End-Stage Renal Disease (ESRD)

Overview

End-stage renal disease (ESRD) is the final, irreversible phase of chronic kidney disease (CKD), in which kidney function is insufficient to sustain life without renal replacement therapy.^[1] In practice, ESRD corresponds to CKD stage 5 (usually defined by an estimated glomerular filtration rate (eGFR) below 15 mL/min/1.73 m²) and is characterized by the need for dialysis or kidney transplantation to manage life-threatening uremia.^[2] This distinguishes ESRD from late-stage CKD (stage 4 and early stage 5), where eGFR is severely reduced (e.g., 15–29 mL/min) but patients may not yet require dialysis if asymptomatic. ESRD carries a grave prognosis: it is a major health burden worldwide with high morbidity and mortality. For example, in the United States over 600,000 individuals live with ESRD, yet the 5-year survival on dialysis is only ~50%^[3] – a survival rate comparable to many cancers. The first year of dialysis is especially perilous (mortality up to 20–30%).^[4] Kidney transplantation dramatically improves outlook, with transplanted patients achieving about 80% five-year survival (versus <50% on dialysis) as noted in clinical registries.^[5] Epidemiologically, the prevalence of ESRD has steadily risen due to increasing rates of diabetes and hypertension globally, and CKD is projected to rank among the top causes of years of life lost by 2040. Overall, ESRD confers a markedly reduced life expectancy and heavy symptom burden, making prevention of progression and timely treatment crucial.

Causes

Diagnosis

Primer

The interplay between impaired metal handling, dysbiosis-driven toxin generation, and global metabolomic disruption in ESRD illustrates how the metallome, microbiome, and metabolome converge on shared pathways of inflammation, oxidative stress, and fibrosis. Loss of renal excretory capacity alters circulating metal availability, reshapes gut microbial communities, and permits accumulation of toxic microbial metabolites such as indoxyl sulfate and p-cresyl sulfate. These combined disturbances amplify endothelial dysfunction, immune activation, and intestinal barrier injury, underscoring the potential of microbiome-based diagnostics and targeted interventions (MBTIs) to detect and modulate pathophysiologic processes that traditional renal markers cannot fully capture.

Etiology

ESRD is the common endpoint of various chronic nephropathies. Diabetic nephropathy (from long-standing diabetes mellitus) is the single leading cause of ESRD worldwide, accounting for roughly 40–50% of new ESRD cases in many regions.^[6]

What are the leading causes of End-Stage Renal Disease (ESRD) worldwide?

ESRD is most commonly caused by long-standing diabetic nephropathy, which accounts for approximately 40–50% of global ESRD cases.^[7] Chronic hyperglycemia produces glomerular hyperfiltration, microvascular injury, and eventually diffuse glomerulosclerosis. Hypertensive nephrosclerosis is the second major cause; poorly controlled blood pressure leads to arteriolar sclerosis, ischemic nephron loss, and interstitial fibrosis. Together, diabetes and hypertension are responsible for the majority of ESRD cases in both developed and developing nations.^[8]

Which other conditions and risk factors contribute to ESRD progression?

Beyond diabetes and hypertension, several chronic nephropathies can progress to ESRD, including IgA nephropathy, focal segmental glomerulosclerosis, membranous nephropathy, and lupus nephritis. Polycystic kidney disease (PKD) is a major genetic cause, with cyst expansion gradually destroying renal parenchyma. Additional contributors include recurrent pyelonephritis, chronic interstitial nephritis, obstructive uropathy, Alport syndrome, and reflux nephropathy. Certain demographics—such as individuals of African ancestry with APOL1 variants—exhibit higher susceptibility. Major risk factors that accelerate CKD progression include poor glycemic control, uncontrolled hypertension, heavy proteinuria, smoking, and chronic exposure to nephrotoxins like NSAIDs. Ultimately, any chronic kidney disorder, if severe or untreated, can culminate in ESRD.^[9]

Pathophysiology

ESRD represents the end result of relentless nephron loss and maladaptive repair processes in the kidneys. As functioning nephron mass declines, the remaining nephrons undergo compensatory hyperfiltration: surviving glomeruli dilate and raise single-nephron GFR to uphold overall filtration. In the short term, this preserves kidney function, but chronically, the intraglomerular hypertension and stretch injury lead to capillary wall damage, podocyte loss, and ultimately segmental sclerosis of glomeruli.^[10] This phenomenon (described in the Brenner hyperfiltration hypothesis) creates a vicious cycle of progressive nephron destruction. Hemodynamic maladaptations are largely mediated by the renin–angiotensin–aldosterone system (RAAS). Decreased renal perfusion triggers renin release and angiotensin II formation, which preferentially constricts efferent arterioles to maintain filtration pressure. However, angiotensin II also promotes inflammatory and fibrogenic pathways (via TGF-β1 and others), accelerating renal scarring.^[11] Indeed, persistent RAAS activation is a central driver of CKD progression, and RAAS inhibitors (ACEis/ARBs) slow decline by lowering glomerular pressure and fibrosis.^[12]

What cellular and metabolic processes further accelerate kidney injury in ESRD?

Progressive CKD shifts from adaptive hyperfunction to destructive remodeling marked by glomerulosclerosis and tubulointerstitial fibrosis. Chronic injury from hypertension, hyperglycemia, or immune-mediated damage drives tubular epithelial cells to release profibrotic cytokines such as TGF-β, activating myofibroblasts and collagen deposition. Uremia intensifies oxidative stress and inflammatory signaling by generating excess reactive oxygen species that impair endothelial and tubular mitochondrial function.

As renal clearance declines, numerous metabolic wastes accumulate, including the validated microbiome-derived uremic toxins indoxyl sulfate (IS) and p-cresyl sulfate (PCS). Their serum levels rise 10- to 50-fold because damaged kidneys cannot secrete them effectively,^[13] and they directly promote oxidative stress, endothelial dysfunction, inflammation, pro-coagulant activity, and profibrotic gene expression.^[14]^[15]

Experimental evidence shows IS stimulates TGF-β1 and epithelial-to-mesenchymal transition, linking microbial metabolites to renal fibrosis.^[16] Strong albumin binding makes IS and PCS poorly dialyzable, allowing substantial accumulation in ESRD. Additional solutes such as advanced glycation end-products and asymmetric dimethylarginine further drive vascular and oxidative injury. Together, these processes establish a self-perpetuating cycle in which nephron loss leads to hyperfiltration and RAAS activation, escalating glomerular hypertension, inflammation, toxin buildup, and progressive destruction of kidney architecture.

Systemic Complications due to ESRD

The loss of kidney function in ESRD has widespread systemic consequences, as failing kidneys no longer maintain internal homeostasis or hormonal functions. Cardiovascular disease (CVD) is the most dire complication, and in fact the leading cause of death in ESRD patients.^[17]

Individuals on dialysis have an extremely high CVD risk owing to both traditional factors (hypertension, dyslipidemia, diabetes) and nontraditional factors associated with uremia (vascular calcification, arterial stiffness, oxidative stress, inflammation). Uremic toxins like indoxyl sulfate and p-cresyl sulfate promote endothelial dysfunction, vascular smooth muscle calcification, and cardiac fibrosis, accelerating atherosclerosis and heart failure.^[18]

ESRD patients commonly develop left ventricular hypertrophy (partly from chronic pressure overload and anemia) and calcific uremic arteriolopathy; arrhythmias and sudden cardiac death are also prevalent, exacerbated by electrolyte shifts (e.g. hyperkalemia) during dialysis. Alongside CVD, Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD) is a hallmark systemic complication: the failing kidneys retain phosphate and cannot activate vitamin D, leading to hyperphosphatemia, hypocalcemia, and low calcitriol.

These trigger secondary hyperparathyroidism, high fibroblast growth factor-23 (FGF23) levels, and resultant bone turnover abnormalities (renal osteodystrophy) with osteomalacia or high-turnover bone disease. Consequences include bone pain, fractures, and metastatic calcification of vessels and soft tissues. The calcium-phosphate product is often elevated in ESRD, driving vascular calcification that further contributes to cardiovascular morbidity.^[19]

Anemia due to ESRD

Anemia is another ubiquitous problem: damaged kidneys produce insufficient erythropoietin (EPO), causing a normocytic, normochromic anemia. Contributing factors include iron deficiency (from poor GI absorption and dialysis-related blood loss), elevated hepcidin (inhibiting iron utilization), and the suppressive effects of inflammation on erythropoiesis.

Untreated, anemia causes fatigue, dyspnea, and cardiac strain (high-output heart failure); fortunately, it can be managed with EPO-stimulating agents and intravenous iron therapy in ESRD. Profound immune dysfunction also occurs. Uremia impairs neutrophil chemotaxis and phagocytosis and causes T-cell dysregulation, leading to an immunocompromised state. As a result, infections are the second leading cause of mortality in ESRD.^[20]

ESRD patients (especially those on hemodialysis with indwelling catheters) are prone to sepsis, pneumonia, and dialysis access infections. Uremic toxins like PCS have been shown to induce a pro-inflammatory phenotype in leukocytes,^[21] which paradoxically coexists with immune paralysis in other contexts – culminating in high infection risk.

Protein-energy wasting and sarcopenia as a result of ESRD

Protein-energy wasting and sarcopenia are common in end stage renal disease, where progressive loss of muscle mass and strength develops through converging metabolic and inflammatory pressures. Persistent inflammation and metabolic acidosis accelerate muscle protein breakdown, while anorexia, reduced appetite, and therapeutic dietary limitations impair nutrient intake.

Dialysis contributes further by removing circulating amino acids during treatment sessions. The cumulative effect is a pronounced decline in muscle and fat reserves, leading to profound fatigue, reduced physical capacity, and increasing frailty.

What are Neurologic complications due to ESRD?

Neurologic complications in end stage renal disease span both peripheral and central systems. Peripheral and autonomic neuropathies present with restless legs, paresthesias, and orthostatic hypotension, while central involvement manifests as uremic encephalopathy. This encephalopathic state produces cognitive slowing, sleep disruption, asterixis, and, when severe, confusion, seizures, or coma, with most symptoms improving once adequate dialysis is restored.

Many individuals with ESRD also experience persistent pruritus and neuropathic pain. Metabolic and endocrine abnormalities are nearly universal, particularly chronic metabolic acidosis that arises from impaired acid excretion and insufficient bicarbonate regeneration. This sustained acidosis drives bone demineralization, accelerates muscle catabolism, and in children contributes to impaired growth.

CVD Complications due to ESRD

Dyslipidemia in ESRD often features elevated triglycerides and reduced HDL, promoting atherosclerosis. Endocrine abnormalities include insulin resistance (uremia causes impaired glucose utilization and hepatic insulin clearance, so some diabetic ESRD patients paradoxically require less insulin), gonadal dysfunction (men often have low testosterone and erectile dysfunction; women can have menstrual irregularities and reduced fertility), thyroid axis changes (low T3 syndrome is common in CKD), and elevated prolactin levels. Secondary hyperparathyroidism, as noted, is an endocrine disorder of mineral metabolism.

Adrenal and cortisol rhythm alterations have also been described. In summary, ESRD affects virtually every organ system – cardiovascular and immune complications are the most life-threatening, while anemia, bone disease, neuropathy, malnutrition, and hormonal imbalances all contribute to the heavy symptom burden and complex management of these patients.

Metabolomic Signature of ESRD

ESRD is marked by a distinct metabolomic signature characterized by the extreme accumulation of protein-bound uremic solutes, nitrogenous waste products, organic acids, and inflammatory metabolites. Indoxyl sulfate and p-cresyl sulfate—derived from microbial metabolism of tryptophan and tyrosine—rise to levels dozens of times higher than in early CKD because damaged kidneys cannot excrete these protein-bound toxins efficiently, and dialysis removes them poorly. These metabolites drive oxidative stress, endothelial injury, vascular stiffness, left ventricular hypertrophy, and fibrotic signaling within the kidney. Parallel increases in endotoxin, or lipopolysaccharide (LPS), advanced glycation end-products, and middle molecules further promote systemic inflammation and cardiovascular risk, establishing a metabolomic milieu tightly linked to mortality and complications in dialysis patients.

Nutritional Immunity

Nutritional immunity becomes profoundly dysregulated in ESRD. Chronic inflammation elevates hepcidin, restricting iron availability for erythropoiesis while paradoxically increasing iron deposition in tissues and fostering microbial dysbiosis. Zinc deficiency, common in ESRD due to impaired absorption and inflammation-mediated sequestration, compromises host tight-junction integrity and antimicrobial defense, promoting barrier disruption and bacterial translocation. Copper handling likewise becomes erratic, contributing to oxidative stress and impaired innate immune signaling. The net effect is a disrupted metal-immune balance that heightens infection susceptibility, sustains systemic inflammation, and reinforces the gut–kidney axis disturbances characteristic of uremia.

Which nutritional-immunity pathways become dysregulated in patients with end-stage renal disease (ESRD)?

Hepcidin

The dysregulation of nutritional immunity in ESRD reflects a coordinated disturbance in iron, zinc, and copper handling driven by chronic inflammation, uremic toxicity, and barrier failure. Persistent inflammatory signaling in advanced CKD markedly elevates hepcidin, the central regulator of iron metabolism, which inhibits intestinal iron absorption and traps iron within the reticuloendothelial system. This inflammation-hepcidin axis is a well-established contributor to functional iron deficiency and the anemia of CKD.^[22]

Zinc Bioavailablity

At the same time due to ESRD, bioavailable zinc levels fall, influenced by dietary restriction, reduced gastrointestinal absorption, and cytokine-mediated sequestration. Zinc deficiency compromises epithelial barrier maintenance and innate immune function, predisposing patients to mucosal vulnerability and infection—patterns consistent with CKD-related immune dysfunction described in nephrology literature.^[23]

Serum Copper and Ceruloplasmin Concentrations

Conversely, serum copper and ceruloplasmin concentrations often rise in ESRD as part of the acute-phase response. Elevated copper contributes to oxidative stress, endothelial injury, and pro-inflammatory signaling, reinforcing the toxic milieu generated by uremic solutes such as indoxyl sulfate and p-cresyl sulfate.^[24] These microbiome-derived uremic toxins further stimulate leukocyte activation, endothelial dysfunction, nitric-oxide depletion, and profibrotic TGF-β signaling,^[25]^[26]amplifying nutritional-immunity perturbations.

Mismetallation in ESRD

The uremic milieu, chronic inflammation, and impaired renal excretion promote the accumulation of circulating toxins and metabolic by-products, many of which disrupt normal protein structure and enzymatic function in a manner analogous to toxic metal substitution. Protein-bound uremic solutes such as indoxyl sulfate and p-cresyl sulfate rise to extremely high concentrations because diseased kidneys cannot secrete them effectively,^[27] and they bind tightly to albumin, preventing efficient dialysis clearance.^[28] Their capacity to induce oxidative stress, inflammation, endothelial dysfunction, and mitochondrial injury^[29][30] mirrors the biochemical consequences of mismetallation, wherein misplaced or excessive metals impair protein stability and cellular redox balance. Through oxidative injury, IS and PCS activate profibrotic pathways including TGF-β1 and epithelial-to-mesenchymal transition,^[31] illustrating how metabolic overload in ESRD functionally produces effects similar to metal dysregulation: protein damage, loss of structural fidelity, and activation of maladaptive signaling cascades. Thus, while not a metal itself, the toxin-driven oxidative microenvironment in ESRD creates conditions under which mismetallation-like injury pathways become pathophysiologically relevant.

Gut–Kidney Axis

The gut–kidney axis reflects the bidirectional relationship between renal failure and microbial dysbiosis. In ESRD, high levels of uremic waste in the blood and gastrointestinal tract, combined with low-fiber dietary restrictions, shift the microbiome toward proteolytic species that generate excess nitrogenous and aromatic metabolites. This results in markedly elevated circulating levels of indoxyl sulfate and p-cresyl sulfate—often dozens-fold above normal.^[32] These validated uremic toxins cause oxidative stress, inflammation, endothelial dysfunction and contribute to cardiovascular pathology, including vascular calcification and left ventricular hypertrophy.^[33] IS also reduces nitric oxide and promotes fibrotic signaling in the kidney,^[34] while PCS activates leukocytes and drives chronic inflammation.^[35] Since both toxins bind tightly to albumin, they are poorly cleared by dialysis and accumulate further in ESRD.^[36] Dysbiosis simultaneously weakens the intestinal barrier: uremia induces mucosal atrophy and disrupts tight junction proteins, facilitating the translocation of endotoxin and microbial fragments into the bloodstream.^[37] This “leaky gut” syndrome amplifies systemic inflammation and contributes to malnutrition, atherosclerosis, and inflammatory anemia. The resulting feedback loop—renal failure worsening dysbiosis, dysbiosis generating toxins and endotoxin, and these factors intensifying systemic and cardiovascular injury—reinforces the central role of the gut–kidney axis in ESRD pathophysiology.^[38]

Interventions

ESRD requires more than replacing filtration—it demands direct intervention against the systemic offenders driving inflammation, oxidative stress, toxin accumulation, and metallomic imbalance. Microbiome-derived uremic toxins, dysfunctional RAAS signaling, chronic acidosis, dysregulated iron metabolism, zinc depletion, copper elevation, endotoxin translocation, and toxic solute retention collectively maintain a biochemical environment that accelerates cardiovascular and renal injury. Interventions must therefore combine dialysis adequacy, pharmacologic therapy, nutritional strategies, and targeted management of metallomic and microbiome-toxin burdens, all supported by the mechanistic pathways described in the referenced literature.

Novel Interventions

Interventions for Microbiome-Derived Uremic Toxins (IS, PCS)

Rationale:
Indoxyl sulfate and p-cresyl sulfate accumulate to extremely high levels in ESRD because damaged kidneys cannot secrete them and standard dialysis clears them poorly due to strong albumin binding.^[39] They induce oxidative stress, endothelial dysfunction, inflammation, and profibrotic signaling,^[40] and stimulate pathways such as TGF-β1 and epithelial-to-mesenchymal transition.^[41]

a. Dialysis Optimization for Toxin Clearance
High-flux hemodialysis, extended-hour nocturnal HD, or hemodiafiltration can improve clearance of middle molecules and partially reduce toxin burden (supported by poor clearance of protein-bound toxins in conventional HD). Ensuring Kt/V adequacy reduces symptoms of under-dialysis.

b. Dietary Prebiotic Fiber Strategies
Increasing fermentable fiber intake reduces production of toxin precursors by shifting microbiota away from proteolytic metabolism (consistent with IS/PCS formation pathways).^[42]

c. Consideration of Oral Sorbents (Where Regionally Approved)
Agents such as AST-120 adsorb indole precursors and lower IS levels supported mechanistically by dependence of IS on microbial tryptophan metabolism.^[43][44]

d. Avoidance of Microbiome-Disrupting Agents
Minimize unnecessary antibiotics, which worsen dysbiosis and raise toxin production (aligned with dysbiosis-driven toxin accumulation described).^[45]

Interventions for Metallomic Dysregulation (Zinc, Copper, Iron, Toxic Metals)

Rationale:
ESRD alters nutritional immunity, elevates hepcidin, sequesters iron, reduces zinc bioavailability, and increases copper as part of the inflammatory acute-phase response.^[46]^[47] These abnormalities contribute to immune dysfunction, oxidative injury, and worsened barrier integrity, reinforcing microbiome and toxin-mediated harm.

a. Treat Inflammation-Driven Iron Sequestration
Use IV iron cautiously and administer ESA therapy to correct functional iron deficiency.^[48]
Correcting anemia reduces oxidative stress and cardiac strain.

b. Zinc Repletion When Indicated
Zinc supplementation may be appropriate in deficiency states to restore epithelial barrier integrity and support innate immunity (supported by zinc roles described in CKD immune dysfunction).^[49]

c. Monitor and Address Copper Excess
Elevated copper—common in inflammatory states—contributes to endothelial oxidative stress; reducing inflammation, improving dialysis adequacy, and avoiding copper-containing supplements help mitigate excess.

d. Reduce Toxin-Associated Oxidative Stress
• Address IS/PCS burden (see Section 1) to indirectly reduce redox stress that parallels mismetallation-like injury patterns.

Endotoxemia and Gut Barrier Dysfunction Correction

Uremia disrupts tight junctions, causing “leaky gut,” endotoxin translocation, and systemic inflammation.^[50] This amplifies cytokine burden, worsens anemia of inflammation, and elevates cardiovascular risk.

a. Improve Dialysis Adequacy
Adequate solute clearance reduces uremic injury to the gut barrier.

b. Dietary Fiber and Microbiome Support
Prebiotic fiber reduces proteolytic fermentation and enhances short-chain fatty acid production, supporting epithelial barrier health (aligned with dysbiosis mechanisms).^[51]

c. Management of Constipation and Dysmotility
ESRD-associated dysmotility worsens dysbiosis; proactive bowel management supports microbial balance.

d. Infection Prevention and Antibiotic Stewardship
Avoid perturbing microbiome stability unless clearly indicated.

Oral Bicarbonate/Citrate

Acidosis worsens muscle wasting and inflammation. Oxidative stress is amplified by IS/PCS and mitochondrial injury.

Oral bicarbonate or citrate to maintain HCO₃⁻ ≥22 mEq/L

Optimize dialysis clearance
Reduce microbial toxin burden (Section 1) to decrease oxidative load

Fecal microbiota transplantation (FMT)

The ability to achieve stable and durable engraftment of transplanted microbial communities is a key determinant of fecal microbiota transplantation (FMT) success. Even so, FMT remains an emerging yet promising therapeutic strategy for CKD and ESRD because it directly targets the dysbiosis-driven mechanisms that contribute to disease progression. Its mechanistic foundation is strong: gut microbial imbalance is known to influence CKD through renin–angiotensin system activation, systemic inflammation, immune dysregulation, and impaired intestinal barrier integrity. Preclinical data consistently show that FMT can normalize dysbiotic microbial profiles, attenuate inflammation, lower circulating uremic toxins, and preserve renal function.

While FMT has not been explored in acute kidney injury (AKI), its application across several CKD subtypes—such as diabetic nephropathy, IgA nephropathy, membranous nephropathy, and focal segmental glomerulosclerosis—has yielded encouraging preclinical and early clinical findings.

Psyllium Husk

Psyllium husk is a soluble, fermentable fiber rich in gel-forming arabinoxylans with emerging therapeutic relevance in end-stage renal disease (ESRD). Through its actions along the gut–kidney axis, psyllium modulates the intestinal microbiota, strengthens epithelial barrier function, lowers systemic inflammation, reduces circulating uremic toxins, and enhances fecal nitrogen excretion. Its principal benefit in ESRD stems from shifting microbial fermentation toward pathways that limit production and systemic absorption of protein-derived toxins such as indoxyl sulfate and p-cresyl sulfate. Clinical studies—primarily short-term prebiotic and fiber-supplementation trials—demonstrate consistent reductions in uremic solutes over 4–12 weeks, including decreases in serum creatinine, pCS, and IS.^[52] Given the central role of uremic toxin burden in ESRD progression, these findings support psyllium husk as a promising adjunctive strategy for mitigating toxin load and inflammatory stress in this population.^[53]

FAQs

What drives the clinical transition from advanced kidney failure to ESRD?

The shift from advanced kidney failure into ESRD is driven by a mix of accelerating physiological stressors that overwhelm the remaining renal reserve. As kidney function declines, patients often experience rising fluid overload, worsening hypertension, and mounting cardiovascular strain. Episodes such as abrupt drops in eGFR—frequently triggered by heart failure events—push the kidneys past a tipping point. This destabilization forces the move to dialysis, not just because filtration capacity has fallen, but because the body can no longer compensate for rapid shifts in volume, toxins, and metabolic waste. These same disruptions also intensify systemic inflammation and elevate gut-derived uremic toxins, illustrating how the microbiome’s metabolic burden becomes more pronounced during the transition. The clinical move to ESRD essentially reflects the moment when these converging stresses make continued conservative management unsafe, signaling that renal replacement therapy is the only path to maintain physiological stability.^[54]

Which uremic toxins are clinically relevant in ESRD, and why are they retained?

Small water-soluble toxins clinically relevant in ESRD include urea, creatinine, uric acid, ADMA, SDMA, guanidinosuccinic acid, methylguanidine, carbamylated compounds, and TMAO. They accumulate because reduced GFR eliminates filtration, and their high production rates exceed residual clearance.^[55]

Middle-molecule toxins include β2-microglobulin, IL-6, IL-8, IL-10, IL-18, PTH, TNF-α, complement factor D, FGF-2, FGF-23, prolactin, kappa and lambda free light chains, myoglobin, CX3CL1, CXCL12, pentraxin-3, and sTNFR1/2. Their larger molecular size prevents passage through conventional dialysis membranes, allowing progressive retention and inflammation-driven complications.^[56]

Protein-bound toxins include indoxyl sulfate, p-cresyl sulfate, AGEs, CMPF, CML, kynurenines, homocysteine, and other aromatic microbial metabolites. They remain in the bloodstream because albumin binding prevents diffusion across dialysis membranes and limits free fraction removal despite adequate dialysis dose.^[57]

Research Feed

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