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BOOK REVIEW
Year : 2013  |  Volume : 137  |  Issue : 6  |  Page : 1213-1215

Controversies in acute kidney injury


Department of Nephrology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Rae Bareli Road, Lucknow 226 014, India

Date of Web Publication4-Jul-2013

Correspondence Address:
R K Sharma
Department of Nephrology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Rae Bareli Road, Lucknow 226 014
India
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Source of Support: None, Conflict of Interest: None


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How to cite this article:
Sharma R K. Controversies in acute kidney injury. Indian J Med Res 2013;137:1213-5

How to cite this URL:
Sharma R K. Controversies in acute kidney injury. Indian J Med Res [serial online] 2013 [cited 2020 Feb 22];137:1213-5. Available from: http://www.ijmr.org.in/text.asp?2013/137/6/1213/114402

Controversies in acute kidney injury, J.A. Kellum, C. Ronco, J.L. Vincent, editors (S. Karger, Basel, Switzerland) 2011. 258 pages. Price: US$ 232.00, CHF 198.00, EUR 165.00
ISBN 978-3-8055-9810-1

This book is broadly divided in to four sections each authored and co-authored by experts in the field of intensive care nephrology. The objective is to look into the various grey areas in acute kidney injury (AKI) beginning with definition to pathogenesis to timing of renal replacement therapy (RRT) and its dosing.

The first section begins with discussion on prerenal azotemic syndromes. The authors discuss the determinants of ultrafiltration. The role of various neurohumoral influence including role of ROS, NO and adrenergic system is discussed in detail. In the chapter on prerenal physiology the authors have identified flaws in the paradigm of prerenal azotemia. They suggest that prerenal azotemia might be a normal response to renal hypoperfusion and it is difficult clinically to identify renal parenchymal damage. Cardiorenal and hepatorenal syndromes are discussed in detail in subsequent chapters.

The second section on Dying 'of' or 'with' Acute Kidney Injury is divided into various sub-sections including clinical consequences of AKI, the details of renal pulmonary crosstalk, and bidirectional mode of sepsis and AKI. The main emphasis is to highlight the need to early recognize and intervene. Early fluid therapy, correction of acid base disorder and treating infection are of paramount importance. AKI and acute living injury (ALI) when occur together increase mortality drastically. AKI modulates lung function in various ways, as it has got both pro-and anti-inflammatory effects in lungs. The role of cytokines IL-6, IL-10 and serum amyloid-3 is discussed. In the last chapter on bidirectional model of sepsis and AKI the authors describe the impact of sepsis on AKI and vice versa.

In the third section, the authors describe pathophysiology of septic AKI. In the first chapter the role of global renal blood flow and renal vascular resistance is described. Sepsis causes AKI by various mechanisms and not merely due to isolated renal hypoperfusion. There are renal microcirculatory changes which increase renal vascular resistance. The earlier belief of reduced rend blood flow (RBF) is now challenged by both animal and human studies. Role of Doppler ultrasonography (USG) in calculating resistive index may play a role in distinguishing prerenal AKI from acute tubular necrosis (ATN). ATN shows a high resistive index as compared to prerenal AKI. The authors discuss the role of endothelium in septic AKI.

Toxic triangle of oxygen, reactive oxygen species and nitric oxide is further discussed in the pathogenesis of acute kidney injury. Inflammation induced leucocyte endothelium interaction causes disturbance of homeostatic balance between O 2 , NO and ROS. Taken together, this causes microcirculatory dysfunction which leads to AKI. In subsequent chapters the effects of remote tissue damage on the kidney are discussed. New emerging evidences argue that injury to the kidney is largely derived from local inflammation and the triggers for this inflammation are derived from remote tissue damage and interactions directed at blocking these signals suppress AKI. Injured and infected tissues release immunological danger signals or danger-associated molecular pattern molecules (DAMPS) such as chromatin-associated protein high-mobility group box 1 (HMGB1), DNA, microRNAs, ATP, adenosine and uric acid. These molecules cause diverse renal injury. New technologies such as real time monitoring of tissue NADH may improve our ability to detect evolving oxidative stress in various tissues during sepsis. The role of maladaptive repair in causing chronic kidney disease from injury is dealt with in the next chapter. With mild injury the repair is usually complete with no residual injury, however, with severe injury repair process can lead to fibrosis which facilitates progression to CKD.

In the fourth section the authors discuss prevention, treatment and rehabilitation. The models of preventable diseases such as contrast-induced nephropathy and cardiac surgery-associated acute kidney injury are discussed in the first chapter of this section. In the next chapter, the focus is on AKI in children. Recent advancement in standardizing the AKI definition (the paediatric modified RIFLE criteria), multi-centre collaboration via the prospective paediatric CRRT registry group and multiple validation studies of novel AKI biomarkers in children have provided the essential components to evaluate preventive and therapeutic strategies to attack paediatric AKI as a disease state. The authors suggest that paediatric population form ideal group to study early biomarkers of kidney damage as they are usually free of confounding comorbities. Long term outcomes of acute kidney injury is further discussed in the next chapter. Progression to chronic kidney disease (CKD) is a known complication of AKI. Risk factors for progression have been identified and include advanced age, diabetes mellitus, baseline GFR, severity of AKI and low serum albumin. Since progression to CKD has been studied, intervention can be planned to halt this progression and recovery phase of AKI provides the best opportunity. The authors described the role of microvesicles (MV) in acute kidney injury. Microvesicles participate in physiological and pathological processes by signaling through specific interactions and transferring gene products. These may provide new diagnostic tools in future as their presence in body fluids make them readily accessible.

The fifth section covers the concept of renal support in AKI. Fluid management is a complex issue in critically ill patients. Adequate balance needs to be maintained. On one hand there is a risk of hyovolemia and hypoperfusion and on the other extreme, there is a risk of fluid overload. Recent evidence suggests that fluid overload leads to adverse outcomes. Several definitions have been proposed to standardize the approaches like daily fluid balance, cumulative fluid balance, percentage of fluid overload adjusted for body weight.

RRT in AKI is another area of controversy. The time of initiation, dose and outcome have been a matter of extensive debate. Areas which need further refinement include timing of RRT (early vs late), fluid and electrolyte management and identification of important uremic toxins. Available evidence suggests a survival benefit of early initiation of RRT. At last, future advancement is dealt with in detail. Specifically designed extracorporeal membrane and drug or cell based therapy are under research. Machine developed feed-back system responding to specific endopoints is also under consideration. Cascade apheresis, use of nanoporous membrane and bioartificial system have expanded the future domain of research.

To conclude, the book is an excellent review of the current controversies in acute kidney injury. This book seems to be more useful for nephrologists dealing with critical care and can guide them in decision making.




 

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