PURPOSE OF REVIEW: Global renal blood flow is considered pivotal to renal function. Decreased global renal blood flow (decreased perfusion) is further considered the major mechanism of reduced glomerular filtration rate responsible for the development of acute kidney injury (AKI) in critically ill patients. Additionally, urinary biochemical tests are widely taught to allow the differential diagnosis of prerenal (functional) AKI and intrinsic [structural AKI (so-called acute tubular necrosis)]. In this review we will examine recent evidence regarding these two key clinical paradigms. RECENT FINDINGS: Recent animal experiments and clinical studies in humans using cine-phase contrast magnetic resonance technology are not consistent with the decreased perfusion paradigm. They suggest instead that changes in the intra-renal circulation including modification in efferent arteriolar function and intra-renal shunting are much more likely to be responsible for AKI, especially in sepsis. Similarly, recent human studies indicate the urinary biochemistry has limited diagnostic or prognostic ability and is dissociated form biomarker and microscopic evidence of tubular injury. SUMMARY: Intra-renal microcirculatory changes are likely more important than changes in global blood flow in the development of AKI. Urinary biochemistry is not a clinically useful diagnostic or prognostic tool in critically ill patients at risk of or with AKI.
PURPOSE OF REVIEW: Global renal blood flow is considered pivotal to renal function. Decreased global renal blood flow (decreased perfusion) is further considered the major mechanism of reduced glomerular filtration rate responsible for the development of acute kidney injury (AKI) in critically illpatients. Additionally, urinary biochemical tests are widely taught to allow the differential diagnosis of prerenal (functional) AKI and intrinsic [structural AKI (so-called acute tubular necrosis)]. In this review we will examine recent evidence regarding these two key clinical paradigms. RECENT FINDINGS: Recent animal experiments and clinical studies in humans using cine-phase contrast magnetic resonance technology are not consistent with the decreased perfusion paradigm. They suggest instead that changes in the intra-renal circulation including modification in efferent arteriolar function and intra-renal shunting are much more likely to be responsible for AKI, especially in sepsis. Similarly, recent human studies indicate the urinary biochemistry has limited diagnostic or prognostic ability and is dissociated form biomarker and microscopic evidence of tubular injury. SUMMARY: Intra-renal microcirculatory changes are likely more important than changes in global blood flow in the development of AKI. Urinary biochemistry is not a clinically useful diagnostic or prognostic tool in critically illpatients at risk of or with AKI.
Authors: Maurizio Cecconi; Glenn Hernandez; Martin Dunser; Massimo Antonelli; Tim Baker; Jan Bakker; Jacques Duranteau; Sharon Einav; A B Johan Groeneveld; Tim Harris; Sameer Jog; Flavia R Machado; Mervyn Mer; M Ignacio Monge García; Sheila Nainan Myatra; Anders Perner; Jean-Louis Teboul; Jean-Louis Vincent; Daniel De Backer Journal: Intensive Care Med Date: 2018-11-19 Impact factor: 17.440
Authors: Hector R Wong; Natalie Z Cvijanovich; Nick Anas; Geoffrey L Allen; Neal J Thomas; Michael T Bigham; Scott L Weiss; Julie Fitzgerald; Paul A Checchia; Keith Meyer; Thomas P Shanley; Michael Quasney; Mark Hall; Rainer Gedeit; Robert J Freishtat; Jeffrey Nowak; Shekhar S Raj; Shira Gertz; Emily Dawson; Kelli Howard; Kelli Harmon; Patrick Lahni; Erin Frank; Kimberly W Hart; Christopher J Lindsell Journal: Crit Care Med Date: 2015-08 Impact factor: 7.598
Authors: Nadikuda Sunil Kumar; Garipalli Nikilesh Kumar; Krushna C Misra; Manimala Rao; Suneetha Chitithoti; Surya Y Prakash Journal: Indian J Crit Care Med Date: 2021-07