Evaluation of the diagnostic characteristics of urinary kidney injury molecule 1 (uKIM-1) and uKIM-1/creatinine ratio in the assessment of incipient diabetic kidney disease

Carvalho, José Antônio Mainardi de; Tatsch, Etiane; Hausen, Bruna S.; Bollick, Yãnaí S.; Torbitz, Vanessa Dorneles; Guarda, Naiara S.; Campos, Luízi P.; Duarte, Thiago; Duarte, Marta M.M.F.; Londero, Sílvia W.K.; Comim, Fábio Vasconcellos; Moresco, Rafael Noal

doi:10.1515/cclm-2014-0655

Cited by 3 publications

(3 citation statements)

References 5 publications

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“…This interpretation is supported by a growing body of literature which suggests that KIM-1 may be a useful marker for the development of chronic kidney disease (CKD) 18 . Urinary KIM-1 has been shown to track disease progression and regression in both IgA nephropathy 19 – 24 and diabetic nephropathy 25 , 26 . In AKI, KIM-1 plays an important protective role, promoting tubular epithelial cell regeneration 27 , and conferring a phagocytic phenotype on epithelial cells which may be important in clearing kidney tubules of apoptotic and necrotic cell debris 28 .…”

Section: Discussionmentioning

confidence: 99%

Urinary Biomarkers of Aminoglycoside-Induced Nephrotoxicity in Cystic Fibrosis: Kidney Injury Molecule-1 and Neutrophil Gelatinase-Associated Lipocalin

McWilliam

Antoine

Jorgensen

et al. 2018

Sci Rep

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Aminoglycosides are commonly used for the treatment of pulmonary exacerbations in patients with cystic fibrosis (CF). However, they are potentially nephrotoxic. This prospective observational cohort study aimed to investigate the potential validity of two urinary renal biomarkers, Kidney Injury Molecule-1 (KIM-1) and Neutrophil Gelatinase-associated Lipocalin (NGAL), in identifying aminoglycoside-induced nephrotoxicity in children with CF. Children and young adults up to 20 years of age with a confirmed diagnosis of CF were recruited from ten United Kingdom hospitals. Participants provided urine samples for measurement of KIM-1 and NGAL concentrations, at baseline, at regular outpatient appointments, and before, during and after exposure to clinically-indicated treatment with the aminoglycoside tobramycin. 37/158 patients recruited (23.4%) received at least one course of IV tobramycin during the study. The median peak fold-change during tobramycin exposure for KIM-1 was 2.28 (IQR 2.69) and 4.02 (IQR 7.29) for NGAL, in the absence of serum creatinine changes. Baseline KIM-1 was positively associated with cumulative courses of IV aminoglycosides (R2 = 0.11; β = 0.03; p < 0.0001). KIM-1, in particular, may be a useful, non-invasive, biomarker of acute and chronic proximal tubular injury associated with exposure to aminoglycosides in patients with CF, but its clinical utility needs to be further evaluated in prospective studies.

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Section: Discussionmentioning

confidence: 99%

Urinary Biomarkers of Aminoglycoside-Induced Nephrotoxicity in Cystic Fibrosis: Kidney Injury Molecule-1 and Neutrophil Gelatinase-Associated Lipocalin

McWilliam

Antoine

Jorgensen

et al. 2018

Sci Rep

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“…All samples were stored at fridge temperature (4 °C) for a total of one week (including time spent at the patient's home) and then aliquoted and stored at −80 °C (or −20 °C for a maximum of 6 months) in the local laboratory. Stability of KIM-1 has previously been reported in urine stored at 4 °C for periods of one week 37,38 .…”

Section: Sample Collectionmentioning

confidence: 97%

A randomised controlled trial of rosuvastatin for the prevention of aminoglycoside-induced kidney toxicity in children with cystic fibrosis

McWilliam

Rosala-Hallas

Jones

et al. 2020

Sci Rep

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The PROteKT study tested the hypothesis that rosuvastatin can inhibit aminoglycoside-induced nephrotoxicity in children with Cystic Fibrosis (CF). This open label, parallel group, randomised controlled trial recruited children and young people aged 6 to 18 years with CF at 13 paediatric CF treatment centres in the UK. Participants were randomised equally to either receive oral rosuvastatin (10 mg once daily) or no intervention (control) throughout clinically indicated treatment with intravenous tobramycin. The primary outcome was the difference between the groups in mean fold-change in urinary Kidney Injury Molecule-1 (KIM-1). Fifty (rosuvastatin n = 23, control n = 27) participants were recruited between May 2015 and January 2017. Primary outcome data was available for 88% (rosuvastatin n = 20, control n = 24). The estimated mean treatment difference in the geometric mean-fold change of normalised KIM-1 was 1.08 (95% CI 0.87–1.35, p = 0.48). In total there were 12 adverse reactions, all mild, reported by five participants randomised to rosuvastatin, and one serious adverse event in each group. Whilst no protective effect of rosuvastatin was seen, there was a lower than expected level of nephrotoxicity in the cohort. Therefore, we can neither confirm nor refute the hypothesis that rosuvastatin protects against aminoglycoside nephrotoxicity.

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“…Therefore, it was recommended to avoid the adjustment of tubular markers to urinary creatinine, especially in patients with acute or even moderate chronic renal failure. Interestingly, a study from our group reported that urinary KIM-1 had a higher ability to discriminate incipient diabetic kidney disease than the urinary KIM-1/creatinine ratio [29]. In contrast, another study showed that both urinary cystatin C and KIM-1 concentrations were positively correlated with urinary creatinine, indicating a rationale for urinary creatinine adjustment [30].…”

Section: Discussionmentioning

confidence: 99%

High Serum Uric Acid Is Associated with Tubular Damage and Kidney Inflammation in Patients with Type 2 Diabetes

et al. 2019

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Background. Uric acid presents different roles in an organism. High serum uric acid concentrations may induce inflammatory pathways and promote kidney damage through different mechanisms. Therefore, this study investigated the association among high serum uric acid concentrations, renal tubular damage, and renal inflammation assessed via estimation of urinary kidney injury molecule-1 (KIM-1) and inflammatory cytokines in patients with type 2 diabetes (T2D). Methods. Urinary concentrations of KIM-1, IL-1, IL-6, IL-10, and TNF-alpha, as well as other biochemical parameters, were assessed in 125 patients with T2D who were grouped into two groups based on the serum uric acid levels (<6.0 mg/dL and ≥6.0 mg/dL). Patients were also stratified according to the tertiles of serum uric acid concentrations. Results. Urinary KIM-1, IL-1, IL-6, and TNF-alpha were higher in patients with serum uric acid concentrations≥6.0 mg/dL. However, the differences between the groups were not statistically significant when the urinary values of KIM-1 and cytokines were normalized by the urinary creatinine concentration. Serum uric acid concentrations were significantly associated with urinary KIM-1 (values normalized by urinary creatinine concentration) and urinary TNF-alpha (absolute values and values normalized by urinary creatinine concentration), independent of the body mass index (BMI) and estimated glomerular filtration rate (eGFR). Conclusions. High serum uric acid concentrations were associated with high urinary KIM-1 levels accompanied by the increase of urinary proinflammatory cytokines in patients with T2D. However, normalization of urinary markers by urine creatinine concentration seems to influence the profile of the results.

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Evaluation of the diagnostic characteristics of urinary kidney injury molecule 1 (uKIM-1) and uKIM-1/creatinine ratio in the assessment of incipient diabetic kidney disease

Cited by 3 publications

References 5 publications

Urinary Biomarkers of Aminoglycoside-Induced Nephrotoxicity in Cystic Fibrosis: Kidney Injury Molecule-1 and Neutrophil Gelatinase-Associated Lipocalin

Urinary Biomarkers of Aminoglycoside-Induced Nephrotoxicity in Cystic Fibrosis: Kidney Injury Molecule-1 and Neutrophil Gelatinase-Associated Lipocalin

A randomised controlled trial of rosuvastatin for the prevention of aminoglycoside-induced kidney toxicity in children with cystic fibrosis

High Serum Uric Acid Is Associated with Tubular Damage and Kidney Inflammation in Patients with Type 2 Diabetes

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