As we delve deep into countless medical journals to uncover the latest on Integrative Medicine’s approach to kidney health, we are always reminded of the value of your time. Our commitment remains steadfast in curating and succinctly summarizing these vital studies for you. Welcome to the December Research and News.
Global Burden of Chronic Kidney Disease Linked to Poor Diet
This Global Burden of Disease 2021 analysis found that poor dietary habits contribute to nearly one-fifth of all chronic kidney disease (CKD) deaths worldwide, about 317,000 annually, with mortality rates continuing to rise.
The study identified low intake of fruits and vegetables as the leading dietary contributor to CKD deaths, while consumption of sugar-sweetened beverages showed the fastest increase in associated mortality.
Red and processed meat intake also played a growing role.
The burden of diet-related CKD was highest in low-socio-demographic index (SDI) countries, though the steepest increases occurred in high-SDI regions, particularly among people born after 1952.
Overall, diet-related CKD mortality rates varied almost 70-fold across countries, reflecting sharp global inequalities.
Why is this important?
These findings emphasize that diet is a major modifiable driver of CKD risk and mortality. The growing impact of unhealthy dietary patterns, especially increased intake of sugary and processed foods, highlights the urgent need for public health interventions promoting balanced, plant-forward diets to curb the rising global burden of CKD.
Fibroblast Growth Factor 23, Urinary Phosphate, and CKD Progression
This study followed 946 adults with non-dialysis-dependent CKD to investigate whether levels of intact fibroblast growth factor 23 (FGF23)—a hormone involved in phosphate regulation—predict kidney disease progression.
Over roughly 27 months, 181 participants reached the composite kidney outcome (kidney failure requiring replacement therapy or a 40% decline in eGFR).
Higher FGF23 levels were strongly associated with faster CKD progression, with those in the highest quartile having more than double the risk compared with the lowest.
Importantly, this association was significantly stronger among individuals with low 24-hour urinary phosphate excretion, suggesting that inadequate phosphate elimination may magnify the harmful effects of elevated FGF23. Fractional excretion of phosphate, however, did not alter the relationship.
Why is this important?
These findings highlight that two available clinical measures, FGF23 and 24-hour urinary phosphate, may together help identify patients at the highest risk for rapid CKD progression.
Elevated FGF23 likely reflects the body’s attempt to compensate for phosphate retention, a key driver of mineral dysregulation, vascular injury, and kidney decline.
When urinary phosphate excretion is low, this compensatory system may be even more strained, amplifying risk. This study reinforces the importance of managing phosphate load in CKD. It suggests that FGF23 could serve not just as a biomarker of risk but also as a potential therapeutic target in efforts to slow kidney disease progression.
Dietary Salt and Protein Intake and Urinary Cystine Excretion in Cystinuria
This retrospective study followed 41 adults with recurrent cystine kidney stones who completed five 24-hour urine collections over several years, evaluating whether changes in dietary salt and protein intake affect urinary cystine excretion.
Protein intake, estimated by urinary urea, showed a moderate within-person association: increasing protein by about 10 g/day led to a 164 µmol rise in urinary cystine.
In contrast, changes in dietary salt intake, estimated by urinary sodium, had only a minimal and statistically nonsignificant effect on cystine excretion.
Cystine levels varied substantially between urine collections, highlighting the disease’s fluctuating nature.
Why is this important?
This study provides real-world evidence that protein moderation may help reduce cystine excretion in this genetic disorder, but salt restriction alone is unlikely to impact stone risk meaningfully.
It reinforces that the most effective strategies for preventing cystine stone formation remain high fluid intake and urine alkalinization, which directly increase cystine solubility. These findings help refine dietary counseling for patients with cystinuria by prioritizing interventions that offer the most significant clinical benefit.
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Three-Month Interim Analysis of Ketogenic Metabolic Therapy in Japanese ADPKD Patients
This interim analysis presented at the latest ASN Kidney Week reports early results from the first clinical study in Asia testing ketogenic metabolic therapy, using a ketogenic diet supported by beta-hydroxybutyrate and alkaline citrate (KetoCitra®), in adults with ADPKD who had never received tolvaptan.
After three months, patients following the ketogenic program showed significantly greater weight loss and, notably, a 5% reduction in total kidney volume, while the control group experienced an 8% increase.
Kidney function (eGFR) remained stable in the intervention group, and no participants discontinued the diet, indicating good tolerability.
These early findings suggest that ketogenic metabolic therapy may be beneficial in slowing structural kidney changes in ADPKD.
Why is this important?
ADPKD lacks many effective therapies, and early metabolic studies have shown that cyst growth is tightly linked to energy dysregulation in kidney cells.
This clinical evidence supports the idea that targeting metabolism, specifically through nutritional ketosis, can directly influence cyst expansion, offering a promising, non-pharmacologic therapeutic option.
Epstein-Barr Virus Reprograms Autoreactive B Cells in Lupus
This study uncovers a mechanism that may explain how Epstein–Barr virus (EBV) may trigger or amplify systemic lupus erythematosus (SLE).
Using a novel EBV-specific single-cell RNA sequencing platform, researchers showed that in people with SLE, EBV infects autoreactive B cells that recognize nuclear antigens and reprograms them into highly active antigen-presenting cells.
These EBV-infected B cells display a distinct transcriptional profile—driven largely by the EBV protein EBNA2—which activates genes that enhance antigen presentation and immune signaling.
Functionally, these modified B cells can activate autoreactive helper T cells, which in turn stimulate additional autoreactive B cells (even those not infected with EBV), amplifying systemic autoimmune activity.
The antibodies produced from EBV-infected SLE B cells directly targeted classic lupus autoantigens, supporting their pathogenic role.
Why is this important?
The findings provide a mechanistic explanation for the long-observed association between EBV and lupus. By showing that EBV selectively infects autoreactive B cells and converts them into potent antigen-presenting cells that fuel a cascade of autoimmune activation, this study strengthens the case for EBV as a causal driver of SLE.
It also highlights antigen-presenting B cells as a potential therapeutic target in lupus—opening the door to strategies that interrupt EBV-driven immune reprogramming and downstream autoimmune amplification.
Review article of the month
Tailoring Low-Protein Diets to Improve CKD Health Outcomes
This review highlights that excessive protein intake can worsen chronic kidney disease by increasing glomerular stress and nitrogenous waste, while a tailored low-protein diet (around 0.6 g/kg/day) may help slow progression and improve metabolic outcomes.
Although study results vary, often due to poor adherence, multiple trials and meta-analyses show benefits, including reduced progression to kidney failure and improvements in phosphorus balance, acidosis, and gut microbiome–related toxins.
The authors claim that most adults consume far more protein than is recommended for CKD, and that plant-based protein sources may offer additional benefits. The authors emphasize that low-protein diets remain a core management strategy for non-dialysis CKD and should be individualized, especially for older adults with changing protein needs.
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