Blood Retention and Kidney Clearance of Renal-Clearable Gold Nanoparticles Strongly Correlate with Renal Injury Biomarkers

Abstract

Renal-clearable engineered nanoparticles are typically filtered through the glomeruli and transported along the renal tubules before entering the bladder. However, the effects of glomerular leakage and tubular injury, two common features of kidney diseases, on nanoparticle transport remains poorly understood. Herein, we investigated the blood retention, kidney accumulation, and renal clearance of Au₂₅(SG)₁₈ in a doxorubicin-induced acute kidney injury (AKI) mouse model. By correlating its transport with proteinuria and urinary kidney injury molecule-1 (KIM-1), endogenous biomarkers of glomerular leakage and proximal tubular injury, respectively, we found that glomerular leakage, as indicated by a >50-fold increase in proteinuria, did not enhance its blood clearance. Instead, tubular injury significantly reduced glomerular filtration, resulting in elevated blood retention, increased kidney accumulation, and reduced renal clearance of Au₂₅(SG)₁₈. Moreover, Au₂₅(SG)₁₈ blood retention exhibited a very strong positive correlation with urinary KIM-1 (Pearson’s coefficient r = 0.90), much stronger than KIM-1 correlations with conventional glomerular filtration blood markers such as serum creatinine. This suggests that Au₂₅(SG)₁₈ could serve as a sensitive exogenous blood marker of tubular injury, expanding the diagnostic potential of renal-clearable nanoparticles in kidney diseases.

Graphical Abstract

In a doxorubicin-induced acute kidney injury model, proximal tubular injury—rather than glomerular leakage—predominantly determines the renal clearance of gold nanoclusters. The blood retention of Au₂₅(SG)₁₈ strongly correlates with proximal tubular injury biomarker KIM-1, highlighting its potential as a sensitive exogenous blood marker for proximal tubular injury.

Introduction

Engineered nanoparticles are increasingly designed to leverage rapid renal clearance pathways to reduce nonspecific accumulation and minimize potential toxicities^[1]. Typically, nanoparticles with hydrodynamic diameters below 5–8 nm under physiological conditions can be efficiently filtered through the glomeruli from the bloodstream into the tubular lumen before ultimately entering the bladder^{[1a, 2]}. This filtration process is highly size-dependent due to the unique anatomical structure of the glomerular basement membrane (pore size: 2–8 nm), fenestrations between endothelia (~70 nm), slit diaphragm of podocytes (4–9 nm) and the dense glycocalyx layer on the endothelium^[2]. These nanoscale structures not only restrict the passage of larger nanoparticles but also prevent filtration of plasma proteins such as albumin of > 8 nm^[3]. However, in diseased kidneys with glomerular injury, these barriers become compromised, allowing proteins to leak into the tubular lumen and eventually into the urine, a condition known as proteinuria, which serves as a key endogenous biomarker for glomerular damage^[4]. While renal-clearable nanoparticles are small enough to be efficiently filtered through normal glomeruli, it remains unclear whether glomerular leakage affects their blood clearance and renal excretion. This knowledge gap highlights the need for systematic investigations correlating blood retention and kidney clearance of engineered nanoparticles with proteinuria levels in diseased kidneys.

Once renal-clearable nanoparticles are filtered through the glomerulus, they enter the proximal tubules, which account for approximately 50% of the kidney’s mass and are also highly susceptible to injury^[5]. Under normal conditions, the retention of engineered nanoparticles in the proximal tubules is largely influenced by their surface charge and electrostatic interactions with the microvilli lining the tubular epithelium^[6]. However, when the proximal tubules are injured, nanoparticle uptake by tubular cells is significantly reduced, and the particles often become obstructed by cellular debris or protein casts in the lumen of proximal tubules^[7] or the loop of Henle^[8], where flow dynamics are substantially reduced. This obstruction further impairs the renal clearance of the nanoparticles. To noninvasively assess tubular injury, several endogenous biomarkers have been identified and clinically tested. Among them, kidney injury molecule-1 (KIM-1) is considered one of the most sensitive markers, as it is upregulated in proximal tubular cells following injury and subsequently released into the urine^[9]. Although reduced renal clearance and prolonged nanoparticle retention have been frequently observed in kidneys with tubular damage^{[7–8, 10]}, the relationship between nanoparticle transport and KIM-1 levels has not been systematically investigated.

Herein, we used a doxorubicin (DOX)-induced kidney disease mouse model, characterized by both leaky glomeruli and patchy tubular necrosis, to investigate how proteinuria and urinary KIM-1 correlate with blood retention, kidney accumulation, and renal clearance of Au₂₅(SG)₁₈, an atomically precise gold nanocluster composed of 25 gold atoms and 18 glutathione surface ligands. Although DOX-induced kidney injury is known to slightly reduce pH and acidify the local environment (down to pH 6.02 ± 0.032)^[11], Au₂₅(SG)₁₈ remains highly stable and no changes in its characteristic absorption even pH 4 due to its unique closed-shell electronic structure^[12] (Figure S1). Contrary to the intuitive assumption that increased glomerular permeability facilitates faster nanoparticle clearance from the blood, our findings show that severe glomerular leakage—reflected by a >50-fold increase in 24-hour proteinuria—did not accelerate Au₂₅(SG)₁₈ clearance. Instead, the 30-minute blood concentration of Au₂₅(SG)₁₈ increased by 1.8-fold compared to healthy controls. This increase was consistent with reduced clearance of serum creatinine (sCr), the most widely used clinical marker for estimated glomerular filtration rate (eGFR)^[13], suggesting impaired filtration as the cause of reduced nanoparticle clearance. Surprisingly, the blood concentration of Au₂₅(SG)₁₈ showed a much stronger correlation with the tubular injury marker urinary KIM-1 (Pearson’s r = 0.90) than with the traditional GFR markers (blood urea nitrogen (BUN), r = 0.40; sCr, r = 0.68; creatinine clearance, r = −0.73), indicating that Au₂₅(SG)₁₈ is more sensitive to GFR reduction when tubular injury plays a key role. Despite reduced filtration into the tubular lumen, Au₂₅(SG)₁₈ accumulation in the injured renal tubules was significantly increased, contributing to a marked reduction in renal clearance alongside impaired blood clearance. Together, these results suggest that both blood and renal clearance of Au₂₅(SG)₁₈ are primarily governed by tubular injury–induced reductions in GFR and enhanced tubular accumulation. Moreover, Au₂₅(SG)₁₈ may serve as a more sensitive and accurate blood-based indicator of early kidney injury than conventional renal biomarkers such as sCr and BUN.

Results and Discussion

Synthesis of Au₂₅(SG)₁₈ and Establishment of Doxorubicin-induced AKI Model

Au₂₅(SG)₁₈ has been widely used as an imaging probe to investigate nanoparticle transport and interactions in the kidneys and tumors^[14]. It exhibits efficient renal clearance (~50% excreted in urine within 2 hours)^[15], is detected by various imaging modalities^{[14a, 15]}, and enables precise quantification via inductively coupled plasma mass spectrometry (ICP-MS) (Figure 1A). The rapid renal clearance of these glutathione coated AuNPs A minimize RES organ retention and reduce the risk of immunological effects^[16]. The synthesis of Au₂₅(SG)₁₈ has been previously described in our earlier work^[15], following the reported method.^[17] Au₂₅(SG)₁₈ exhibits distinct UV–Vis absorption peaks at 400, 445, and 675 nm and near-infrared fluorescence emission at 740 and 802 nm, attributed to its discrete energy states, which are comparable in scale to the electron Fermi wavelength^[18] (Figure 1B–C). To establish a kidney disease model involving both glomerular and tubular injuries, BALB/c mice were randomly assigned to receive either saline or doxorubicin (DOX; 20 mg/kg, intravenous injection), with 8–10 mice per group to reduce biological variability inherent in in vivo studies (Figure 1D). We chosen 20 mg/kg doses of DOX because it can induce dual compartment injuries. Lowering the dose to 15 mg/kg resulted in high inter-animal variability in proteinuria levels, and histopathological analysis revealed no consistent evidence of glomerular damage (Figure S2). In contrast, 20 mg/kg DOX consistently induced pronounced proteinuria and pathological features characteristic of both glomerular and tubular injury, supporting its selection as the optimal dose for this disease model. A post-hoc power analysis conducted using G*Power further supported the sufficiency of the chosen group size, demonstrating a statistical power exceeding 0.80, which is considered the minimum acceptable threshold for detecting significant effects^[19] (Figure S3). For each mouse, we measured its renal biomarkers while quantifying gold distribution as follows. Kidney injury and filtration function were evaluated by collecting 24-hour urine samples on days 3–4 post-injection to measure proteinuria, KIM1/creatinine ratio, urine output, and 24-hour urinary creatinine (uCr) clearance. Four days post-treatment, DOX-treated mice exhibited a 9.5 ± 1.9% loss in body weight, in contrast to control mice, which gained 0.12 ± 1.2% (Figure 1E). To account for body weight differences, Au₂₅(SG)₁₈ was administered intravenously at 100 mg/kg based on individual body weight to both saline- and DOX-treated mice, four days after saline or DOX injection. Thirty minutes after injection of Au₂₅(SG)₁₈, blood, kidney, and urine samples were collected for gold quantification using ICP-MS. The 30-minute time point was selected based on our previous pharmacokinetic study of Au₂₅(SG)₁₈, which identified it as the turning point between the initial rapid distribution phase and the subsequent slower elimination phase^[15–16]. Our earlier research also demonstrated that the kidney is the primary organ responsible for both the accumulation and clearance of renal-clearable Au₂₅(SG)₁₈ nanoclusters, with long-term biodistribution studies showing that less than 1.5% of the injected dose remains in any organ, including the kidney, one-month post-injection^[15]. Serum samples were obtained to measure classical blood biomarkers of GFR, including BUN and sCr, while kidneys were harvested for pathological analysis.

Figure 1.

Experimental design for evaluating the effects of glomerular and tubular injuries on nanoparticle kidney clearance in a Doxorubicin (DOX)-Induced Acute Kidney Injury (AKI) Model. A) Au25(SG)18, a renal-clearable gold nanoparticle with a core of 25 gold atoms, was selected as a model particle. B) UV–Vis absorption spectrum of synthesized Au25(SG)18 showing characteristic peaks at 400 nm, 445 nm, and 675 nm, confirming successful synthesis and high purity. C) Fluorescence emission spectrum of Au25(SG)18 showing peaks at 740 nm and 802 nm under 350 nm excitation, enabling fluorescence microscopy imaging of Au25(SG)18 distribution in kidney tissue sections. D) The DOX-induced AKI mouse model was established by a single intravenous injection of 20 mg/kg DOX. Saline-injected mice served as the normal control group. Urine was collected over 24 hours on days 3–4 post-DOX injection for analysis of proteinuria (glomerular injury biomarker), Kidney Injury Molecule-1 (KIM-1, tubular injury biomarker), 24-hour urinary creatine clearance (GFR biomarker), and urine output (urine volume, indicator of AKI). On day 4, 30 minutes after intravenous injection of 100 mg/kg Au25(SG)18, blood, kidney, and urine samples were collected for ICP-MS quantification of gold. Serum samples were analysed for BUN and sCr (clinical eGFR biomarkers). Kidneys were harvested for pathological evaluation. E) Significant body weight loss was found in DOX-treated mice 4 days post-injection (20 mg/kg). Each group consisted of 10 mice. Data are presented as mean ± standard deviation. Statistical significance was assessed using a two-tailed Student’s t-test (α = 0.05).

Reduced Glomerular Filtration of Nanoparticles Despite Glomerular Protein Leakage

DOX is a widely used first-line chemotherapeutic agent, but it is also known to cause damage to both the glomeruli and proximal tubules^[20]. In the glomerulus, DOX injures podocytes, disrupting the slit diaphragm and increasing glomerular permeability, which leads to significant proteinuria^[21]. Indeed, four days after DOX administration, mice developed marked proteinuria. As shown in Figure 2A, 24-hour urinary protein excretion increased 51-fold—from 544 ± 190 μg/24 h in control mice to 27,803 ± 2639 μg/24 h in DOX-treated mice and urinary protein concentration rose by an average of 70-fold, from 611 ± 105 μg/mL in controls to 42,927 ± 26,361 μg/mL in DOX-treated mice, while 24-hour urine volume remained comparable between the two groups (Figure 2B and 2C). These substantial increases in both total protein excretion and urine protein concentration confirm that the slit diaphragm was severely compromised and glomerular permeability significantly elevated. Despite this, the renal-clearable gold nanoparticle Au₂₅(SG)₁₈ with a core size of ~1.2 nm^[17], much smaller than plasma proteins (e.g., albumin, >8 nm^[3]), did not show enhanced blood clearance. Instead, its 30-minute blood concentration increased by 1.8-fold, from 30 ± 2.7 μg/mL in control mice to 54 ± 9 μg/mL in DOX-treated mice (Figure 2D). This rise was consistent with an elevated sCr level from 0.15 to 0.32 ± 0.16 mg/dL after DOX treatment (Figure 2E), a well-established eGFR marker. The 24-hour urine creatinine clearance declined by nearly half from 0.32 ± 0.08 mL/min in normal controls to 0.17 ± 0.10 mL/min in DOX-treated mice (Figure 2F; see Supplementary Information for calculation). Together, these findings indicate that while DOX induces glomerular injury and increases protein leakage, it simultaneously reduces GFR, leading to impaired blood clearance and elevated blood retention of Au₂₅(SG)₁₈. Since proteinuria (quantified by urine protein concentrations) exhibited continuous changes in normal and DOX-treated mice, we analyzed its correlation with Au₂₅(SG)₁₈ clearance using Pearson correlation analysis^[22]. Proteinuria showed a strong negative correlation with the renal excretion of Au₂₅(SG)₁₈ (r = −0.83), a good positive correlation with the blood concentration of Au₂₅(SG)₁₈ (r = 0.74), and a positive but moderate correlation with nanoparticle kidney accumulation (r = 0.68) (Figure 2G-I). The opposite trends in kidney clearance between proteinuria and Au₂₅(SG)₁₈ suggest their distinct elimination mechanisms.

Figure 2.

Reduced glomerular filtration of Au25(SG)18 in the presence of protein-leaky glomeruli in DOX-treated mice. A-C) DOX treatment resulted in significantly increased total 24-hour proteinuria (A) and elevated urinary protein concentration (B), while urine output remains comparable to that of normal mice (C). D-F) Impaired glomerular filtration in DOX-treated mice was evidenced by increased 30-minute blood concentration of Au25(SG)18 (D), elevated serum creatinine (sCr) level (E), and decreased 24-hour urinary creatinine clearance (F). For panels A-F, each group consisted of 8 mice. Data are presented as mean ± standard deviation. Statistical significance was assessed using a two-tailed Student’s t-test (α = 0.05). G-I) Pearson correlation analysis between proteinuria (quantified by urinary protein concentration) and Au₂₅(SG)₁₈ biodistribution at 30 minutes post-injection, including kidney accumulation (G), blood retention (H), and urinary excretion (I, %ID = percentage of injected dose). Data from both normal control and DOX-injected mice were plotted. The relationships were indicated by Pearson correlation coefficient values (r_p). N = 16, with no outliers detected.

Kidney Transport of Au₂₅(SG)₁₈ Altered by Tubular Injury

In addition to inducing glomerular leakage, DOX also damages proximal tubules^[23] by disrupting epithelial cell polarity and reducing reabsorptive capacity, which promotes the formation of proteinaceous casts and sloughed epithelial cells that obstruct the tubules. These tubular obstructions contribute to a decline in GFR and an elevation in sCr. As one of the most sensitive markers of tubular injury, the urinary KIM-1/creatinine ratio increased approximately 4.4-fold—from 15.5 ± 9 ng/mg in normal controls to 68 ± 19 ng/mg following DOX treatment (Figure 3A and S4), corresponding to a 4.5-fold increase in total urinary KIM-1 excretion over 24 hours (Figure 3B). This impairment was further supported by pathological analyses. The predominant renal damage in DOX-injected mice was patchy tubular necrosis, primarily localized to the outer cortical (subcapsular) region of the kidney (Figure 3C and S5). In addition, proximal tubules showed loss of brush border integrity, enlarged pale-staining cytoplasm, and cytoplasmic vacuolization. Necrotic epithelial cells often detached and sloughed into the tubular lumen, leading to luminal obstruction by cellular debris and proteinaceous casts. Moreover, increased protein permeability due to glomeruli abnormalities (Figure S6) enhanced accumulation of plasma proteins in the tubules, exacerbating luminal obstruction and tubular stress, ultimately reducing GFR.

Figure 3.

DOX-induced proximal tubular injury leads to delayed blood clearance, enhanced kidney accumulation, and reduced urinary excretion of Au25(SG)18. A,B) Urinary KIM-1/creatinine ratio (A) and the total amount of KIM-1 excreted over 24 hours (B) were significantly elevated in DOX-treated mice compared to controls, indicating proximal tubular injury. C) H&E staining of paraffin-embedded kidney sections showed normal proximal tubules in control mice, while DOX-treated mice exhibited hallmark features of tubular damage, including patchy necrotic tubules with pale and degenerative cytoplasm (pointed by black arrows), enlarged nuclei (pointed by blue arrows), and lumen obstruction due to protein casts (pointed by green arrows). D) Kidney accumulation of Au25(SG)18 was markedly higher in DOX-treated mice compared to controls. E) Renal clearance efficiency of Au25(SG)18 was significantly reduced after DOX treatment. F-H) Silver enhancement imaging of Au25(SG)18 on kidney tissues revealed increased renal accumulation of Au25(SG)18 in DOX-treated mice (G, enhanced proximal tubular accumulation was pointed by yellow arrows) compared to control mice (F, filtered nanoparticles in the proximal tubular lumen for clearance were found and pointed by yellow arrows), with H showing a magnified image highlighting specific localization of Au₂₅(SG)₁₈ (brown color, silver-stained) in necrotic tubules. I-L) Direct fluorescence imaging of Au25(SG)18 distribution on kidney tissues revealing its enhanced kidney accumulation after DOX treatment due to prolonged blood retention and interaction with necrotic proximal tubules. (K,L) Zoomed-in fluorescence images showing co-localization of Au25(SG)18 fluorescence (L, red signal) with necrotic tubules (K, pointed by arrows) and accumulation of gold in peritubular capillaries (white triangles in panels J and L). For panels A, B, D, E, each group consisted of 8 mice. Data are presented as mean ± standard deviation. Statistical significance was assessed using a two-tailed Student’s t-test (α = 0.05).

Despite the slower glomerular filtration, kidney accumulation of Au₂₅(SG)₁₈ increased significantly from 75.3 ± 47 μg/g tissue in controls to 242.8 ±97 μg/g tissue in DOX-treated mice (Figure 3D) due to impaired excretion and tubular accumulation. Although a single 20 mg/kg dose of DOX was administered, individual variability in drug response resulted in varying degrees of tubular injury across the treated mice, leading to a spectrum of kidney damage severity (Figure S7). Consistent with this pattern, selective accumulation of Au₂₅(SG)₁₈ in necrotic tubules containing detached cells was observed in kidney tissues from DOX-treated mice using both silver staining of gold nanoparticles (Figures 3F-H) and direct fluorescence imaging of Au₂₅(SG)₁₈ (Figures 3I-L). On the other hand, morphologically more preserved (though still damaged) tubules exhibited lower gold accumulation, consistent with partial clearance of Au₂₅(SG)₁₈ into the tubular lumen (Figure S7). In addition, Au₂₅(SG)₁₈ fluorescence and silver-stained nanoparticles were also clearly seen in peritubular capillaries, consistent with prolonged blood retention (Figures 3G and 3J). In contrast, significantly lower amount of Au₂₅(SG)₁₈ were detected in the lumen of renal tubules in normal kidneys, and the vascular Au₂₅(SG)₁₈ signal was negligible (Figures 3F and 3I). Therefore, reduced blood clearance and enhanced retention in the kidneys are responsible for ultimate reduction in the renal clearance of Au₂₅(SG)₁₈ (Figure 3E), from 58.7 ± 12% of the injected dose (%ID) in normal mice to 16.6 ± 12 %ID in DOX-treated mice.

Strong Correlation of Au₂₅(SG)₁₈ Blood Clearance with Proximal Tubular Injury Biomarker KIM-1

A strong Pearson’s correlation (r = 0.90) between blood clearance of Au₂₅(SG)₁₈ and urinary KIM-1 was observed (Figure 4A), confirming that tubular injury-induced GFR reduction rather than glomerular leakage is primarily responsible for the altered blood clearance of Au₂₅(SG)₁₈. Although Pearson’s correlation analysis revealed that the urinary KIM-1/creatinine ratio was also associated with Au₂₅(SG)₁₈ kidney accumulation, and urinary excretion (Figure 4B and 4C), its correlation with Au₂₅(SG)₁₈ blood concentration (r =0.90) was stronger than with kidney accumulation (r = 0.73) or urinary excretion (r = –0.81). Moreover, the correlation between Au₂₅(SG)₁₈ blood retention and urinary KIM-1 (Pearson’s r = 0.90) exceeded that with conventional GFR biomarkers, including blood urea nitrogen (BUN, r = 0.4; Figure S8), sCr (r = 0.68), and 24-hour urinary creatinine clearance (r = −0.73) (Figure 4D-F). These findings suggest that renal-clearable nanoparticles can serve as an effective exogenous blood marker for kidney disease, particularly for detecting tubular injury. While KIM-1 is one of the most sensitive biomarkers for detecting proximal tubular injury, its clinical and experimental utility is limited by the need for urine collection and normalization to urinary creatinine—an approach prone to variability due to differences in hydration status, muscle mass and renal function^[24]. These challenges make urinary biomarkers less practical in clinical settings. As a result, blood-based markers such as BUN and sCr remain the standard for routine kidney function assessment, despite their limited sensitivity and specificity for early-stage injury. When comparing the correlation of urinary KIM-1 with BUN (r = 0.54; Figure 4G), serum creatinine (r = 0.60; Figure 4H) and creatinine clearance (r = −0.66; Figure 4I), the correlation of urinary KIM-1 with blood retention of Au₂₅(SG)₁₈ is significantly stronger (r = 0.90; Figure 4A), indicating that Au₂₅(SG)₁₈ could be a more sensitive and robust blood-based biomarker for tubular injury than either BUN or sCr.

Figure 4.

Pearson correlation analysis reveals a strong association between the proximal tubular injury marker KIM-1 with the kidney clearance of Au25(SG)18, with the strongest correlation observed between urinary KIM-1 and Au25(SG)18 blood clearance. A-C) Urinary KIM-1 levels showed strong correlations with Au25(SG)18 in blood (A), kidney (B), and urine (C) at 30 minutes post intravenous injection. D-F) Correlations between Au25(SG)18 blood concentration with conventional GFR biomarkers: BUN (D), sCr (E), and 24-hour urinary creatinine clearance (F). G-I) Correlations between urinary KIM-1 and traditional GFR biomarkers: BUN (G), sCr (H), and creatinine clearance (I). J) Heatmap summarizing Pearson’s r values for correlations between kidney-determined Au25(SG)18 biodistribution parameters (blood concentration, kidney accumulation, and urinary excretion) and renal injury/function biomarkers. The relationships were indicated by Pearson correlation coefficient values (r_p). N = 16, with no outliers detected.

Conclusion

Kidney elimination is increasingly utilized as a primary pathway for clearing engineered nanoparticles from the body. Therefore, a fundamental understanding of how kidney disease affects the in vivo transport of renal-clearable nanoparticles is essential for both enhancing their biomedical applications and minimizing potential side effects. In this study, we quantitatively evaluated how glomerular leakage and tubular injury influence the blood retention, kidney accumulation, and renal clearance of Au₂₅(SG)₁₈ in a DOX-induced kidney injury mouse model. Our results demonstrate that increased glomerular permeability did not enhance the blood clearance of Au₂₅(SG)₁₈. Instead, its clearance was primarily governed by reduced glomerular filtration resulting from tubular injury. Notably, as summarized in the heatmap of Pearson’s r values (Figure 4J and S9-S13), among the renal injury and function biomarkers tested, the blood clearance of Au₂₅(SG)₁₈ exhibited the strongest correlation with urinary KIM-1 (r = 0.90), substantially stronger than with conventional clinical GFR markers such as BUN, serum creatinine and creatinine clearance (r < 0.8). This suggests that renal clearable gold nanoparticle like Au₂₅(SG)₁₈ could serve as a sensitive and accurate exogenous blood marker for tubular injury, complementing its potential use as a urinary markers and contrast agents^{[15, 25]} for kidney disease diagnosis. Not limited to DOX-induced AKI, cisplatin-induced tubular injury—despite the absence of glomerular damage—also resulted in increased blood retention of Au₂₅(SG)₁₈ nanoclusters (Figure S14). These findings unraveled that it is glomerular filtration reduction resulted from tubular injury rather than glomerular leakage that governs blood clearance of renal clearable nanoparticles, laying down a foundation for renal clearable nanoparticles as a blood marker in kidney disease diagnosis.

Supplementary Material

The data that supports the findings of this study are available from the submitted supporting information file.