Determinants and impact of calcium oxalate crystal deposition on renal outcomes in acute kidney injury patients
Objectives Calcium oxalate (CaOx) crystal deposition in acute kidney injury (AKI) patients is under recognized but impacts renal outcomes. This study investigates its determinants and effects.Methods We studied 814 AKI patients with native kidney biopsies from 2011 to 2020, identifying CaOx crystal...
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Taylor & Francis Group
2024-12-01
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| Series: | Renal Failure |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/0886022X.2024.2334396 |
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| author | Weiwei Yang Tao Zhao Xuejing Chen Suxia Wang Yu Wang Tao Su |
| author_facet | Weiwei Yang Tao Zhao Xuejing Chen Suxia Wang Yu Wang Tao Su |
| author_sort | Weiwei Yang |
| collection | DOAJ |
| description | Objectives Calcium oxalate (CaOx) crystal deposition in acute kidney injury (AKI) patients is under recognized but impacts renal outcomes. This study investigates its determinants and effects.Methods We studied 814 AKI patients with native kidney biopsies from 2011 to 2020, identifying CaOx crystal deposition severity (mild: <5, moderate: 5–10, severe: >10 crystals per section). We assessed factors like urinary oxalate, citrate, urate, electrolytes, pH, tubular calcification index, and SLC26A6 expression, comparing them with creatinine-matched AKI controls without oxalosis. We analyzed how these factors relate to CaOx severity and their impact on renal recovery (eGFR < 15 mL/min/1.73 m2 at 3-month follow-up).Results CaOx crystal deposition was found in 3.9% of the AKI cohort (32 cases), with 72% due to nephrotoxic medication-induced tubulointerstitial nephritis. Diuretic use, higher urinary oxalate-to-citrate ratio induced by hypocitraturia, and tubular calcification index were significant contributors to moderate and/or severe CaOx deposition. Poor baseline renal function, low urinary chloride, high uric acid and urea nitrogen, tubular SLC26A6 overexpression, and glomerular sclerosis were also associated with moderate-to-severe CaOx deposition. Kidney recovery was delayed, with 43.8%, 31.2%, and 18.8% of patients having eGFR < 15 mL/min/1.73 m2 at 4, 12, and 24-week post-injury. Poor outcomes were linked to high urinary α1-microglobulin-to-creatinine (α1-MG/C) ratios and active tubular injury scores. Univariate analysis showed a strong link between this ratio and poor renal outcomes, independent of oxalosis severity.Conclusions In AKI, CaOx deposition is common despite declining GFR. Factors worsening tubular injury, not just oxalate-to-citrate ratios, are key to understanding impaired renal recovery. |
| format | Article |
| id | doaj-art-d7519ea8f18144188159b3c5904b54b1 |
| institution | Kabale University |
| issn | 0886-022X 1525-6049 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Renal Failure |
| spelling | doaj-art-d7519ea8f18144188159b3c5904b54b12025-01-23T04:17:47ZengTaylor & Francis GroupRenal Failure0886-022X1525-60492024-12-0146110.1080/0886022X.2024.2334396Determinants and impact of calcium oxalate crystal deposition on renal outcomes in acute kidney injury patientsWeiwei Yang0Tao Zhao1Xuejing Chen2Suxia Wang3Yu Wang4Tao Su5Department of medicine, Renal Division, Peking University First Hospital, Peking University, Institute of Nephrology, Renal Pathology Center, Institute of Nephrology, Peking University, Beijing, PR ChinaDepartment of medicine, Renal Division, Peking University First Hospital, Peking University, Institute of Nephrology, Renal Pathology Center, Institute of Nephrology, Peking University, Beijing, PR ChinaDepartment of medicine, Renal Division, Peking University First Hospital, Peking University, Institute of Nephrology, Renal Pathology Center, Institute of Nephrology, Peking University, Beijing, PR ChinaLaboratory of Electron Microscopy, Pathological Center, Peking University First Hospital, Beijing, PR ChinaDepartment of medicine, Renal Division, Peking University First Hospital, Peking University, Institute of Nephrology, Renal Pathology Center, Institute of Nephrology, Peking University, Beijing, PR ChinaDepartment of medicine, Renal Division, Peking University First Hospital, Peking University, Institute of Nephrology, Renal Pathology Center, Institute of Nephrology, Peking University, Beijing, PR ChinaObjectives Calcium oxalate (CaOx) crystal deposition in acute kidney injury (AKI) patients is under recognized but impacts renal outcomes. This study investigates its determinants and effects.Methods We studied 814 AKI patients with native kidney biopsies from 2011 to 2020, identifying CaOx crystal deposition severity (mild: <5, moderate: 5–10, severe: >10 crystals per section). We assessed factors like urinary oxalate, citrate, urate, electrolytes, pH, tubular calcification index, and SLC26A6 expression, comparing them with creatinine-matched AKI controls without oxalosis. We analyzed how these factors relate to CaOx severity and their impact on renal recovery (eGFR < 15 mL/min/1.73 m2 at 3-month follow-up).Results CaOx crystal deposition was found in 3.9% of the AKI cohort (32 cases), with 72% due to nephrotoxic medication-induced tubulointerstitial nephritis. Diuretic use, higher urinary oxalate-to-citrate ratio induced by hypocitraturia, and tubular calcification index were significant contributors to moderate and/or severe CaOx deposition. Poor baseline renal function, low urinary chloride, high uric acid and urea nitrogen, tubular SLC26A6 overexpression, and glomerular sclerosis were also associated with moderate-to-severe CaOx deposition. Kidney recovery was delayed, with 43.8%, 31.2%, and 18.8% of patients having eGFR < 15 mL/min/1.73 m2 at 4, 12, and 24-week post-injury. Poor outcomes were linked to high urinary α1-microglobulin-to-creatinine (α1-MG/C) ratios and active tubular injury scores. Univariate analysis showed a strong link between this ratio and poor renal outcomes, independent of oxalosis severity.Conclusions In AKI, CaOx deposition is common despite declining GFR. Factors worsening tubular injury, not just oxalate-to-citrate ratios, are key to understanding impaired renal recovery.https://www.tandfonline.com/doi/10.1080/0886022X.2024.2334396Acute kidney injuryacute tubular injuryhypocitraturiacalcium oxalatetubular calcification |
| spellingShingle | Weiwei Yang Tao Zhao Xuejing Chen Suxia Wang Yu Wang Tao Su Determinants and impact of calcium oxalate crystal deposition on renal outcomes in acute kidney injury patients Renal Failure Acute kidney injury acute tubular injury hypocitraturia calcium oxalate tubular calcification |
| title | Determinants and impact of calcium oxalate crystal deposition on renal outcomes in acute kidney injury patients |
| title_full | Determinants and impact of calcium oxalate crystal deposition on renal outcomes in acute kidney injury patients |
| title_fullStr | Determinants and impact of calcium oxalate crystal deposition on renal outcomes in acute kidney injury patients |
| title_full_unstemmed | Determinants and impact of calcium oxalate crystal deposition on renal outcomes in acute kidney injury patients |
| title_short | Determinants and impact of calcium oxalate crystal deposition on renal outcomes in acute kidney injury patients |
| title_sort | determinants and impact of calcium oxalate crystal deposition on renal outcomes in acute kidney injury patients |
| topic | Acute kidney injury acute tubular injury hypocitraturia calcium oxalate tubular calcification |
| url | https://www.tandfonline.com/doi/10.1080/0886022X.2024.2334396 |
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