Serum myo-inositol oxygenase levels at hospital discharge predict progression to chronic kidney disease in community-acquired acute kidney injury

Abstract

Acute kidney injury (AKI) increases the risk of morbidity, mortality, and progression to chronic kidney disease (CKD). There are few data on the risk of CKD following community-acquired AKI (CA-AKI) and its predictors from developing countries. We evaluated the association of a panel of serum and urine biomarkers at the time of hospital discharge with 4-month renal outcome in CA-AKI. Patients of either sex, aged between 18 and 70 years, with no underlying CKD, and with CA-AKI were recruited at the time of discharge from hospital in this prospective observational study. Levels of serum and urine biomarkers were analyzed and association between these markers and development of CKD, defined as eGFR < 60 ml/min/1.73 m2 or dialysis dependence at 4 month after discharge, were analyzed using multivariate logistic regression analysis and penalized least absolute shrinkage and selection operator logistic regression. Out of a total 126 patients followed up for 4 months, 25 developed CKD. Those who developed CKD were older (p = 0.008), had higher serum creatinine (p < 0.001) and lower serum albumin (p = 0.001) at discharge. Adjusted logistic regression showed that each 10% increase in standardized serum myo-inositol oxygenase (MIOX) level increased the odds of progression to CKD by 13.5%. With 10% increase in standardized urine Neutrophil gelatinase-associated lipocalin (NGAL), serum creatinine and urine protein creatinine ratio (uPCR), increase in the odds of progression to CKD was 10.5%, 9.6% and 8%, respectively. Multivariable logistic model including serum MIOX, discharge serum creatinine and discharge uPCR, was able to predict the progression of CKD [AUC ROC 0.88; (95% CI 0.81, 0.95)]. High level serum MIOX levels at the time of discharge from hospital are associated with progression to CKD in patients with CA-AKI.

Identification of novel prognostic targets in acute kidney injury using bioinformatics and next generation sequencing data analysis

“…BMI1 [327], AMH (anti-Mullerian hormone) [328], E2F1 [329], PF4 [330], VASH2 [331], GRIN1 [332], CYP11B2 [333], COMP (cartilage oligomeric matrix protein) [334], DES (desmin) [335], ANGPTL3 [336], CYP3A5 [337], DPEP1 [338], LRP2 [339], AGXT2 [340], FABP1 [341], SLC22A12 [342], CUBN (cubilin) [343], MIOX (myo-inositol oxygenase) [344], ARG2 [345], KHK (ketohexokinase) [346], CYP2C8 [347], SLC2A9 [348], GC (GC vitamin D binding protein) [349], VNN1 [350], NOX4 [351], EPHX2 [352], AKR1C3 [353], NR4A3 [354], PFKFB2 [355], SLC22A6 [356], F11 [357], SLC22A2 [358], AQP2 [171], EGF (epidermal growth factor) [359], KNG1 [360], SERPINA5 [361], KL (klotho) [362], ACE2 [363], NPNT (nephronectin) [364], SLC47A1 [358], MGAM (maltase-glucoamylase) [365], AQP3 [366], AZGP1 [367], GALNT3 [368], DPP4 [369], STC1 [370], ABCB1 [371], ERRFI1 [372], TREH (trehalase) [373], MANBA (mannosidase beta) [374], ERBB4 [375], VCAM1 [376] and ALB (albumin) [377] might play an important role in the pathophysiology of AKI. BMI1 [378], IGF2 [379], PRKCB (protein kinase C beta) [380], CCL5 [381], E2F1 [382], PF4 [111], CYP11B2 [383], WNT3A [384], COMP (cartilage oligomeric matrix protein) [385], DES (desmin) [335], ANGPTL3 [386], CYP3A5 [387], LRP2 [388], PAH (phenylalanine hydroxylase) [389], HMGCS2 [390], AGXT2 [391], FABP1 [392], CUBN (cubilin) [393], DIO1 [394], MIO...…”

Characterization and Proteomic Analysis of Plasma EVs Recovered from Healthy and Diseased Dogs with Canine Leishmaniosis

“…The upregulation of this enzyme in the kidney is associated with increased production of inflammatory cytokines and ROS [ 49 ]. The plasma levels in humans were associated with the progression of chronic kidney disease [ 50 ]. Still, the biological implications of the reduced detection of Myo-inositol oxygenase are not evident because kidney damage is a frequent clinical sign in CanL dogs.…”