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Renal Disease Biomarkers 14/2/11 Mcllroy, D. R., et al (2010) “Biomarkers of Acute Kidney Injury – An Evolving Domain” Anesthesiology, Vol 112 (4), page 998-1004 - AKI is a common problem associated with increased morbidity and mortality incidence increasing all biomarkers to date have differing problems: -> -> -> -> elevate too late. associated with only some sorts of renal injury. lack significant sensitivity and specificity. elevations don’t correlate well with predicting clinically relevant outcomes. Clinical - reducing urine output and anuria clinically relevant surrogate for end-organ perfusion can measure accurately familiarity invasive hard to use in some circumstances (TURP, haematuria) catheter can block oliguria can be caused by other factors (ADH secretion) not related to renal dysfunction Creatinine Clearance - estimates GFR requires 24 hours collection accuracy limited due to creatinine secretion thus overestimates GFR assumes steady state in GFR which may be incorrect Plasma Creatinine - commonly used - well validated - more a marker of renal function rather than injury - production may increase with trauma, fever or immobilization. - GFR may deteriorate by more than 50% prior to a significant rise in serum creatinine - influenced by a number of nonrenal factors: age, race, gender, muscle mass, drug metabolism, protein intake, perioperative fluid administration, hydration. - injury is often taking place prior to the rise in creatinine Plasma Urea - simple to measure - cheap Jeremy Fernando (2011) - widely available - not specific for renal function - affected by: renal disease, protein intake, catabolic state, volume status, GI bleeding, drug therapy (corticosteroids). Plasma and Urinary NGAL = neutrophil gelatinase-associated lipcalin - gene that is maximally induced in a renal ischaemia-reperfusion model - synthesized and secreted by tubular cells - can be rapidly detected in plasma and urine - rapid rise means that it can be used to detect injury - endogenous role is unclear ?possible renoprotective role in ischaemic injury - shown to correlated well in post cardiac bypass renal injury in paediatrics (not so conclusive in adults) Plasma and Urinary Cystatin-C = small cysteine proteinase inhibitor - filtered freely and catabolised entirely by the proximal tubular cells - if there is renal damage it appears in urine - t ½ = 2 hours - mixed results when compared to creatinine Interleukin-18 - ischaemia-reperfusion injury of the proximal tubules producers an active form of IL-18. - it has been shown to accurate predict delayed graft function post transplant. - able to predict AKI only 24 hour prior to creatinine. Kidney Injury Molecule-1 - released from proximal tubule after a variety of injuries. can be measured in urine. best sensitivity and specificity best at prognosticating early detection of AKI N-Acetyl-Beta-D-Glucosaminidase - released from the proximal tubular cells -> into lymph and then not normally filtered to its appearance in the urine is a pathological sign. Other biomarkers - CD11b IL-6 IL-8 IL-10 matrix metalloproteinase-9 glutathione-S-transferase microglobulins Jeremy Fernando (2011) - retinol binding protein in urine Jeremy Fernando (2011)
