Discrepant Urinary Findings Between Dipstick Protein and Sulfosalicylic Acid Test in a Patient With Hyaline Casts: A Case Report

ABSTRACT

Background

Routine urinalysis is a foundational screening tool; however, increased hyaline casts accompanied by a negative dipstick protein result may complicate laboratory interpretation. In patients at high risk of acute kidney injury (AKI), this discordant pattern may warrant confirmatory protein testing and correlation with renal‐function trends.

Case Presentation

A 31‐year‐old female with hemophagocytic lymphohistiocytosis (HLH) underwent routine urinalysis after allogeneic hematopoietic stem cell transplantation (allo‐HSCT). Automated sediment analysis detected elevated hyaline casts (5.8/μL), whereas the concurrent dipstick protein result was negative. Protocol‐based sulfosalicylic acid (SSA) verification yielded a visually graded positive (++) reaction. Serial renal‐function monitoring showed that serum creatinine (SCr) increased from 53 μmol/L on December 10 to 62 μmol/L on December 12, followed by progressive deterioration and a peak SCr of 132 μmol/L with an estimated glomerular filtration rate (eGFR) nadir of 46.3 mL/min/1.73 m² on December 24. Follow‐up urinalysis on December 26 showed normalization of this urinary phenotype, with negative dipstick protein, negative SSA testing, and a decrease in hyaline casts to 0.5/μL. These findings were consistent with a transient urinary abnormality occurring during evolving AKI rather than persistent kidney disease.

Conclusion

In this high‐risk post‐transplant patient, increased hyaline casts with negative dipstick protein and positive SSA testing occurred during evolving AKI and resolved as renal function improved. The finding may indicate acid‐precipitable non‐albumin urinary material, but its molecular basis and relationship to tubular injury remain uncertain.

In this post‐transplant patient, increased hyaline casts with negative dipstick protein but positive SSA testing occurred during evolving acute kidney injury and resolved with renal recovery. This discordant urinalysis pattern may warrant confirmatory protein testing and correlation with serial renal function in patients at high risk of AKI.

1. Introduction

Routine urinalysis serves as a fundamental, noninvasive screening tool in clinical medicine, providing simultaneous morphological and biochemical insights into renal function [1, 2]. The consistency between urinary casts in the sediment and urinary protein levels is crucial for the early diagnosis of renal tubular and glomerular disorders [1, 3]. This concurrent evaluation is particularly critical in high‐risk populations, such as patients undergoing allogeneic hematopoietic stem cell transplantation (allo‐HSCT) for hemophagocytic lymphohistiocytosis (HLH), whose kidneys are highly vulnerable to tubular injury secondary to cytokine storms and nephrotoxic interventions [4, 5, 6].

A small number of physiological hyaline casts generally have no clinical significance; however, pathological positivity of hyaline casts often suggests abnormal function of renal tubular epithelial cells [1]. A specific and clinically perilous diagnostic trap arises when automated urine sediment analysis detects positive hyaline casts while the concurrent dipstick protein result is negative [7, 8]. This discordant pattern can easily mislead clinicians into attributing the casts to benign physiological causes, creating a false sense of security and potentially missing a critical window for early intervention in subclinical renal tubular injury [9].

The underlying explanation for this discrepancy lies in a fundamental methodological limitation of urine protein testing. The standard dipstick reagent strip is primarily albumin‐sensitive and usually requires approximately 100–150 mg/L albumin to yield a positive result [7, 10]. In contrast, the sulfosalicylic acid (SSA) test precipitates a broader spectrum of urinary proteins, including non‐albumin proteins, with a lower detection range of approximately 50–100 mg/L [11, 12]. This difference in analytical sensitivity and protein reactivity provides a plausible analytical explanation for a dipstick‐negative but SSA‐positive pattern. Hyaline casts are composed predominantly of Tamm–Horsfall glycoprotein, also known as uromodulin, a non‐albumin protein that may therefore be missed by routine dipstick testing [13, 14, 15]. Uromodulin expression and urinary excretion may change under conditions of renal stress, although the clinical significance of these changes remains context dependent [9, 16]. Although SSA testing can detect urinary proteins that may be missed by albumin‐sensitive dipsticks, the clinical significance of this specific discordant pattern, including its relationship with tubular stress, remains uncertain and requires further validation [8, 11].

Systematic guidance on the interpretation of increased hyaline casts accompanied by negative dipstick protein remains limited, particularly in clinically complex post‐transplant patients. Here, we describe the analytical evaluation and clinical course of this discordant urinalysis finding in a patient with HLH after allo‐HSCT and discuss its interpretation in the context of evolving renal dysfunction.

2. Case Presentation

2.1. Patient Information and Clinical Context

A 31‐year‐old female with a 2‐year history of hemophagocytic lymphohistiocytosis was admitted to the Department of Hematology on December 9, 2025, 19 days after undergoing allo‐HSCT. The admission was for routine post‐transplant monitoring and management of chemotherapy‐associated myelosuppression rather than for renal complications, and no clinical evidence of GVHD was documented during hospitalization. No urinary symptoms, edema, flank pain, or documented oliguria were present at admission. At the time of admission, her body temperature was normal with no fever; C‐reactive protein (CRP) was 6.5 mg/L (reference range: 0–10 mg/L); and serum ferritin was 1998.00 ng/mL on December 10 (reference range: 11–306.8 ng/mL), indicating persistent systemic inflammatory activation despite clinical stability [4, 5]. The patient reported no urinary symptoms, including frequency, urgency, dysuria, hematuria, or foamy urine. There was no history of diabetes mellitus, hypertension, or chronic kidney disease. No family history of malignancy was reported. No strenuous exercise or documented fever was identified in the week before urinalysis. However, nausea, vomiting, poor oral intake, and possible volume depletion were present and were considered potential contributors to altered renal hemodynamics and cast formation. This case report was conducted in accordance with the Declaration of Helsinki. Given the retrospective nature of this clinical observation and the use of de‐identified clinical data, formal ethical review was waived by the Ethics Committee of Shanghai Tongren Hospital, with an exemption approval number of Lunmian 2026–003. Written informed consent for publication was obtained from the patient.

2.2. Treatment History and Clinical Course

Following admission, the patient received comprehensive post‐transplant management. Anti‐infective therapy included cefoperazone–sulbactam for bacterial infection, oral posaconazole for antifungal prophylaxis, letermovir for cytomegalovirus (CMV) prevention, and trimethoprim–sulfamethoxazole (SMZ) for Pneumocystis jirovecii pneumonia (PJP) prophylaxis. For graft‐versus‐host disease (GVHD) prevention, the patient was treated with mycophenolate mofetil (MMF) and cyclosporine A (CSA). Ursodeoxycholic acid was administered to promote bile excretion. Due to cytopenia, supportive treatments included granulocyte colony‐stimulating factor (G‐CSF) for leukocyte recovery, thrombopoietin (TPO) and romiplostim for platelet production, as well as component blood transfusions. On December 24, 2025, the patient received ruxolitinib for the treatment of the primary disease. During hospitalization, the patient experienced nausea, vomiting, and poor oral intake, requiring gastrointestinal protection, antiemetic therapy, and parenteral nutritional support. During progressive renal‐function deterioration, nephrology consultation considered drug‐induced AKI, most likely related to CSA exposure in the context of post‐transplant multidrug therapy. On December 24, 2025, when serum creatinine (SCr) reached its peak, CSA was reduced and replaced with tacrolimus to reduce suspected cyclosporine‐related nephrotoxicity. Intravenous hydration was optimized, and additional nephrotoxic medications, including aminoglycosides and nonsteroidal anti‐inflammatory drugs, were avoided. After these interventions, renal function gradually improved, and the patient was discharged on December 29, 2025, with an SCr of 70 μmol/L. The chronological clinical course, major medication exposure, renal‐function changes, and management are summarized in Table 1.

TABLE 1.

Chronological clinical course, renal‐function changes, and management.

Date	Clinical event	Treatment/Exposure	Renal‐related findings	Interpretation/Management
2023	HLH with chronic active EBV infection diagnosed	Steroids, CSA, anti‐infective/supportive therapy	No recorded renal dysfunction	Baseline disease background
2025‐12‐09	Admission after allo‐HSCT	CSA + MMF for GVHD prophylaxis; antimicrobial and supportive therapy	No urinary symptoms or edema	Routine post‐transplant observation; no GVHD diagnosis
2025‐12‐10	Baseline renal assessment	Continued post‐transplant treatment	SCr 53 μmol/L; eGFR 121.5 mL/min/1.73 m2; blood β2‐MG 4.0 mg/L; CRP 6.5 mg/L; ferritin 1998 ng/mL; uric acid 168 μmol/L	Preserved glomerular filtration; blood β2‐MG elevated, with nonspecific clinical significance in the post‐transplant setting
2025‐12‐12	Earliest detectable SCr increase	Continued CSA exposure	SCr 62 μmol/L; blood β2‐MG 5.3 mg/L	Earliest detectable renal‐function deterioration; this isolated increase did not independently meet the KDIGO creatinine criterion for AKI
2025‐12‐16	Key urinalysis	Continued CSA; supportive therapy	Dipstick protein negative; SSA positive; hyaline casts 5.8/μL	Discordant urinalysis during evolving renal dysfunction
2025‐12‐19	Nephrology evaluation; drug‐induced AKI clinically suspected	Continued monitoring	SCr 75 μmol/L; eGFR 92.2 mL/min/1.73 m2; blood β2‐MG 6.7 mg/L	Clinical suspicion of drug‐induced AKI based on progressive SCr elevation, nephrotoxic exposure, and the overall clinical course
2025‐12‐24	Peak SCr; KDIGO creatinine criterion fulfilled	CSA reduced/replaced; fluids optimized	SCr 132 μmol/L; eGFR 46.3 mL/min/1.73 m2; blood β2‐MG 8.0 mg/L	SCr peaked at 132 μmol/L; the available serial SCr data fulfilled the KDIGO criterion for AKI; CSA‐related nephrotoxicity was considered and treatment was adjusted
2025‐12‐26	Recovery phase	Adjusted treatment regimen	SCr 86 μmol/L; eGFR 77.5 mL/min/1.73 m2; SSA negative; hyaline casts 0.5/μL	Renal and urinary findings improved
2025‐12‐29	Discharge	Outpatient monitoring	SCr 70 μmol/L; blood β2‐MG 3.7 mg/L; CRP 0.6 mg/L	Improved renal function

Abbreviations: β2‐MG, beta‐2 microglobulin; AKI, acute kidney injury; allo‐HSCT, allogeneic hematopoietic stem cell transplantation; CRP, C‐reactive protein; CSA, cyclosporine A; EBV, Epstein–Barr virus; eGFR, estimated glomerular filtration rate; GVHD, graft‐versus‐host disease; HLH, hemophagocytic lymphohistiocytosis; MMF, mycophenolate mofetil; SCr, serum creatinine; SSA, sulfosalicylic acid.

2.3. Routine Urinalysis and Verification Procedure

On December 16, 2025, a fresh clean‐catch midstream morning urine sample was collected and analyzed within 1 h, strictly adhering to standard operating procedures [2]. A clear discordance emerged between the automated morphological and biochemical analyses. Automated urine sediment analysis was performed using a Mindray EH‐2090C analyzer, and dipstick testing was performed using a Mindray UA‐5600 analyzer. The sediment analyzer detected elevated hyaline casts at 5.8/μL (reference: 0–1.0/μL), while no pathological casts, red blood cells, or white blood cells were observed. Conversely, the concurrent dipstick protein result was completely negative. The urine pH was 5.5, the specific gravity was 1.013, and all other parameters remained unremarkable. Under our laboratory's quality‐control protocol, the combination of increased casts and a negative dipstick protein result triggered a predefined verification procedure [2, 17]. Initial manual microscopy confirmed the presence of a small number of morphologically intact hyaline casts without cellular attachments, thereby reducing concern for an analyzer‐related false‐positive result [1, 3]. Subsequently, SSA verification was conducted as a manual confirmatory precipitation test by adding 100 g/L SSA reagent to the urine specimen and visually assessing turbidity according to national clinical laboratory procedures. The reaction produced immediate moderate white turbidity without visible precipitation and was visually graded as positive (++), consistent with the presence of acid‐precipitable urinary protein [1, 12]. Targeted assessment did not identify high urinary ascorbic acid or bilirubin as potential interfering factors. However, other sources of nonspecific precipitation or analytical interference could not be excluded. These verification steps confirmed that the observed findings were reproducible across sediment microscopy, dipstick testing, and SSA testing. However, they did not determine the molecular composition of the SSA‐reactive material or completely exclude nonspecific precipitation and other analytical interference.

2.4. Concurrent Renal Function and Biochemical Profile

Baseline biochemical data from December 10, 2025, showed preserved renal function, with a SCr of 53 μmol/L, blood urea nitrogen of 4.8 mmol/L, uric acid of 168 μmol/L, and an estimated glomerular filtration rate (eGFR) of 121.5 mL/min/1.73 m². Blood β2‐microglobulin (β2‐MG) was elevated at 4.0 mg/L, whereas serum albumin was mildly reduced at 35 g/L [18]. To evaluate possible non‐albumin or paraprotein‐related causes of SSA positivity, serum protein assessment showed a total protein level of 59 g/L, albumin of 35 g/L, globulin of 24 g/L, and an albumin‐to‐globulin ratio of 1.46. Serum protein electrophoresis did not reveal a monoclonal M‐protein peak, and the serum free light‐chain κ/λ ratio was within the normal range. The 24‐h urinary total protein level was 0.64 g/24 h.

Serial monitoring showed that SCr increased from 53 μmol/L on December 10 to 62 μmol/L on December 12, representing the first observed rise from baseline, although the KDIGO creatinine criterion for AKI was not met at that time. On December 16, routine urinalysis revealed the key discrepancy of elevated hyaline casts, negative dipstick protein, and positive SSA testing (++). Renal function continued to deteriorate thereafter, with SCr reaching 87 μmol/L on December 22 and peaking at 132 μmol/L on December 24, accompanied by an eGFR nadir of 46.3 mL/min/1.73 m². Based on the available serial measurements, the increase in SCr from 87 to 132 μmol/L over approximately 48 h first clearly fulfilled the KDIGO serum creatinine criterion for AKI, defined as an increase in SCr of ≥ 26.5 μmol/L within 48 h [19]. After reduction and replacement of CSA, optimization of intravenous fluid management, and avoidance of additional nephrotoxic agents, SCr decreased to 123.1 μmol/L on December 25, 86 μmol/L on December 26, and 70 μmol/L on December 29.

Therefore, the dipstick‐negative/SSA‐positive urinary protein discrepancy observed on December 16 did not precede the first detectable increase in SCr, but it occurred during the early progression of renal dysfunction and before the peak of renal injury. This pattern should therefore be interpreted as a laboratory abnormality associated with evolving renal dysfunction rather than as definitive standalone evidence of preclinical tubular injury. Urinary uromodulin concentration was not measured in this patient; therefore, the contribution of uromodulin to the SSA‐positive result could not be directly quantified.

Follow‐up urinalysis was performed on December 26, 2025. At that time, the dipstick protein remained negative, SSA testing became negative, and hyaline casts decreased from 5.8 to 0.5/μL, within the reference range. This follow‐up result indicated that the urinary abnormality was transient rather than persistent. In parallel, SCr decreased to 86 μmol/L and eGFR improved to 77.5 mL/min/1.73 m² after modification of nephrotoxic therapy and renal‐supportive management. These serial findings indicate that the discordant urinary phenotype was temporally associated with a reversible episode of AKI and subsequent clinical recovery. However, the observational sequence does not establish that the urinary phenotype was caused by AKI or that its normalization resulted from a specific intervention. The serial urinalysis and paired renal‐function findings are summarized in Table 2.

TABLE 2.

Chronological urinalysis and renal‐function findings.

Date	Dipstick protein	SSA	Hyaline casts (/μL)	SG	pH	SCr (μmol/L)	eGFR (mL/min/1.73 m2)	Blood β2‐MG (mg/L)	CRP (mg/L)/Ferritin (ng/mL)	Clinical interpretation
2025‐12‐16	Negative	Positive	5.8	1.013	5.5	NA a	NA a	NA	Not measured on the same day a	Key discordant urinalysis during evolving renal dysfunction
2025‐12‐26	Negative	Negative	0.5	1.007	7.0	86	77.5	6.0	CRP 2.9; Ferritin 1831	Urinary phenotype normalized; renal function improving

Abbreviations: β2‐MG, beta‐2 microglobulin; CRP, C‐reactive protein; eGFR, estimated glomerular filtration rate; NA, not available; SCr, serum creatinine; SG, specific gravity; SSA, sulfosalicylic acid.

^a No paired same‐day renal‐function or inflammatory‐marker results were available for December 16. The nearest available renal‐function values were SCr 68 μmol/L on December 15 and SCr 77 μmol/L on December 17. Baseline values from December 10, including SCr 53 μmol/L, eGFR 121.5 mL/min/1.73 m², blood β2‐MG 4.0 mg/L, CRP 6.5 mg/L, and ferritin 1998 ng/mL, are summarized in Table 1.

3. Discussion

3.1. Potential Analytical Basis and Relevant Uromodulin Biology

The discordance observed in this case may reflect the analytical limitations of the urine dipstick together with the presence of non‐albumin urinary proteins; the possible contribution of uromodulin remains inferential. The standard urine dipstick utilizes a colorimetric reaction with bromophenol blue that is highly specific to albumin, featuring a detection threshold of approximately 100–150 mg/L. Consequently, non‐albumin proteins, including globulins and Tamm–Horsfall glycoprotein (uromodulin), fail to trigger a positive reaction. In contrast, the SSA method precipitates a broad range of urinary proteins at an approximate visual detection range of 50–100 mg/L, providing a plausible analytical explanation for the positive SSA reaction [7, 11, 12]. Biologically, uromodulin is exclusively secreted by the epithelial cells of the thick ascending limb of the loop of Henle and forms the primary structural matrix of hyaline casts [13, 14, 15]. Previous studies suggest that uromodulin expression and secretion may change under certain renal stress conditions, although this response was not directly evaluated in the present patient [9, 16, 20]. The relatively low urine specific gravity of 1.013 suggested that urinary concentration alone might not fully explain the increased cast count. Nevertheless, without urinary uromodulin quantification or protein characterization, the molecular basis of the SSA‐positive result remains uncertain. The observed pattern should therefore be interpreted as a nonspecific finding of acid‐precipitable urinary material during transient renal dysfunction rather than as evidence of uromodulin‐mediated tubular injury [20, 21].

3.2. Potential Clinical Significance in a High‐Risk Cohort

The clinical context of this discrepancy is paramount. Patients with HLH, particularly those undergoing allo‐HSCT, are at an exceptionally high risk for AKI driven by cytokine storms, nephrotoxic conditioning regimens, and immunosuppressive therapies [4, 5, 17, 22]. In this patient, the initially preserved conventional renal‐function parameters did not exclude evolving renal dysfunction. Although the elevated blood β2‐MG level of 4.0 mg/L is a recognized risk marker for AKI in patients with HLH [18], its elevation in this post‐transplant setting could also partially reflect high cellular turnover and systemic inflammation. However, the concurrent presence of SSA positivity and increased hyaline casts provided a laboratory clue suggesting that non‐albumin urinary proteins and possible tubular stress should be considered in the context of evolving renal dysfunction [8, 9]. Without urinary uromodulin quantification or direct urinary tubular injury biomarkers, this pattern cannot be regarded as definitive evidence of uromodulin‐mediated tubular injury. In this setting, the discordant finding supported repeat urinalysis, review of potentially nephrotoxic drug exposure, and continued monitoring of renal function. It should therefore be regarded as a laboratory finding requiring clinical correlation rather than as a standalone marker of tubular injury or AKI.

3.3. Alternative Explanations and Clinical Confounders

The interpretation of the urinary findings was complicated by several concurrent factors, including the post‐transplant state, systemic inflammation, poor oral intake with possible volume depletion, and exposure to multiple potentially nephrotoxic medications. These factors may have contributed to altered renal hemodynamics, transient tubular stress, and hyaline cast formation, thereby limiting the specificity of the observed urinary phenotype [4, 22]. In this patient, the nephrology team considered CSA‐associated nephrotoxicity a possible contributor to the deterioration in renal function in the context of multidrug post‐transplant therapy. Moreover, because SSA testing detects a broad range of urinary proteins rather than uromodulin specifically, SSA positivity alone cannot establish uromodulin‐predominant proteinuria without urinary uromodulin quantification or protein profiling [11]. Accordingly, the dipstick‐negative/SSA‐positive pattern should be interpreted as a laboratory clue prompting closer renal evaluation, rather than as a specific diagnostic marker of uromodulin‐mediated tubular injury.

We also considered whether SSA positivity could reflect nonspecific protein precipitation or analytical interference rather than uromodulin‐associated proteinuria. The available serum protein studies did not support monoclonal gammopathy as the main explanation. However, urinary Bence‐Jones protein testing, urine protein electrophoresis, and urine immunofixation electrophoresis were not available. In addition, the patient received corticosteroids, intravenous immunoglobulin, transplant‐related immunosuppressants, and broad‐spectrum antimicrobial agents. Although the specific effects of these treatments on the SSA reaction were not directly assessed, treatment‐related interference or precipitation of other urinary constituents could not be excluded. Therefore, the positive SSA reaction was interpreted as indicating acid‐precipitable urinary material, but not as proof of uromodulin predominance, a specific drug metabolite, or tubular injury.

3.4. Laboratory Strategies and Clinical Insights

This case illustrates a potential quality‐control issue when increased hyaline casts are accompanied by a negative dipstick protein result and highlights the value of integrated laboratory‐clinical interpretation. Within locally validated procedures, laboratories may consider using this discordance as a trigger for secondary review, including manual microscopy and, where clinically appropriate, repeat or complementary urinary protein testing [2, 17]. Because SSA testing is nonspecific and precipitates a broad range of urinary proteins, a positive reaction should be interpreted as evidence of acid‐precipitable urinary protein rather than attributed specifically to uromodulin or tubular injury [7, 10, 11]. Laboratory reports may include an interpretive comment recommending correlation with quantitative urinary protein measurements, serial renal‐function results, hydration status, systemic inflammation, and nephrotoxic drug exposure, particularly in clinically complex patients at risk of AKI [4, 20, 23]. Clinical management decisions should be based on the overall clinical assessment rather than on the SSA result alone. A proposed verification and clinical‐correlation workflow is shown in Figure 1.

FIGURE 1.

Proposed laboratory verification and clinical‐correlation workflow for discordant urinalysis findings in transplant patients. When increased urinary casts coexist with a negative dipstick protein result, manual confirmation and complementary urinary protein testing may be considered. A positive SSA reaction indicates the presence of acid‐precipitable urinary material but does not establish its molecular composition or confirm tubular injury. Subsequent evaluation and management should be based on serial renal‐function results, clinical context, and medication exposure rather than on the SSA result alone. eGFR, estimated glomerular filtration rate; SCr, serum creatinine; SSA, sulfosalicylic acid.

3.5. Limitations and Future Directions

While this case underscores a clinically relevant diagnostic pitfall, several limitations must be acknowledged. First, as a retrospective observation of a single patient, the generalizability and diagnostic performance of this discordant urinalysis pattern require validation in larger, prospective multicenter cohorts. Second, the clinical evidence for tubular injury in this case remains indirect. Direct urinary tubular damage markers, such as urinary β2‐MG and N‐acetyl‐β‐D‐glucosaminidase (NAG), were not available, and renal biopsy was not performed; therefore, the extent and histopathological nature of tubular dysfunction could not be quantitatively confirmed. In addition, urinary uromodulin concentration was not measured, which represents a major limitation of this case. Although hyaline casts are primarily composed of uromodulin, direct urinary uromodulin quantification would be necessary to determine whether the SSA‐positive result was truly driven by uromodulin‐predominant proteinuria. Urinary total protein profiling or mass spectrometry was also not performed; therefore, we could not confirm whether the dipstick‐negative/SSA‐positive pattern was dominated by uromodulin or by other non‐albumin urinary proteins. Third, the complex post‐allo‐HSCT setting introduced multiple nephrotoxic and physiological confounders, including calcineurin inhibitor exposure, antimicrobial therapy, systemic inflammation, poor oral intake, and possible hemodynamic vulnerability. Accordingly, this urinary phenotype should be regarded as a hypothesis‐generating laboratory signal rather than definitive evidence of a specific uromodulin‐mediated mechanism. Future prospective studies should incorporate serial urinalysis, absolute urinary uromodulin quantification, direct tubular injury biomarkers, and urinary total protein mass spectrometry to validate this phenotype and determine its relationship with AKI progression and long‐term renal outcomes.

4. Conclusion

This case documents a transient dipstick‐negative/SSA‐positive urinary protein discrepancy accompanied by increased hyaline casts during evolving AKI after allo‐HSCT. The pattern may warrant manual verification and correlation with serial renal‐function results, hydration status, and nephrotoxic exposure. Its molecular basis and value as an indicator of tubular injury require prospective validation.

Author Contributions

Yifei Jia and Binquan Chu carried out the studies, participated in collecting data, and drafted the manuscript. Fengjun Chen, Xiangyu Zhu, Chen Hang, and Xiaoling Yu participated in its design. Jinpiao Lin participated in the acquisition, analysis, or interpretation of data and drafted the manuscript. All authors read and approved the final manuscript.

Funding

The authors have nothing to report.

Ethics Statement

This case report was conducted in accordance with the Declaration of Helsinki. Formal ethical review was waived by the Ethics Committee of Shanghai Tongren Hospital due to the retrospective nature of the report and the use of de‐identified clinical data, with an exemption approval number of Lunmian 2026‐003.

Consent

Written informed consent was obtained from the patient for publication of this case report and any accompanying clinical data.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

All data generated or analysed during this study are included in this published article.