Fanconi syndrome developing and worsening during anti-myeloma therapy in multiple myeloma: a case report and literature review.

Introduction

Multiple myeloma (MM) is a hematologic malignancy characterized by clonal proliferation of plasma cells. Renal impairment is frequent in MM, with 20%–40% of newly diagnosed patients demonstrating varying degrees of renal dysfunction ( 1 ). Common renal pathologies include light−chain cast nephropathy, amyloidosis, and monoclonal immunoglobulin deposition disease ( 2 ). Light−chain proximal tubulopathy (LCPT) is rare and typically presents as Fanconi syndrome (FS).

FS is a clinical disorder caused by impaired proximal tubular transport, leading to defective reabsorption of multiple solutes. Key features include normoglycemic glycosuria, hyperphosphaturia, hypophosphatemia, aminoaciduria, hypouricemia, hypokalemia, and proximal renal tubular acidosis (RTA). Etiologies are hereditary or acquired; monoclonal gammopathy is a leading cause of adult−onset acquired FS, termed light chain−associated FS (LCFS). Most LCFS cases occur with monoclonal gammopathy of undetermined significance (MGUS) or MM, with rare associations with Waldenström macroglobulinemia (WM), lymphoplasmacytic lymphoma (LPL), and chronic lymphocytic leukemia (CLL) ( 3 ). FS is usually diagnosed before or at MM diagnosis ( 4 ); onset during anti−myeloma therapy is rare, and non−specific gastrointestinal symptoms are often misdiagnosed as drug−related adverse events. Here, we report a rare case of MM-associated FS that developed during induction therapy and recurred after autologous stem cell transplantation (ASCT), and a relevant literature review is also conducted herein to improve the clinical recognition and management of this disorder.

Case report

On September 20, 2024, a 55−year−old woman was admitted to Qilu Hospital, Shandong University, China, with a 5−month history of lower back and rib pain. She denied fatigue, nausea, or anorexia, and had no history of hypertension, diabetes mellitus, or chronic kidney disease. Physical examination was unremarkable. Laboratory results are summarized in Table 1 .

At admission, complete blood count and liver function tests were normal. Serum creatinine level was 103 μmol/L (reference range, 53-97 μmol/L), serum uric acid level was 100 μmol/L (reference range,155-357 μmol/L), estimated glomerular filtration rate(eGFR)was 53.22 mL/min and serum calcium level was 2.54 mmol/L (reference range, 2.11-2.5 mmol/L). Serum sodium, chloride, potassium, phosphorus, fasting glucose, and lactate dehydrogenase were within normal limits. β2-microglobulin level was 6.42 mg/L (reference range, 0.7-1.8mg/L). Urinalysis showed pH 6.0, glucose 1+, occult blood 2+, and protein 2 +. Arterial blood gas analysis indicated compensated metabolic acidosis: pH 7.38, PaCO 2 33 mmHg, PaO 2 101 mmHg, anion gap 8.5 mmol/L, actual base excess -4.8 mmol/L, and actual bicarbonate level was 19.5 mmol/L. Renal tubular function tests revealed urinary microalbumin level was 129 mg/L (reference range, <30 mg/L), α1-microglobulin level of 194 mg/L (reference range, <20 mg/L), and β2-microglobulin level was 144 mg/L (reference range, <0.22 mg/L). Serum immunofixation electrophoresis identified a κ light chain type. The serum free λ light chain level was 4.8 ng/L (reference range, 5.71-25.3 ng/L), the serum free κ light chain level was 20071.99 ng/L (reference range, 3.3-19.4 ng/L), and the κ/λ ratio was 4181.6646 (reference range, 0.26-1.65).

Bone marrow examination showed 32% immature plasma cells, and immunophenotyping revealed 19.5% abnormal plasma cells expressing CD38, CD138, CD56dim, CD27dim, BCMA, and cytoplasmic κ light chains. MM-FISH analysis was negative. Whole-body ECT and spinal CT demonstrated osteoporosis with fractures of the T9 vertebra and bilateral ribs. Bone mineral density showed a T-score was -3.1.

Based on these findings, the patient was diagnosed with κ light chain multiple myeloma, ISS stage III. Renal glycosuria and elevated tubular markers suggested subclinical tubular dysfunction, which was initially overlooked. After written informed consent, she started VRD therapy (bortezomib, lenalidomide, dexamethasone) and received denosumab 120 mg for bone disease. On day 5 of treatment, serum potassium level of 3.16 mmol/L, serum phosphorus level of 0.45 mmol/L, serum creatinine decreased to 70 μmol/L, and eGFR increased to 84 mL/min. The patient reported no significant discomfort and was discharged after potassium supplementation alone.

After one cycle, bone pain resolved, serum free κ light chain fell to 181.45 ng/L, and renal function normalized. However, she developed nausea, vomiting, anorexia, and limb numbness. Biochemical testing showed hypokalemia (3.11 mmol/L) and hypophosphatemia (0.34 mmol/L). Symptoms were initially attributed to drug toxicity and insufficient intake; antiemetics and electrolyte replacement were given. Electromyography confirmed bortezomib−induced peripheral neuropathy. Treatment was switched to IRD (ixazomib, lenalidomide, dexamethasone) in cycle 2, but symptoms persisted. Preparing for cycle 3, she presented with poor performance status and severe malnutrition. She reported a progressive worsening of nausea, vomiting and anorexia, which led to a marked reduction in oral intake, severely disrupted her daily activities and resulted in a significant decline in her self-assessed quality of life. Repeat testing showed severe electrolyte disturbances: potassium 3.09 mmol/L, phosphorus 0.24 mmol/L (calcium and magnesium normal). Arterial blood gas: pH 7.36, base excess −9.5 mmol/L, bicarbonate 14.7 mmol/L. Urinalysis: pH 5.5, glucose 4+, occult blood 3+, protein 1 +.

For a patient with persistent unexplained electrolyte disturbances and progressive gastrointestinal symptoms despite hematologic remission of MM, we organized a multidisciplinary consultation involving the Departments of Hematology, Nephrology, and Endocrinology. A diagnosis of MM-related FS was established based on glycosuria, hypophosphatemia, hypokalemia, metabolic acidosis, and hypouricemia. 24-hour urine biochemistry panel showed potassium 33.48 mmol/L (reference range, 50–100 mmol/L), sodium 220 mmol/L (reference range, 130–217 mmol/L), chloride 123 mmol/L (reference range, 173–250 mmol/L), phosphorus 10.75 mmol/L (reference range, 3.5–8.4 mmol/L), glucose 202.68 mmol/L, creatinine 1396 µmol/L (reference range,7000-14000 µmol/L), and fractional excretion of phosphate (FEPO 4 ) is 49% (reference range, 10%–20%). Increased FEPO 4 further supported the diagnosis of FS. Urinary uric acid, bicarbonate, and aminoaciduria were not available. Subsequently, she received oral and intravenous potassium and phosphorus supplementation, symptoms improved within 3 days. She continued regular IRD therapy plus oral electrolyte replacement for 4 months; electrolytes normalized, and glycosuria/proteinuria resolved. The patient reported recovery of the ability to perform basic daily activities and a marked improvement in overall health status.

After 6 cycles, she achieved VGPR, but urinalysis showed recurrent glycosuria. On August 29, 2025, she underwent ASCT with melphalan conditioning. On post - ASCT day 5, hypokalemia, hypophosphatemia, nausea, vomiting, and anorexia recurred (urine protein 1+, glucose 3+), indicating FS recurrence. Symptoms resolved with electrolyte replacement. She remains stable in follow−up. The patient’s clinical course is illustrated in Figure 1 .

Literature review

A systematic review of LCFS was performed via PubMed, Embase, and Cochrane Library (inception to December 2025) using keywords: “Fanconi syndrome”, “light chain proximal tubulopathy”, “multiple myeloma”, “monoclonal gammopathy”.

The inclusion criteria were case reports and case series that meet the diagnosis of both monoclonal gammopathy and FS, with relatively complete records of treatment and prognosis. Exclusion criteria were the presence of another cause of FS, especially the use of any drugs known to induce proximal tubular (PT) dysfunction. A total of 18 case reports and 6 case series were included ( 5 – 26 ) (summarized in Tables 2 , 3 ). The limitations of this review lie in its nature as a narrative synthesis and the potential publication bias inherent in case reports.

LCFS is a recognized but rare renal complication of monoclonal gammopathies such as MM. Its pathogenesis is associated with the deposition of abnormal free light chains (FLCs) produced by monoclonal plasma cells in proximal tubular cells of the kidney. Under normal physiological conditions, small amounts of FLCs are reabsorbed via the megalin/cubilin scavenger receptor on the apical surface of proximal tubular epithelium and subsequently degraded through the lysosomal pathway. In the setting of dysproteinemias, however, the proximal tubules endocytose excessive FLCs, predominantly κ-type light chains, whose variable domains possess intrinsic physicochemical properties that confer resistance to proteolysis and promote self-aggregation and crystal formation. The reabsorbed but undegraded monoclonal light chains accumulate in the proximal tubules in either crystalline or non-crystalline forms, a condition termed light chain proximal tubulopathy (LCPT) ( 27 ). Approximately 68% of LCPT cases manifest as FS ( 28 ).

FS is classically characterized by normoglycemic glycosuria, aminoaciduria, hypophosphatemia or hyperphosphaturia, hypouricemia, and RTA. When all these features are present, the condition is classified as full-blown FS; if one or two features are missing as well as specific PT injuries confirmed by kidney biopsy, incomplete FS was diagnosed ( 24 ). Full-blown FS is typically more common than incomplete FS ( 21 ). Most patients also exhibiting proteinuria and varying degrees of renal dysfunction at initial diagnosis ( 24 ). Proteinuria is considered a feature of FS, likely resulting from impaired proximal tubular reabsorption. The diagnosis of LCFS requires the presence of classic FS-related proximal tubular dysfunction, confirmation of monoclonal light chains by serum/urine free light chain assays or immunofixation electrophoresis, exclusion of other secondary FS etiologies, and is further supported by pathological findings of light chain-induced proximal tubular injury on renal biopsy.

In most cases, FS is an early manifestation of monoclonal gammopathy ( 4 ). FS is usually diagnosed before or concurrently with monoclonal gammopathy, with a clinical history ranging from several months to years before diagnosis. The most common manifestations include renal insufficiency, proteinuria, glycosuria, fatigue, bone pain, and osteomalacia ( 5 – 26 ) ( Tables 2 , 3 ). Delayed diagnosis is common until typical features emerge. Late-onset FS is often drug-related, such as cisplatin and ifosfamide, which cause direct damage to proximal tubular epithelial cells via metabolites, leading to generalized solute reabsorption dysfunction ( 29 ). In recent years, several cases of lenalidomide-induced FS have been reported, typically occurring months after treatment initiation, with a clear temporal association with lenalidomide exposure but no correlation with FLC levels. Pathological findings show pan-tubulopathy, although the precise mechanism remains unclear. Notably, this adverse effect is usually reversible upon drug discontinuation ( 30 , 31 ).

Over the past few decades, management of LCFS has mainly consisted of electrolyte replacement and correction of acidosis to relieve symptoms. Conventional chemotherapy based on alkylating agents shows low efficacy and carries a risk of secondary malignancies ( 22 ). In recent years, bortezomib-based regimens have been shown to stabilize or improve renal and tubular function and are currently recommended as first-line therapy for LCFS ( 25 ). Renal response occurs only in patients achieving at least a partial hematologic response (PR), and early diagnosis and treatment significantly shorten the time to tubular function recovery ( 24 ).

Regarding the role of ASCT in LCFS, some studies suggest that chemotherapy plus ASCT yields superior renal or tubular responses compared with chemotherapy alone ( 19 ). Nevertheless, MM remains incurable, and FS may recur with disease relapse, requiring further investigation of optimal therapeutic strategies ( 32 ).

Discussion

In this case, the patient was diagnosed with MM. At initial presentation, she exhibited typical features of proximal renal tubular dysfunction, including renal glycosuria and proteinuria. Urinary microalbumin mainly reflects early glomerular filtration barrier impairment but also indicates defective proximal tubular reabsorption of small-molecular-weight proteins. Urinary α 1 -microglobulin is a specific marker of proximal tubular injury, and its elevation directly indicates impaired reabsorptive capacity. Urinary β 2 -microglobulin is a highly sensitive indicator of proximal tubular dysfunction, as even mild injury leads to a marked increase due to impaired reabsorption and degradation. In this patient, all three key biomarkers of proximal tubular injury were significantly elevated, further supporting the diagnosis of proximal tubular damage. After excluding secondary etiologies including hereditary disorders, drug toxicity, and autoimmune diseases, LCPT was suspected clinically.

Shortly after anti-myeloma therapy, the patient rapidly developed hypokalemia and hypophosphatemia. Severe malnutrition and rapid calorie repletion were absent before treatment, excluding refeeding syndrome. Persistent diarrhea or vomiting was not present during electrolyte disturbances, excluding gastrointestinal losses. Drug-induced diarrhea was excluded because no diarrhea occurred after starting anti-myeloma therapy. In addition, renal function gradually improved without hyperkalemia or hyperphosphatemia, making tumor lysis syndrome (TLS) unlikely.

Therefore, combined with features including hypophosphatemia, hypokalemia, increased urinary phosphate excretion, proximal renal tubular acidosis, and hypouricemia, the patient fulfilled the diagnostic criteria for FS. Although the absence of important parameters such as aminoaciduria and urinary uric acid may limit the comprehensive evaluation of tubular function, it does not negate the diagnosis.

Renal biopsy is the gold standard for diagnosing LCFS, as it identifies characteristic monoclonal light chain deposition in proximal tubules, confirms the diagnosis, and differentiates LCFS from other causes of FS. Its diagnostic value is well documented in the literature ( 27 ). Unfortunately, renal biopsy was not performed because the patient’s renal function was relatively preserved at the time and clinical awareness of the disease was limited. Despite the lack of pathological confirmation, the patient’s clinical manifestations were consistent with LCFS in the setting of pre−existing LCPT. This case underscores the necessity for more comprehensive evaluation of such patients in the future.

The development of FS during induction therapy in this patient is a rare clinical event. We analyzed its underlying pathogenesis in detail. First, pre-existing proximal renal tubular dysfunction served as a predisposing factor. Monoclonal light chains had already induced subclinical and compensated tubular injury, providing the pathological basis for subsequent FS. Second, the synergistic tubular toxicity of anti-myeloma agents likely contributed. Lenalidomide and bortezomib are core components of anti-myeloma treatment. Lenalidomide has been previously associated with FS ( 30 , 31 ) and may play a central role in triggering proximal tubular damage. In animal studies, bortezomib impairs proteasome function and cellular metabolism in tubular epithelial cells, thereby exerting direct tubular toxicity ( 33 ). The combination of these two agents may have aggravated tubular injury, resulting in defective reabsorption of multiple solutes and the typical clinical features of FS. Third, disordered calcium-phosphate homeostasis further compromised tubular ion transport. Denosumab, a RANKL inhibitor, markedly reduces osteoclast activity and can cause severe hypocalcemia and hypophosphatemia ( 34 ). Phosphate regulates tubular epithelial function via Na+-Pi cotransporters and calcium channels and abnormal calcium-phosphate levels directly impair tubular reabsorption ( 35 ). Denosumab likely precipitated calcium-phosphate imbalance and worsened tubular ion handling. Notably, FS progressed despite hematological remission, partly because electrolyte disturbances were not corrected promptly. In our patient, early hypophosphatemia was not adequately treated with phosphate supplementation. Sustained hypophosphatemia caused intestinal smooth muscle dysfunction, leading to nausea, anorexia, and reduced oral intake, while further injuring proximal tubules and worsening reabsorptive capacity. This created a vicious cycle: renal electrolyte loss → hypokalemia/hypophosphatemia → gastrointestinal symptoms/tubular injury → reduced oral intake/renal electrolyte loss → severe electrolyte disturbance. Subsequent electrolyte replacement, especially phosphate supplementation, markedly alleviated symptoms, supporting this mechanism.

However, the complexity of this case did not end with the induction phase. A particularly challenging observation was that the patient experienced a recurrence of FS only a few days after high−dose melphalan conditioning. Before ASCT, renal glycosuria reappeared in our patient, despite complete hematologic remission. This indicates that although effective treatment suppressed light chain production, tubular recovery was incomplete and residual tubular defects persisted in some patients ( 24 ). Melphalan is an alkylating agent secreted and reabsorbed via renal tubules and is generally considered to have low nephrotoxicity. Nevertheless, case reports of melphalan−induced acute kidney injury exist, especially in patients with pre−existing tubular dysfunction ( 29 ). The development of FS in this patient likely occurred through a similar mechanism. Janina et al. described 5 cases of acute FS following ASCT, with an average onset of 10.2 days. While one case could not exclude lenalidomide involvement, the pathogenesis remained unclear in others. All cases recovered rapidly after electrolyte replacement, leading the authors to hypothesize that this phenomenon may represent a self-limiting and transient feature after ASCT. However, based on the reported laboratory data, all five patients had varying degrees of renal dysfunction (eGFR 41–105 mL/min) before ASCT, and four had glucosuria, suggesting that these cases may be similar to ours, with pre-existing tubular dysfunction present before treatment, although this was not recognized by the authors. Notably, only one patient was diagnosed with LCPT by renal biopsy prior to ASCT [36].

In summary, we report a rare case of MM-related FS. The patient developed and progressed with FS during anti-myeloma induction therapy on the basis of pre-existing subclinical renal tubular dysfunction, with recurrence following ASCT. Through review of the entire clinical course and analysis of relevant literature, we have further strengthened the holistic management of FS.

This study has several limitations: first, it is a single case report with a limited sample size, which restricts the generalizability of the conclusions; second, renal biopsy was not performed, so histological evidence of tubular injury is lacking, and incomplete key quantitative data, such as the fractional excretion of phosphate, uric acid, bicarbonate, aminoaciduria, and urea nitrogen, limited the comprehensive evaluation of renal tubular damage; third, no in vitro or in vivo experimental data were available to verify the proposed hypothesis of synergistic tubular toxicity. The generalizability and causal relationship require validation in prospective studies.

Conclusion

LCFS is a rare renal complication of multiple myeloma. Renal glycosuria may be its sole presentation. When glycosuria occurs in the setting of normal blood glucose, comprehensive evaluation of renal tubular function should be performed to investigate the possibility of FS. Early identification of FS and timely electrolyte replacement are critical. For patients with pre-existing renal tubular injury or confirmed FS, individualized adjustment of anti-myeloma regimens is necessary to avoid synergistic renal tubular toxicity induced by multiple medications. It should also be highlighted that FS may persist as a chronic complication even after the effective remission of the primary disease, hence long-term renal function follow-up is recommended to monitor recurrent renal tubular damage.

Edited by: Robert Ohgami , The University of Utah, United States

Reviewed by: Antonio Giovanni Solimando , University of Bari Aldo Moro, Italy

Nina Nurarifah , Saiful Anwar Region Hospital, Indonesia

Data availability statement

The original contributions presented in the study are included in the article/supplementary material. Further inquiries can be directed to the corresponding author.

Ethics statement

The studies involving humans were approved by Shandong University Qilu Hospital Ethics Committee. The studies were conducted in accordance with the local legislation and institutional requirements. The participants provided their written informed consent to participate in this study. Written informed consent was obtained from the individual(s) for the publication of any potentially identifiable images or data included in this article.

Author contributions

PZ: Investigation, Writing – review & editing, Data curation, Writing – original draft. PL: Formal analysis, Writing – review & editing. XZ: Writing – review & editing, Formal analysis. YX: Writing – review & editing, Formal analysis. YN: Writing – review & editing, Formal analysis. XL: Writing – review & editing, Formal analysis. XQ: Supervision, Conceptualization, Writing – review & editing.

Conflict of interest

The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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The author(s) declared that generative AI was not used in the creation of this manuscript.

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References

1 Lu J Lu J Chen W Huo Y Huang X Hou J . Clinical features and treatment outcome in newly diagnosed Chinese patients with multiple myeloma: results of a multicenter analysis . Blood Cancer J . ( 2014 ) 4 : e239 . doi: 10.1038/bcj.2014.55 , PMID: 25127393 PMC4219472

2 Song J Jiang F Liu H Ding K Ren Y Li L . Effect factors related to a high probability of hemodialysis independence in newly diagnosed multiple myeloma patients requiring hemodialysis . J Clin Lab Anal . ( 2020 ) 34 : e23057 . doi: 10.1002/jcla.23057 , PMID: 31663630 PMC7031559

3 Daniel W Ross R . Light chain Fanconi syndrome in a patient with acute myeloid leukemia and monoclonal gammopathy of undetermined significance . CEN Case Rep . ( 2016 ) 5 : 238–41 . doi: 10.1007/s13730-016-0232-3 , PMID: 28508985 PMC5413759

4 Maldonado JE Velosa JA Kyle RA Wagoner RD Holley KE Salassa RM . Fanconi syndrome in adults. A manifestation of a latent form of myeloma . Am J Med . ( 1975 ) 58 : 354–64 . doi: 10.1016/0002-9343(75)90601-4 , PMID: 163583

5 Engle RL Wallis LA . Multiple myeloma and the adult Fanconi syndrome . Am J Med . ( 1957 ) 22 : 5 – 12 . doi: 10.1016/0002-9343(57)90333-9 , PMID: 13381734

6 Harrison JF Blainey JD . Adult Fanconi syndrome with monoclonal abnormality of immunoglobulin light chain . J Clin Pathol . ( 1967 ) 20 : 42 . doi: 10.1136/jcp.20.1.42 , PMID: 6016886 PMC473418

7 Salman M Gailani R Byeong-Kuk M . κ light chain — myeloma associated with adult Fanconi syndrome: Response of the nephropathy to treatment of myeloma . Med Pediatr Oncol . ( 1978 ) 4 : 141–7 . doi: 10.1002/mpo.2950040210 , PMID: 96325

8 Uchida S Matsuda O Yokota T Takenmura T Ando R Kanemitsu H . Adult fanconi syndrome secondary to K-light chain myeloma: improvement of tubular functions after treatment for myeloma . Nephron . ( 1990 ) 55 : 332–5 . doi: 10.1159/000185986 , PMID: 2115147

9 Yonemura K Matsushima H Kato A Isozaki T Hishida A . Acquired Fanconi syndrome associated with IgG kappa multiple myeloma: observations on the mechanisms of impaired renal acid excretion . Nephrol Dial Transplant . ( 1997 ) 12 : 1251–3 . doi: 10.1093/ndt/12.6.1251 , PMID: 9198061

10 Narvaez J Domingo-Domenech E Narvaez JA . Acquired hypophosphatemic osteomalacia associated with multiple myeloma . Joint Bone Spine . ( 2005 ) 72 : 424–6 . doi: 10.1016/j.jbspin.2004.10.012 , PMID: 16112595

11 Toly-Ndour C Peltier J Piedagnel R Coppo P Sachon E Ronco P . Acute renal failure with lambda light chain-derived crystals in a patient with IgD myeloma . Nephrol Dial Transplant . ( 2011 ) 26 : 3057–9 . doi: 10.1093/ndt/gfr377 , PMID: 21737515

12 Nishida Y Iwama KI Yamakura M Takeuchi M Matsue K . Renal Fanconi syndrome as a cause of chronic kidney disease in patients with monoclonal gammopathy of undetermined significance: partially reversed renal function by high-dose dexamethasone with bortezomib . Leuk Lymphoma . ( 2012 ) 53 : 1804–1806 . doi: 10.3109/10428194.2012.671483 , PMID: 22385229

13 Ugai T Tsuda K Sugihara H Nishida Y Yamakura M Takeuchi M . Renal Fanconi syndrome associated with monoclonal κ free light chain in a patient with Waldenstrm macroglobulinemia . Br J Haematol . ( 2013 ) 162 : 1 – 1 . doi: 10.1111/bjh.12398 , PMID: 23758066

14 Yao Y Wang SX Zhang YK Wang Y Liu L Liu G . Acquired fanconi syndrome with proximal tubular cytoplasmic fibrillary inclusions of λ Light chain restriction . Internal Med . ( 2014 ) 53 : 121–4 . doi: 10.2169/internalmedicine.53.0836 , PMID: 24429451

15 Kim DH Lim AY Gwag HB Lee JH Jung KS Lee K . A case of Fanconi syndrome accompanied by crystal depositions in tubular cells in a patient with multiple myeloma . Kidney Res Clin Pract . ( 2014 ) 33 : 112–5 . doi: 10.1016/j.krcp.2014.04.002 , PMID: 26877961 PMC4714179

16 Reyskens M Sleurs K Verresen L Janssen M van den Bergh J Geusens P . Hypophosphatemic osteomalacia: an unusual clinical presentation of multiple myeloma . Osteoporos Int . ( 2015 ) 26 : 2039–42 . doi: 10.1007/s00198-015-3090-5 , PMID: 25906239 PMC4483244

17 Tojo A Asaba K Kinugasa S Ikeda Y Shintani Y Fukayama M . The reduced expression of proximal tubular transporters in acquired Fanconi syndrome with κ light chain deposition . Med Mol Morphology . ( 2016 ) 49 : 1 – 5 . doi: 10.1007/s00795-015-0114-3 , PMID: 26141649

18 Mathur M Chacko B Vankalakunti M Patil C . Fanconi syndrome due to light chain proximal tubulopathy in a patient with multiple myeloma . Saudi J Kidney Dis Transpl . ( 2016 ) 27 : 805 . doi: 10.4103/1319-2442.185268 , PMID: 27424703

19 Kono A Bando K Takahata A Toyota S . Successful autologous stem cell transplantation for light chain proximal tubulopathy with severe kidney injury . Clin Case Rep . ( 2023 ) 11 : e8337 . doi: 10.1002/ccr3.8337 , PMID: 38094139 PMC10717174

20 Messiaen T Deret S Mougenot B Bridoux F Dequiedt P Dion JJ . Adult Fanconi syndrome secondary to light chain gammopathy. Clinicopathologic heterogeneity and unusual features in 11 patients . Med (Baltimore) . ( 2000 ) 79 : 135–54 . doi: 10.1097/00005792-200005000-00002 , PMID: 10844934

21 Ma CX Lacy MQ Rompala JF Dispenzieri A Rajkumar SV Greipp PR . Acquired Fanconi syndrome is an indolent disorder in the absence of overt multiple myeloma . Blood . ( 2004 ) 104 : 40–2 . doi: 10.1182/blood-2003-10-3400 , PMID: 15010372

22 Liu Y Zhu T Xu L Qin Y Zhuang J . A single-center case series of eight patients with the rare plasma cell dyscrasia of acquired Fanconi syndrome secondary to monoclonal gammopathy . Leuk Lymphoma . ( 2015 ) 56 : 3124–8 . doi: 10.3109/10428194.2015.1025392 , PMID: 25791236

23 Vignon M Javaugue V Alexander MP El-Karoui K Karras A Roos-Weil D . Current anti-myeloma therapies in renal manifestations of monoclonal light chain-associated Fanconi syndrome: a retrospective series of 49 patients . Leukemia . ( 2017 ) 31 : 123–9 . doi: 10.1038/leu.2016.195 , PMID: 27435002

24 Wu X Zhang L Feng J Mao YY Cao XX Zhou DB . Bortezomib-based chemotherapy can improve renal and tubular functions in patients with light chain-associated Fanconi syndrome . Ann Hematol . ( 2019 ) 98 : 1095–100 . doi: 10.1007/s00277-018-3572-6 , PMID: 30511139

25 Chen Z Li J Shi X Wang Y Xia P Ye W . Clinicopathological characteristics and long-term prognosis of monoclonal immunoglobulin light chain associated Fanconi syndrome . Ther Adv Hematol . ( 2021 ) 12 : 2040620720983127 . doi: 10.1177/2040620720983127 , PMID: 33796233 PMC7970675

26 Stokes MB Valeri AM Herlitz L Khan AM Siegel DS Markowitz GS . Light chain proximal tubulopathy: clinical and pathologic characteristics in the modern treatment era . J Am Soc Nephrol . ( 2016 ) 27 : 1555–65 . doi: 10.1681/ASN.2015020185 , PMID: 26374607 PMC4849818

27 Lin Y Xing G Hu R Liu S Li G Zhang P . Clinicopathological characteristics of light chain proximal tubulopathy: a multicentre case series . J Clin Pathol . ( 2025 ) 78 : 562–8 . doi: 10.1136/jcp-2024-209620 , PMID: 39667850

28 Hall AM Bass P Unwin RJ . Drug-induced renal Fanconi syndrome . QJM . ( 2014 ) 107 : 261–9 . doi: 10.1093/qjmed/hct258 , PMID: 24368854

29 Wesner N Bihan K Cez A Simon L Biour M Roos-Weil D . Two cases of reversible Fanconi syndrome induced by lenalidomide . Leuk Lymphoma . ( 2019 ) 60 : 1092–4 . doi: 10.1080/10428194.2018.1515941 , PMID: 30277123

30 Sharra I Lhoir M Des Grottes JM Vaes M Guerisse F . Recurrent fanconi syndrome induced by lenalidomide: A case report . Cureus . ( 2024 ) 16 : e66118 . doi: 10.7759/cureus.66118 , PMID: 39108773 PMC11300179

31 Solimando AG Malerba E Leone P Prete M Terragna C Cavo M . Drug resistance in multiple myeloma: Soldiers and weapons in the bone marrow niche . Front Oncol . ( 2022 ) 12 : 973836 . doi: 10.3389/fonc.2022.973836 , PMID: 36212502 PMC9533079

32 Zhang XZ Han F Ding CG Dou M Wang YX Xue WJ . Different roles of bortezomib and ONX 0914 in acute kidney injury . Int Immunopharmacol . ( 2020 ) 82 : 106259 . doi: 10.1016/j.intimp.2020.106259 , PMID: 32143000

33 Flood MG Jr Rowley MA Basnet A . Diagnosis and management of denosumab-induced hypocalcemia and hypophosphatemia in the setting of metastatic prostate cancer . Cureus . ( 2022 ) 14 : e20928 . doi: 10.7759/cureus.20928 , PMID: 35145817 PMC8812272

34 Adhikari S Mamlouk O Rondon-Berrios H Workeneh BT . Hypophosphatemia in cancer patients . Clin Kidney J . ( 2021 ) 14 : 2304–15 . doi: 10.1093/ckj/sfab078 , PMID: 34754427 PMC8572986

35 Sy-Go JPT Dingli D Gertz MA Kapoor P Buadi FK Dispenzieri A . Acute acquired fanconi syndrome in multiple myeloma after hematopoietic stem cell transplantation . Kidney Int Rep . ( 2020 ) 6 : 857–64 . doi: 10.1016/j.ekir.2020.12.007 , PMID: 33733003 PMC7938074