic Kidney Disease Clinical Chemistry (2012) Thin

    This study investigates the effectiveness of using a combination of serum cystatin C and standardized serum creatinine for estimating glomerular filtration rates (GFR) in a multiethnic Asian population with chronic kidney disease, finding that ethnicity coefficients are unnecess…

    DOI: 10.1373/clinchem.2011.172346
  34. Antithrombotic therapy for stable coronary artery disease: the difficult quest for the holy balance European Heart Journal (2015) Thin

    An editorial analyzing how renal function shapes the efficacy and safety of prolonged ticagrelor therapy in stable coronary artery disease (PEGASUS trial data), finding no interaction for relative ischemic benefit but larger absolute benefits and increased bleeding in CKD, leavi…

    DOI: 10.1093/eurheartj/ehv471
  35. Checkpoint inhibitors in chronic kidney failure and an organ transplant recipient European Journal of Cancer (2016) Thin

    This study reports on the safety and efficacy of immune-checkpoint inhibitors in patients with chronic kidney failure and an organ transplant recipient, highlighting that kidney function remained stable during treatment without allograft rejection.

    DOI: 10.1016/j.ejca.2016.07.026
  36. Assessment of intravenous adipose-derived allogeneic mesenchymal stem cells for the treatment of feline chronic kidney disease: a randomized, placebo-controlled clinical trial in eight cats Journal of Feline Medicine and Surgery (2015) Thin

    This study evaluates the effectiveness of intravenous administration of allogeneic mesenchymal stem cells (MSCs) derived from adipose tissue in treating feline chronic kidney disease (CKD) through a randomized, placebo-controlled trial involving eight cats, finding no significan…

    DOI: 10.1177/1098612X15576980
  37. Exercise Performance Falls over Time in Patients with Chronic Kidney Disease Despite Maintenance of Hemoglobin Concentration Clinical Journal of the American Society of Nephrology (2006) Thin

    This study investigates the decline in exercise performance over time in patients with chronic kidney disease (CKD) stages 3 to 4, despite stable hemoglobin levels, revealing significant reductions in both aerobic capacity and leg strength as renal function deteriorates.

    DOI: 10.2215/cjn.01501005

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