Contributions to nephrology
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In order to prevent a disease, its temporal nature (or at least when it starts) needs to be clearly defined. In acute kidney injury (AKI), this is usually not possible because the current diagnostic criteria are retrospective. Contrast-induced nephropathy (CIN) and cardiac surgery-associated acute kidney injury (CSA-AKI) are both thought of as potentially preventable acute renal lesions because the timing of the insult is known precisely. ⋯ Despite this, progress in prevention has been slow, and to date there are no therapies indicated for preventing either CIN or CSA-AKI. The best we can currently do is to recommend aggressive parenteral hydration, avoid compounds we know are nephrotoxic, and avoid unnecessary hypoxia and hypotension. While there is still clearly a long way to go before either of these acute kidney conditions can be described as preventable, the use of major adverse kidney events - death, dialysis and incident or progressive chronic kidney disease at 90 days - as a composite endpoint in clinical trials of putative prevention agents would represent a significant step forwards.
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Acute kidney injury (AKI) is a serious condition that affects many intensive care unit (ICU) patients. The most common causes of AKI in the ICU are severe sepsis and septic shock. The mortality of AKI in septic critically ill patients remains high despite our increasing ability to support vital organs. ⋯ It would seem logical, therefore, to focus on the glomerulus in trying to understand why such loss of GFR occurs. Recent experimental observations suggest that, at least in the initial phases of septic AKI, profound changes occur which involve glomerular hemodynamics and lead to loss of GFR. These observations imply that changes in the vasoconstrictor tone of both the afferent and efferent arterioles are an important component of the pathogenesis of septic AKI.
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In the US and Europe, approximately 90% of heart failure (HF) hospitalizations are due to symptoms and signs of sodium and fluid excess. Congestion is associated with HF progression. According to data from large national registries, approximately 40% of hospitalized HF patients are discharged with unresolved congestion, which may contribute to unacceptably high rehospitalization rates. ⋯ Clinical studies of ultrafiltration have shown that removal of isotonic fluid relieves symptoms of congestion, improves cardiac filling pressures and exercise capacity, and restores diuretic responsiveness in patients with diuretic resistance, concomitantly with favorable effects on pulmonary function, ventilatory efficiency, and neurohormonal activation. Ultrafiltration has been shown to reduce rehospitalizations in a randomized controlled trial of patients with decompensated HF. Future larger controlled clinical trials should evaluate the effect of ultrafiltration on survival.
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Sepsis is the most common cause of acute kidney injury (AKI). There has been a growing body of evidence demonstrating the association between worsening of kidney function during sepsis and the risk of short- and long-term mortality. AKI in sepsis is associated with poor outcome and independently predicts increased mortality. ⋯ The expanding population of patients with sepsis and AKI, and the associated excess mortality provide a strong basis for further research aimed at addressing more rigorously all potentially modifiable factors to reduce this burden to patients and health care systems. Better insights into bidirectional and synergistic pathways linking sepsis and AKI might open the window for new therapeutic approaches that interrupt this vicious circle. Here, we discuss the rationale for and the current understanding of the bidirectional relationship between AKI and sepsis.
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Acute kidney injury (AKI) has been shown to be associated with progression to chronic kidney disease (CKD). Multiple studies have shown that subsets of AKI survivors are at high risk for progression to advanced stage CKD and death. Risk factors associated with AKI survivors progressing to CKD have been identified and include advanced age, diabetes mellitus, decreased baseline glomerular filtration rate, severity of AKI and a low concentration of serum albumin. ⋯ The maintenance phase of AKI is longer in duration in comparison to the initiation phase, and thus the logistics are more amenable to study. However, the mainstay of treatment for the maintenance phase of AKI (renal replacement therapy) has been tested extensively and increasing the dose of renal replacement therapy has not been shown to improve outcome. Therefore, the recovery phase of AKI may represent the best opportunity to intervene in the negative outcomes of AKI.