Temporal Changes in Incidence of Dialysis-Requiring AKI
The population epidemiology of AKI is not well described. Here, we analyzed data from the Nationwide Inpatient Sample, a nationally representative dataset, to identify cases of dialysis-requiring AKI using validated International Classification of Diseases, Ninth Revision (ICD-9) codes. From 2000 to 2009, the incidence of dialysis-requiring AKI increased from 222 to 533 cases per million person-years, averaging a 10% increase per year (incidence rate ratio=1.10, 95% CI=1.10-1.11 per year). Older age, male sex, and black race associated with higher incidence of dialysis-requiring AKI. The rapid increase in incidence was evident in all age, sex, and race subgroups examined. Temporal changes in the population distribution of age, race, and sex as well as trends of sepsis, acute heart failure, and receipt of cardiac catheterization and mechanical ventilation accounted for about one third of the observed increase in dialysis-requiring AKI among hospitalized patients. The total number of deaths associated with dialysis-requiring AKI rose from 18,000 in 2000 to nearly 39,000 in 2009. In conclusion, the incidence of dialysis-requiring AKI increased rapidly in all patient subgroups in the past decade in the United States, and the number of deaths associated with dialysis-requiring AKI more than doubled.
Available from: PubMed Central
- "Acute kidney injury (AKI) is common and appears to be increasing among hospitalized patients
[1-3]. Observational studies demonstrate that even transient AKI is associated with adverse events ranging from increased hospital length of stay, to the development of end-stage renal disease and death
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A translational study in renal transplantation suggested YKL-40, a chitinase 3-like-1 gene product, plays an important role in acute kidney injury (AKI) and repair, but data are lacking about this protein in urine from native human kidneys.
This is an ancillary study to a single-center, prospective observational cohort of patients with clinically-defined AKI according to AKI Network serum creatinine criteria. We determined the association of YKL -40 ≥ 5 ng/ml, alone or combined with neutrophil gelatinase-associated lipocalin (NGAL), in urine collected on the first day of AKI with a clinically important composite outcome (progression to higher AKI stage and/or in-hospital death).
YKL-40 was detectable in all 249 patients, but urinary concentrations were considerably lower than in previously measured deceased-donor kidney transplant recipients. Seventy-two patients (29%) progressed or died in-hospital, and YKL-40 ≥ 5 ng/ml had an adjusted odds ratio (95% confidence interval) for the outcome of 3.4 (1.5-7.7). The addition of YKL-40 to a clinical model for predicting the outcome resulted in a continuous net reclassification improvement of 29% (P = 0.04). In patients at high risk for the outcome based on NGAL concentrations in the upper quartile, YKL-40 further partitioned the cohort into moderate-risk and very high-risk groups.
Urine YKL-40 is associated with AKI progression and/or death in hospitalized patients and improves clinically determined risk reclassification. Combining YKL-40 with other AKI biomarkers like NGAL may further delineate progression risk, though additional studies are needed to determine whether YKL-40 has general applicability and to define its association with longer-term outcomes in AKI.
Available from: molpharm.aspetjournals.org
- "Acute kidney injury (AKI) leads to adverse outcomes in hospitalized patients including prolonged length of stay, higher health care costs, and increased mortality (Chertow et al., 2005; Hsu et al., 2013). In addition to these short-term complications, recovery of renal function after AKI is often impaired resulting in chronic kidney disease or end-stage renal disease (Coca et al., 2009; Triverio et al., 2009). "
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ABSTRACT: Heterotrimeric G-proteins play a crucial role in the control of renal epithelial cell function during homeostasis and in response to injury. In this report, Gβγ dimer activity was evaluated during the process of renal tubular repair following renal ischemia-reperfusion injury (IRI) in male Sprague Dawley rats. Rats were treated with a small molecule inhibitor of Gβγ activity, gallein (30 or 100 mg/kg), 1 hr after reperfusion and every 24 hours for 3 additional days. Following IRI, renal dysfunction was prolonged following the high-dose gallein treatment in comparison to vehicle treatment during the 7 day recovery period. Renal tubular repair in the outer medulla 7 days after IRI was significantly (P<0.001) attenuated following treatment with high-dose gallein (100 mg/kg) in comparison to low-dose gallein (30 mg/kg), or the vehicle and fluorescein control groups. Gallein treatment significantly reduced (P<0.05) the number of PCNA-positive tubular epithelial cells after 24 hours following the ischemia-reperfusion phase in vivo. In vitro application of gallein on normal rat kidney (NRK-52E) proximal tubule cells significantly reduced (P<0.05) S-phase cell cycle entry compared to vehicle-treated cells as determined by 5'-bromo-2'-deoxyuridine incorporation. Taken together, these data suggest that Gβγ signaling contributes to the maintenance and repair of renal tubular epithelium, and may be a novel therapeutic target for the development of drugs to treat acute kidney injury.
Available from: Eric McArthur
- "Acute kidney injury (AKI) is a common and serious complication of hospitalization; in severe cases, urgent renal replacement therapy (hereafter referred to as dialysis) is needed to address complications of AKI and to support the patient in overcoming the acute illness. Between 2000 and 2009, the incidence of dialysis requiring AKI (AKI-D) in the United States increased by 10% annually from 222 to 533 cases per million person-years
. The increased incidence of AKI will result in greater numbers of patients who are faced with persistent health challenges after the acute phase of their illness has resolved. "
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Survivors of acute kidney injury are at an increased risk of developing irreversible deterioration in kidney function and in some cases, the need for chronic dialysis. We aimed to determine predictors of chronic dialysis and death among survivors of dialysis-requiring acute kidney injury.
We used linked administrative databases in Ontario, Canada, to identify patients who were discharged from hospital after an episode of acute kidney injury requiring dialysis and remained free of further dialysis for at least 90 days after discharge between 1996 and 2009. Follow-up extended until March 31, 2011. The primary outcome was progression to chronic dialysis. Predictors for this outcome were evaluated using cause-specific Cox proportional hazards models, and a competing risk approach was used to calculate absolute risk.
We identified 4 383 patients with acute kidney injury requiring temporary in-hospital dialysis who survived to discharge. After a mean follow-up of 2.4 years, 356 (8%) patients initiated chronic dialysis and 1475 (34%) died. The cumulative risk of chronic dialysis was 13.5% by the Kaplan-Meier method, and 10.3% using a competing risk approach. After accounting for the competing risk of death, previous nephrology consultation (subdistribution hazard ratio (sHR) 2.03; 95% confidence interval (CI) 1.61-2.58), a history of chronic kidney disease (sHR3.86; 95% CI 2.99-4.98), a higher Charlson comorbidity index score (sHR 1.10; 95% CI 1.05-1.15/per unit) and pre-existing hypertension (sHR 1.82; 95% CI 1.28-2.58) were significantly associated with an increased risk of progression to chronic dialysis.
Among survivors of dialysis-requiring acute kidney injury who initially become dialysis independent, the subsequent need for chronic dialysis is predicted by pre-existing kidney disease, hypertension and global comorbidity. This information can identify patients at high risk of progressive kidney disease who may benefit from closer surveillance after cessation of the acute phase of illness.
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