The Real Importance of Pre-Existing Comorbidities on Long-Term Mortality after Acute Kidney Injury

Division of Nephrology, School of Medicine, University of São Paulo, São Paulo, Brazil.
PLoS ONE (Impact Factor: 3.23). 10/2012; 7(10):e47746. DOI: 10.1371/journal.pone.0047746
Source: PubMed


The causes of death on long-term mortality after acute kidney injury (AKI) have not been well studied. The purpose of the study was to evaluate the role of comorbidities and the causes of death on the long-term mortality after AKI.
We retrospectively studied 507 patients who experienced AKI in 2005-2006 and were discharged free from dialysis. In June 2008 (median: 21 months after AKI), we found that 193 (38%) patients had died. This mortality is much higher than the mortality of the population of São Paulo City, even after adjustment for age. A multiple survival analysis was performed using Cox proportional hazards regression model and showed that death was associated with Khan's index indicating high risk [adjusted hazard ratio 2.54 (1.38-4.66)], chronic liver disease [1.93 (1.15-3.22)], admission to non-surgical ward [1.85 (1.30-2.61)] and a second AKI episode during the same hospitalization [1.74 (1.12-2.71)]. The AKI severity evaluated either by the worst stage reached during AKI (P = 0.20) or by the need for dialysis (P = 0.12) was not associated with death. The causes of death were identified by a death certificate in 85% of the non-survivors. Among those who died from circulatory system diseases (the main cause of death), 59% had already suffered from hypertension, 34% from diabetes, 47% from heart failure, 38% from coronary disease, and 66% had a glomerular filtration rate <60 previous to the AKI episode. Among those who died from neoplasms, 79% already had the disease previously.
Among AKI survivors who were discharged free from dialysis the increased long-term mortality was associated with their pre-existing chronic conditions and not with the severity of the AKI episode. These findings suggest that these survivors should have a medical follow-up after hospital discharge and that all efforts should be made to control their comorbidities.

Download full-text


Available from: Regina C R M Abdulkader,
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Haemorrhagic shock is a common cause of acute kidney injury, which is a major risk factor for developing chronic kidney disease. The mechanism is superficially straightforward. An arterial pressure below the kidney's autoregulatory region leads to a direct reduction in filtration pressure and perfusion, which in turn cause renal failure with reduced glomerular filtration rate (GFR), and AKI because of hypoxia. However, the kidney's situation is further worsened by the hormonal and neural reactions to reduced perfusion pressure. There are three major systems working to maintain arterial pressure in shock: Sympathetic signaling, the renin-angiotensin-system, and vasopressin. These work to retain electrolytes and water, and to increase peripheral resistance and cardiac output. In the kidney the increased electrolyte reabsorption consumes oxygen. At the same time, at the signaling level seen in shock, all of these hormones reduces renal perfusion, and thereby oxygen delivery. This creates an exaggerated hypoxic situation that is liable to worsen the AKI. The present review will examine this mechanistic background and identify a number of areas that require further studies. At this time the ideal treatment of haemorrhagic shock appears to be slow fluid resuscitation, possibly with hyperosmolar sodium, low chloride, and no artificial colloids. From the standpoint of the kidney, renin-angiotensin system inhibitors appear fruitful for further study. This article is protected by copyright. All rights reserved.
    Acta Physiologica 07/2013; 209(1). DOI:10.1111/apha.12147 · 4.38 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Acute kidney injury (AKI) is characterized by an abrupt decline in renal function, resulting in an inability to secrete waste products and maintain electrolyte and water balance, and is associated with high risks of morbidity and mortality. This study retrospectively analyzed clinical data, treatment, and prognosis of 271 hospitalized patients (172 males and 99 females) diagnosed with AKI from December, 2008 to December, 2011. In addition, this study explored the association between the cause of AKI and prognosis, severity and treatment of AKI. The severity of AKI was classified according to the Acute Kidney Injury Network (AKIN) criteria. Renal recovery was defined as a decrease in a serum creatinine level to the normal value. Prerenal, renal, and postrenal causes accounted for 36.5% (99 patients), 46.5% (126 patients) and 17.0% (46 patients), respectively, of the incidence of AKI. Conservative, surgical, and renal replacement treatments were given to 180 (66.4%), 30 (11.1%) and 61 patients (22.5%), respectively. The overall recovery rate was 21.0%, and the mortality rate was 19.6%. Levels of Cl(-), Na(+) and carbon dioxide combining power decreased with increasing severity of AKI. Cause and treatment were significantly associated with AKI prognosis. Likewise, the severity of AKI was significantly associated with cause, treatment and prognosis. Multivariate logistic regression analysis found that respiratory injury and multiple organ dysfunction syndrome (MODS) were associated with AKI patient death. Cause, treatment and AKIN stage are associated with the prognosis of AKI. Respiratory injury and MODS are prognostic factors for death of AKI patients.
    PLoS ONE 02/2014; 9(2):e85214. DOI:10.1371/journal.pone.0085214 · 3.23 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Identifying individuals who are at increased risk for accelerated progressive chronic kidney disease (CKD) and who might benefit from preventive interventions is an important challenge. The present observational study evaluated the effect of an episode of Acute Kidney Injury (AKI) on the evolution of the renal trajectory in a cohort of 311 ambulatory CKD patients. We analyzed the evolution of eGFR in this cohort within a 5-year time window around an AKI episode. The mean of the available eGFR-values over a 6 month period was calculated once at the start and once at the end of the 5-year period. Slow and fast CKD progression were defined as a decrease by respectively ≤ or >1 category of 15 ml/min/1.73 m(2) over the 5-year time window. The influence of AKI on progression status was analyzed. Median eGFR decline over the 5 year period was 11, 22 and 6 ml/min/1.73 m(2) in the total, AKI and no AKI group respectively. AKI occurred in 44/72 versus 50/239 of fast versus slow progressors (odds ratio: 5.9, 95 % confidence interval: 3.4-10.5). An incomplete recovery of eGFR after an AKI episode (median in overall, fast progressors, slow progressors 11, 20 and 4 ml/min/1.73 m(2) respectively) was the major component for the overall loss of renal function over the 5-year window. Our data failed to provide evidence that the CKD progression became more accelerated once kidney function was stabilized after the AKI episode. Incomplete recovery of AKI was related with accelerated CKD-progression. Episodes of AKI were not associated with an accelerated decline of kidney function once the AKI episode had resolved. In the group without AKI episode, the progression was similar to that of the general population without CKD.
    Journal of nephrology 02/2015; 28(6). DOI:10.1007/s40620-015-0181-5 · 1.45 Impact Factor
Show more