Liver Type Fatty Acid Binding Protein (L-FABP): A Marker of Contrast Induced -Acute Kidney Injury

Background: Urinary Liver type fatty acid binding protein (L-FABP) is an early biomarker for renal damage. A few studies have been published analyzing the potential use of urinary Liver type fatty acid binding protein (L-FABP) as a biomarker for acute kidney injury. However no study has been done related to Acute Kidney Injury associated with contrast administration. Aim: To search for new markers to identify Acute Kidney Injury (AKI) associated with contrast administration earlier than serum creatinine. Material and Methods: We studied 100 consecutive patients with normal serum creatinine undergoing angiographic procedure. We assessed urinary liver type fatty acid binding protein (L-FABP) levels at basal, 2h 4h, 12h, 24 h and 48 hours after the angiographic procedure. Serum creatinine was measured at basal, 24h and 48 hours after the procedure. Results: There was a significant rise in urinary L-FABP levels at 12 hours after the angiographic procedure. The presence of contrast induced nephropathy associated with acute Kidney Injury was 9%. Conclusion: The present study highlighted the importance of urinary L-FABP in detecting Acute Kidney Injury associated with contrast administration earlier than Serum creatinine. Keywords: Liver type fatty acid binding protein (L-FABP).   Glomerular Filtration Rate (GFR), Contrast induced acute kidney injury (CI-AKI)

Kidney injury molecule-1: a urinary biomarker for contrast induced acute kidney injury.

Back ground: Urinary kidney injury molecule 1 (KIM-1) is early biomarker for renal damage. A few studies have been published analyzing the potential use of urinary kidney injury molecule-1 (KIM-1) as a biomarker for acute kidney injury. However no study has been done related to Acute Kidney Injury associated with contrast administration. Aim: To search for new markers to identify Acute Kidney Injury (ARF) associated with contrast administration earlier than serum creatinine. Material and Methods: We studied 100 consecutive patients with normal serum creatinine undergoing angiographic procedure. We assessed urine KIM-1, at 4h, 8h, and 24 hours after the angiographic procedure. Serum creatinine was measured at basal, 24h and 48 hours after the procedure. Results: There was a significant rise in urinary KIM-1 levels at 24 hours after the angiographic procedure. The presence of contrast induced nephropathy associated with acute Kidney Injury was 12%. Conclusion: The present study highlighted the importance of urinary KIM-1 in detecting Acute Kidney Injury associated with contrast administration earlier than Serum creatinine. Key words: Neutrophil-gelatinase-associated lipocalin. Contrast-induced nephropathy. Cystatin C. Glomerular Filtration Rate (GFR), Kidney injury molecule -1 (KIM-1)

GUT MICROBIOTA AND DIABETES MELLITUS - AN INTERLINKAGE

  In recent years, the curiosity to investigate the relationship between gut microbiota and diabetes development has increased. Evidence from previous studies suggests that gut microbiota manipulation may assure to prevent diabetes development in future, primarily in susceptible individuals. Here, we reviewed special gut microbiota types proposing development of Type 1 (T1D) and Type 2 diabetes (T2D) in humans and laboratory animals. The available data we found are still inconclusive and required more attention in discriminating specific groups of gut microbiomes strongly indicating T1D and T2D development or prevention. Further, we suggested for the first time to study the gut microbiota in different ways to find the root cause of diabetes development

GUT MICROBIOTA AND DIABETES MELLITUS - AN INTERLINKAGE

  In recent years, the curiosity to investigate the relationship between gut microbiota and diabetes development has increased. Evidence from previous studies suggests that gut microbiota manipulation may assure to prevent diabetes development in future, primarily in susceptible individuals. Here, we reviewed special gut microbiota types proposing development of Type 1 (T1D) and Type 2 diabetes (T2D) in humans and laboratory animals. The available data we found are still inconclusive and required more attention in discriminating specific groups of gut microbiomes strongly indicating T1D and T2D development or prevention. Further, we suggested for the first time to study the gut microbiota in different ways to find the root cause of diabetes development

Kidney injury molecule-1: A urinary biomarker for contrast-induced acute kidney injury

Background: Urinary kidney injury molecule 1 (KIM-1) is an early biomarker for renal damage. A few studies have been published analyzing the potential use of urinary KIM-1 as a biomarker for acute kidney injury (AKI). However, no study has been done related to AKI associated with contrast administration. Aim: To search for new markers to identify AKI associated with contrast administration earlier than serum creatinine. Materials and Methods: We studied 100 consecutive patients with normal serum creatinine undergoing angiographic procedure. We assessed urine KIM-1, at 4, 8, and 24 hours after the angiographic procedure. Serum creatinine was measured at basal, 24, and 48 hours after the procedure. Results: There was a significant rise in urinary KIM-1 levels at 24 hours after the angiographic procedure. The presence of contrast induced nephropathy associated with AKI was 12%. Conclusion: The present study highlighted the importance of urinary KIM-1 in detecting AKI associated with contrast administration earlier than Serum creatinine

Evaluation of the diagnostic performance of new markers for acute kidney injury associated with contrast administration

Background: Contrast-induced nephropathy (CIN) is a form of acute kidney injury (AKI) that is caused by exposure to contrast media in diagnostic imaging and interventional procedures such as angiography. At present serum creatinine is the only standard test for it. A few studies have been published analyzing the potential use of neutrophil-gelatinase-associated lipocalin (NGAL) in AKI. Aim: The aim of this study is to search for new markers to identify AKI acute renal failure earlier than serum creatinine. Materials and Methods: We studied 100 consecutive patients with normal serum creatinine undergoing angiographic procedure against Urine NGAL, serum NGAL, serum Cystatin C and urinary interleukin-18 (IL-18) at basal, and 2 h, 4 h, 8 h, 24 h, and 48 h after the angiography. Results: There was a significant rise in serum NGAL levels at 2 h, 4 h, and 8 h after angiography and in urinary NGAL levels at 4 h, 8 h, and 24 h after the procedure. Cystatin C rose significantly at 8 h and 24 h after the procedure, On the other hand, there was mild rise in urinary Il-18 levels at 24 h, but not significant. The presence of CIN associated with AKI was 13%. Conclusion: The present study highlighted the importance of serum NGAL, urine NGAL and Cystatin C in detecting AKI associated with contrast administration earlier than serum creatinine