Hyperkalemia is a common complication of kidney disease and incidence increases as kidney function declines. Renin-angiotensin system blockade, which improves renal and cardiovascular outcomes, increases the risk of hype...Hyperkalemia is a common complication of kidney disease and incidence increases as kidney function declines. Renin-angiotensin system blockade, which improves renal and cardiovascular outcomes, increases the risk of hyperkalemia. Unfortunately, hyperkalemia often leads to discontinuation of these medications, which can increase adverse outcomes. Treatment of chronic hyperkalemia includes diet and pharmacologic interventions. However, the association of dietary potassium intake with serum potassium levels is weak and does not consider important internal and external balance factors that affect serum levels. Traditional dietary interventions that limit dietary potassium lead to a restrictive diet that limits fruits and vegetables, whole-grains, and plant-based proteins. This restrictive approach may unnecessarily limit dietary quality and variety in a population already at risk for poor nutritional status and complications of chronic kidney disease (CKD). The management of hyperkalemia requires a comprehensive, individualized approach that moves beyond blanket dietary restriction. The objective of this review is to describe the role of diet and pharmacological approaches to manage hyperkalemia, highlighting newer dietary approaches.
Protein is a unique, essential component of our diet. There is currently great emphasis on high protein diets, not only in the commercial food market and social media, but also in the scientific literature, with a contin...Protein is a unique, essential component of our diet. There is currently great emphasis on high protein diets, not only in the commercial food market and social media, but also in the scientific literature, with a continuous debate on the need of changing current protein recommendations, in particular in older adults. Here we provide an updated perspective on the debate on high protein intakes for maintaining muscle mass and function, with focus on people who are affected by kidney diseases. Several conditions such as aging, inactivity, and many chronic conditions including dialysis-treated chronic kidney disease are characterized by anabolic resistance, i.e. the need of ingesting higher amounts of protein to maximally stimulate muscle protein synthesis. In addition, sedentarianism and inactivity, conditions very common in developed countries, contribute to decreased muscle mass and strenght. Protein intake and physical activity as the major anabolic stimuli for muscle health and function. However, protein ingestion is associated with oxidation of excess amino acids, ureagenesis, and production of toxins. In addition, protein supplementation in the absence of resistance training produces relatively marginal effects on strength and performance in healthy subjects and older adults. On these grounds, for persons who are inactive, muscle mass and function can be better maintained by physical exercise without the use of high protein diets.
Husser F, Aubert O, Chhun S
… +12 more, Ferriere E, Hummel A, Servais A, Dao M, Le Moal P, Padden M, Sakhi H, Joly D, Knebelmann B, Anglicheau D, Rabant M, Boudhabhay I
Cacciapuoti M, Bahrainwala JZ, Weng WK
… +3 more, Scott SA, Bhalla V, Abra G
Am J Kidney Dis
· 2026 Jun · PMID 42379468
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Hypophosphatemia is a frequent complication of chimeric antigen receptor T-cell therapy. In this setting, hypophosphatemia has been previously associated with cytokine release syndrome. The mechanisms underlying this ele...Hypophosphatemia is a frequent complication of chimeric antigen receptor T-cell therapy. In this setting, hypophosphatemia has been previously associated with cytokine release syndrome. The mechanisms underlying this electrolyte derangement are not fully understood. Extracellular phosphate consumption by chimeric antigen receptor T-cells was demonstrated in vitro, but inflammation is also thought to play a contributing role. We present a case of severe, refractory hypophosphatemia with renal phosphate wasting triggered by hemophagocytic lymphohistiocytosis in acute lymphoblastic leukemia. The diagnosis of phosphate wasting was made at the onset of leukemia and a clinical exacerbation occurred after chimeric antigen receptor T-cell therapy. Diagnostic workup revealed very high FGF23 levels in the absence of recognized, acquired or genetic causes of impaired FGF23 cleavage. This case suggests that inflammation associated with hemophagocytic lymphohistiocytosis may induce FGF23 as a potential mechanism for hypophosphatemia. In this context, we recommend evaluation of renal phosphate wasting and subsequently FGF23 in patients with persistent hypophosphatemia despite standard supplementation.
Khan Z, Dadhania DM, Brailovski E
… +2 more, Landau H, Shaikh A
Am J Kidney Dis
· 2026 Jun · PMID 42379467
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Kidney disease affects approximately half of patients with multiple myeloma (MM), and kidney failure is associated with poor prognosis. Kidney transplantation is rarely pursued in MM due to concerns of relapse, infection...Kidney disease affects approximately half of patients with multiple myeloma (MM), and kidney failure is associated with poor prognosis. Kidney transplantation is rarely pursued in MM due to concerns of relapse, infection, and allograft rejection. However, advances in therapy, including B-cell maturation antigen (BCMA)-directed chimeric antigen receptor (CAR) T-cell therapy, have led to deep and durable hematologic responses, creating new opportunities for transplantation in select patients. We report a 71-year-old man with stage III MM and high-risk cytogenetics [del(17p)] who developed end-stage kidney disease requiring hemodialysis during his treatment course. Despite multiple lines of therapy, he had never achieved a deep remission until he received ciltacabtagene autoleucel (cilta-cel) CAR T-cell therapy, which led to minimal residual disease (MRD)-negative disease status. One year following CAR T-cell therapy, he underwent living donor kidney transplantation with basiliximab induction, and tacrolimus/mycophenolate maintenance immunosuppression. His course was complicated by hypogammaglobulinemia, cytopenia, BK viremia, and acute rejection, all managed with immunosuppression adjustment and supportive therapies. At 17 months post-transplant, allograft function remains stable (creatinine 1.8 mg/dL), and he has achieved an MRD-negative, complete hematologic remission. This case highlights both the feasibility and the challenges of kidney transplantation after CAR T-cell therapy in MM.
Bursic AE, Ernecoff NC, Maurer L
… +2 more, Taylor R, Schell JO
Am J Kidney Dis
· 2026 Jun · PMID 42372938
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The current dialysis care model is largely disease-focused, designed to preserve longevity and minimize sequelae of end-stage kidney disease (ESKD), often with a goal of transplantation. As many patients living with ESKD...The current dialysis care model is largely disease-focused, designed to preserve longevity and minimize sequelae of end-stage kidney disease (ESKD), often with a goal of transplantation. As many patients living with ESKD experience high rates of comorbidity, frailty, and mortality, these goals may not be realistic nor align with their priorities and preferences. Instead, these patients benefit from a person-centered approach to care which emphasizes quality of life; minimizes disease and treatment-associated burdens; and promotes timely transitions to end of life care. Palliative dialysis aims to align dialysis treatment with patients' goals and preferences to optimize quality of life and adapt to patients' evolving individual needs throughout the disease course including at end of life. This narrative review describes person-centered care throughout the dialysis care continuum using palliative dialysis. We describe innovative end of life care models such as concurrent hospice and dialysis care. We then outline necessary steps for implementation of person-centered dialysis care at a system and policy level.
Choi Y, Jacobs DR, Kramer HJ
… +16 more, Coresh J, Cushman M, Reiner AP, Demmer RT, Tracy RP, Sun Y, Balte PP, Raffield LM, Min YI, Vasan RS, Xanthakis V, Regan EA, Kanaya AM, Lash JP, Umans JG, Oelsner EC
Am J Kidney Dis
· 2026 Jun · PMID 42362101
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RATIONALE & OBJECTIVE: While kidney failure is associated with severe COVID-19, data on early-stage chronic kidney disease (CKD) and its relationship to acute and post-acute COVID-19, as well as post-vaccination antibody...RATIONALE & OBJECTIVE: While kidney failure is associated with severe COVID-19, data on early-stage chronic kidney disease (CKD) and its relationship to acute and post-acute COVID-19, as well as post-vaccination antibody responses, are limited. We evaluated pre-pandemic CKD stage in relation to these outcomes. STUDY DESIGN: Prospective cohort. SETTING & PARTICIPANTS: Adults in nine US population-based studies established since 1971, with pre-pandemic CKD measurements and follow-up for COVID-19 outcomes. EXPOSURE: CKD stages (low CKD stage [reference], moderate CKD stage, high CKD stage, and very high CKD stage) defined by creatinine-based eGFR and urinary albumin-to-creatinine ratio. OUTCOMES: (i) COVID-19 hospitalization or death (self-report/medical records, 2020‒2023); (ii) RECOVER Long COVID Research Index score ≥11 (LCRI-positivity by questionnaires, 2023‒2024); (iii) post-vaccination anti-Spike 1 (S1) IgG levels (dried blood spots, 2021‒2022). ANALYTICAL APPROACH: Cause-specific hazards for severe COVID-19, logistic regression for LCRI-positivity, and generalized additive models for anti-S1 IgG. RESULTS: Among 26,039 participants, CKD stage was low in 81.7%, moderate in 13.0%, high in 3.6%, and very high in 1.7%. Over a median 550-day follow-up (P25-P75: 314‒636), 734 had severe COVID-19; 12.1% of infected (669/5,527) were classified as LCRI-positive; and 3.1% (82/2,679) were anti-S1 IgG antibody non-reactive. A more severe CKD stage was associated with a greater risk for severe COVID-19: the HR for moderate stage CKD was 1.27 (95% CI, 1.03‒1.56), for high stage CKD, 2.33 (1.77‒3.06), and for very high stage CKD, 2.72 (1.88‒3.92). Higher CKD stages were associated with lower anti-S1 IgG levels: ‒12.00% (95% CI: ‒21.14% to ‒1.78%) for moderate stage CKD, ‒27.03% (95% CI, ‒40.00% to ‒11.25%) for high stage CKD, and ‒48.9% (95% CI, ‒61.60% to ‒32.01%) for very high stage CKD. A higher prevalence of LCRI positivity was observed only among infected individuals with very high stage CKD (OR=2.20; 95% CI: 1.16‒4.18). LIMITATIONS: Some outcomes were self-reported. CONCLUSION: Higher CKD stages were associated with a greater risk for severe COVID-19 and a lower anti-S1 antibody response. No consistent association was observed between CKD stage and LCRI-positivity except in individuals with very high stage CKD. INDEX WORDS: Chronic kidney disease, kidney dysfunction, SARS-CoV-2 infection, severe COVID-19, Long COVID, anti-S1 IgG antibody, Prospective cohort.
Beynon-Cobb B, Visser W, Hoorn EJ
… +1 more, Morris A
Am J Kidney Dis
· 2026 Jun · PMID 42349771
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Whilst observational evidence suggests that metabolic acidosis in chronic kidney disease (CKD) is a driver of CKD progression, there remains significant debate regarding the quantity and quality of published evidence to...Whilst observational evidence suggests that metabolic acidosis in chronic kidney disease (CKD) is a driver of CKD progression, there remains significant debate regarding the quantity and quality of published evidence to support treatment. The Kidney Disease: Improving Global Outcomes (KDIGO) guidance on metabolic acidosis in CKD highlighted this controversy by publishing practice points, not recommendations, based primarily on placebo-controlled randomized controlled trials. These practice points suggest considering treatment to prevent metabolic acidosis with a proposed cut-off for serum bicarbonate < 18 mmol/L. However, this approach means a substantial number of individuals with CKD may now remain untreated for their metabolic acidosis which may impact CKD progression and associated adverse health outcomes. Additionally, the guidance does not include all the available evidence. From our critical appraisal we suggest that the evidence cited could have been interpreted differently. We recommend that the practice points published are revised based upon critical appraisal of the cited evidence to inform the clinical management of individuals with metabolic acidosis in CKD. We also suggest a research agenda for future studies to help resolve this issue.
Am J Kidney Dis
· 2026 Jun · PMID 42340294
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Ketoacidosis is a metabolic state characterized by overproduction and accumulation of ketone bodies (ketoacids), leading to potentially life-threatening drops in blood pH. Common to these disorders is a reduction in the...Ketoacidosis is a metabolic state characterized by overproduction and accumulation of ketone bodies (ketoacids), leading to potentially life-threatening drops in blood pH. Common to these disorders is a reduction in the insulin-glucagon ratio signaling a lack of available cellular fuel. This change promotes lipolysis and subsequent hepatic β-oxidation of fatty acids, yielding acetyl-CoA that is converted into ketone bodies (acetoacetate, β-hydroxybutyrate, and acetone). Additionally, increased levels of other counterregulatory hormones (eg, catecholamines, cortisol, and growth hormone) often play a key role in exacerbating ketogenesis and the catabolic state. This core curriculum explores the physiological and pathological spectrum of ketoacidosis, beginning with the benign state of starvation ketosis. Diabetic ketoacidosis is a severe complication of diabetes mellitus resulting from profound absolute or relative insulin deficiency and counterregulatory hormone excess. Other forms discussed include pregnancy-associated ketoacidosis (often triggered by starvation or illness), alcoholic ketoacidosis (resulting from the metabolism of alcohol in association with reduced food intake), ketoacidosis associated with chronic salicylate poisoning, sodium/glucose cotransporter 2 inhibitor-induced ketoacidosis, and development of euglycemic ketoacidosis in patients undergoing continuous kidney replacement therapy. Understanding the distinct pathophysiology of each condition is crucial for accurate diagnosis and timely, targeted therapeutic intervention.
Pinzon-Cortes JA, Narongkiatikhun P, Yuan L
… +11 more, Meister J, Hampson H, van Raalte D, Blondin DP, Capozzi M, Sweet IR, Nelson RG, Jandeleit-Dahm K, Forbes JM, Cooper ME, Bjornstad P
Am J Kidney Dis
· 2026 Jun · PMID 42331132
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Mitochondrial alterations are increasingly recognized as central to the pathogenesis of chronic kidney disease (CKD), contributing to impaired energy metabolism, oxidative stress, and maladaptive cellular responses. This...Mitochondrial alterations are increasingly recognized as central to the pathogenesis of chronic kidney disease (CKD), contributing to impaired energy metabolism, oxidative stress, and maladaptive cellular responses. This review highlights recent advances in our understanding of mitochondrial remodeling in both diabetic and non-diabetic CKD (NDKD), including changes in bioenergetics, dynamics, redox balance, and biogenesis. We discuss state-of-the-art approaches to assess mitochondrial health, ranging from high-resolution respirometry and metabolomic profiling to transcriptomic analysis and advanced imaging techniques such as functional magnetic resonance imaging (MRI) and positron emission tomography (PET) radiotracers with metabolic readouts. Therapeutically, several agents show promise in modulating mitochondrial pathways, including sodium glucose cotransporter 2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, and non-steroidal mineralocorticoid receptor antagonists (nsMRAs), as well as emerging interventions such as glucose-dependent insulinotropic polypeptide and glucagon receptor agonist, nicotinamide adenine dinucleotide (NAD) boosters, and coenzyme Q10 (CoQ10) derivatives. Multi-omics integration and spatial profiling are enabling precision phenotyping and the development of mitochondrial health scores to guide individualized therapy. Targeting mitochondrial adaptation offers a compelling avenue to improve outcomes in CKD.
Lin LC, Tao-Min Huang T, Wu YT
… +4 more, Chiang S, Teng NC, Chen L, Wu VC
Am J Kidney Dis
· 2026 Jun · PMID 42320580
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RATIONALE & OBJECTIVE: The impact of iodinated contrast media (ICM) on kidney outcomes remains debated, especially among patients recovering from dialysis-requiring acute kidney injury (AKI-D). Despite apparent clinical...RATIONALE & OBJECTIVE: The impact of iodinated contrast media (ICM) on kidney outcomes remains debated, especially among patients recovering from dialysis-requiring acute kidney injury (AKI-D). Despite apparent clinical recovery, these individuals may remain vulnerable to repeat kidney insults. STUDY DESIGN: Retrospective cohort study. SETTING & PARTICIPANTS: Adults recovering from AKI-D were identified using Taiwan's National Health Insurance Research Database between January 2015 and December 2022. EXPOSURE: Intravenous ICM. OUTCOME: The primary kidney event was recurrent treatment with dialysis; the secondary was persistent kidney dysfunction, defined as at least 0.3 mg/dL or 50% increase in serum creatinine from post-AKI recovery levels at one year after index date. ANALYTICAL APPROACH: Observational analysis using inverse probability of treatment weighting (IPTW) within a target trial emulation framework to compare patients exposed to ICM with unexposed counterparts. RESULTS: Among 23,263 patients recovering from dialysis after AKI-D (mean age, 69.6 years; 58.5 % men), 1,551 (6.7 %) received contrast-enhanced computed tomography in the first 30 days. After IPTW, ICM was independently associated with a higher hazard of recurrent treatment with dialysis (subdistribution hazard ratio (sHR) 1.37 [95 % CI, 1.20-1.56]) and persistent kidney dysfunction (sHR 1.11 [95 % CI, 1.01-1.23]). Generalized-additive modeling showed that the risk for kidney events were greatest when the post-AKI-D estimated glomerular filtration rate (eGFR) fell below 36 mL/min/1.73 m in the patients who received contrast, compared with 22.8 mL/min/1.73 m in patients who did not. External validation in an independent, multi-hospital cohort of 1,195 AKI-D survivors confirmed the excess risk of kidney events after contrast exposure. LIMITATION: The observational nature of this study precludes definitive causal inference. CONCLUSION: Among adults recently recovering from AKI-D and no longer dependent on dialysis, ICM exposure was associated with an increased risk of a recurrent treatment with dialysis and persistent kidney dysfunction. These findings inform clinical management of these patients and the use of contrast in this high-risk population. PLAIN-LANGUAGE SUMMARY: The effects of iodinated contrast on kidney function remain controversial and are even less well understood in patients recovering from dialysis-requiring acute kidney injury (AKI-D). In this nationwide observational study using a target trial emulation framework, we evaluated adults with AKI-D whose recovery permitted discontinued dialysis. We found that patients who underwent contrast-enhanced CT scans within 30 days of dialysis cessation were more likely to require dialysis again and to develop persistent kidney dysfunction compared with those who did not receive contrast. These findings suggest that kidney function may remain vulnerable after apparent recovery and support careful consideration of contrast use in this high-risk population.