Nephron Clinical Practice最新文献

Background: Despite the great interest in acute kidney injury (AKI), there have been very few studies that examined the economic impact and costing methodologies of AKI. We aimed to examine the cost and income of AKI in hospitalised patients over a period of 1 year using the NHS costing system related to that year.

Methods: A total of 627 patients discharged between January 2008 and December 2008 with AKI were identified by International Classification of Disease 10 codes (ICD-10). Basic demographic data were collected using the hospital electronic records, and the severity of AKI was classified according to the Acute Kidney Injury Network (AKIN) classification. We calculated the total income and isolated the AKI income related to AKI-specific finished consultant episodes. Then we conducted a patient level costing exercise using relative value units (RVU) to compare the cost of AKI to the actual income.

Results: The total spell income for all patients was GBP 1,954,922.7; the mean total income per patient was GBP 3,752.3 (95% CI 3,594.6-3,903.9). AKIN stage 3 generated significantly higher total spell and AKI income. The estimated overall cost of treating AKI was higher than the AKI income to the Primary Care Trust (GBP 1,984,543.9 vs. 1,755,395).

Conclusion: AKIN stage 3 has a significant economic impact when compared with AKIN stages 1 and 2. The move towards a patient level costing using RVU could be a more efficient way to match cost and income.

The recent recognition that acute kidney injury (AKI) may lead to the development of chronic kidney disease and end-stage renal disease, with the attendant increase in mortality, has led to interest in the clinical epidemiology and the mechanistic understanding of renal recovery after an episode of AKI. At present, no uniform definition for recovery after AKI exists and various considerations should be taken into account in the development of a definition. Renal recovery after an AKI episode may affect clinical decision making around the initiation of renal replacement therapy, and has significant implication for biomarker assessment and identification of mechanistic targets to guide potential future clinical trials.

Novel biomarkers are required to improve the timely detection of early acute kidney injury (AKI) and to improve the differential diagnosis, prognostic assessment, and management of AKI cases. It is anticipated that novel biomarkers of early structural AKI ('acute kidney damage') will provide critical diagnostic and prognostic stratification and complement functional markers such as serum creatinine. Further studies are required to conclusively demonstrate the association between early kidney damage biomarkers and clinical outcomes, both with and independently of functional markers, and to discern whether or not randomization to a treatment for AKI based on high structural/damage biomarker levels results in an improvement in kidney function and clinical outcomes.

The provision of continuous renal replacement therapies (CRRT) to small children has generally required the adaptation of adult machines and modified operational characteristics. CRRT prescription for younger and smaller children versus adults differs significantly due to problems concerning the extracorporeal blood volume, the need for circuit blood priming, and the adaptation of machines designed for adult-sized patients. Moreover, the provision of renal replacement therapy to infants and neonates presents a unique problem: no more than 10-15% of their blood volume should be removed by the extracorporeal circuit to prevent hypotension and anemia. In 2012, a dedicated machine, i.e. the Cardio-Renal, Pediatric Dialysis Emergency Machine (CARPEDIEM), was developed and launched the 'fitted era' for pediatric CRRT. In this review, we analyze how CRRT techniques have evolved for pediatric application and describe the first in vivo application of the CARPEDIEM for the safe and efficacious provision of CRRT to infants.

Background/aims: Acute kidney injury (AKI) following cardiac surgery is a complication associated with high rates of morbidity and mortality. We compared staging systems for the diagnosis of AKI after cardiac surgery, and assessed pre-operative factors predictive of post-operative AKI.

Methods: Clinical data, surgical risk scores, procedure and clinical outcome were obtained on all 4,651 patients undergoing cardiac surgery to the Royal Infirmary of Edinburgh between April 2006 and March 2011, of whom 4,572 had sufficient measurements of creatinine before and after surgery to permit inclusion and analysis. The presence of AKI was assessed using the AKIN and RIFLE criteria.

Results: By AKIN criteria, 12.4% of the studied population developed AKI versus 6.5% by RIFLE criteria. Any post-operation AKI was associated with increased mortality from 2.2 to 13.5% (relative risk 7.0, p < 0.001), and increased inpatient stay from a median of 7 (IQR 4) to 9 (IQR 11) days (p < 0.05). Patients identified by AKIN, but not RIFLE, had a mean peak creatinine rise of 34% from baseline and had a significantly lower mortality compared to RIFLE-'Risk' AKI (mortality 6.1 vs. 9.7%; p < 0.05). Pre-operative creatinine, diabetes, NYHA Class IV dyspnoea and EuroSCORE-1 (a surgical risk score) all predicted subsequent AKI on multivariate analysis. EuroSCORE-1 outperformed any single demographic factor in predicting post-operative AKI risk, equating to an 8% increase in relative risk for each additional point.

Conclusion: AKI after cardiac surgery is associated with delayed discharge and high mortality rates. The AKIN and RIFLE criteria identify patients at a range of AKI severity levels suitable for trial recruitment. The utility of EuroSCORE as a risk stratification tool to identify high AKI-risk subjects for prospective intervention merits further study.

Introduction of the standard immunosuppressive treatment has dramatically changed the outcome of patients with both ANCA-associated vasculitis and lupus nephritis, transforming them from incurable diseases with very high short-term mortality to chronic debilitating diseases with much lower short-term, but still relatively high long-term, morbidity/mortality. Long-term morbidity with damage accumulating partly due to the adverse events of the available treatment (namely gonadal toxicity, malignancy, bone disease, cataracts, diabetes, and thromboembolic and cardiovascular disease) has become a major concern. Although cyclophosphamide-based regimens have been partly replaced by newer agents in both ANCA-associated vasculitis and lupus nephritis (namely rituximab or mycophenolate, respectively) their short-term and medium-term adverse events may not be significantly less frequent and we can only hope that new treatments will translate into better long-term outcomes including better long-term safety.

Background: Previous studies have shown that obesity is a risk factor for estimated glomerular filtration rate (eGFR) decline and chronic kidney disease (CKD). However, the relationship between fat mass directly measured by bioimpedance analysis and eGFR is not well known.

Methods: We analyzed 21,859 participants without CKD at baseline who underwent two health checkups at a 5-year interval during 2002-2009. Fat mass was measured by Inbody 3.0 (Biospace, Seoul, Korea). eGFR decline was defined as eGFR <60 ml/min/1.73 m(2) at second checkup. Logistic regression analysis was used to analyze factors related to eGFR decline.

Results: Participants were divided into tertiles according to their fat mass change over 5 years: lower tertile (n = 7,042; <-0.7 kg), middle tertile (n = 7,478; -0.7 to 1.2 kg) and higher tertile (n = 7,339; >1.2 kg). After 5 years, 246 cases of eGFR decline were observed. Multivariate logistic analysis revealed that age (OR 1.03, 95% CI 1.02-1.05, p < 0.001), diabetes mellitus (OR 2.04, 95% CI 1.22-3.40, p = 0.007), baseline eGFR (OR 0.80, 95% CI 0.78-0.83, p < 0.001) and higher tertile of fat mass change (OR 1.58, 95% CI 1.16-2.13, p = 0.003) were associated with eGFR decline after adjustment for sex, hypertension, dyslipidemia, cardiovascular disease, smoking status, body mass index, and high-density lipoprotein cholesterol level.

Conclusions: Fat mass gain over 5 years was independently associated with eGFR decline to <60 ml/min/1.73 m(2) in a relatively healthy Korean population. This finding suggests that lifestyle changes to prevent fat mass gain could be protective against the development of CKD.

Rituximab, a monoclonal antibody directed against the CD20 antigen, found on certain B-cell subsets, results in significant B-cell depletion and has been increasingly used in immune-mediated renal disease and transplantation. Although originally applied to what were considered antibody-mediated diseases, it has become clear that auto- and alloreactive B cells contribute in many ways to immune dysfunction, and the benefit of B-cell depletion extends beyond reduction in auto- or alloantibody levels. Most positive data regarding the benefit of rituximab in immune-mediated kidney disease have come from uncontrolled cohort studies, with the only positive controlled clinical trials demonstrating efficacy for the treatment of systemic vasculitis. While negative trials may have potentially missed clinical effects due to trial design, there may be significant differences in responses in different diseases or lack of efficacy due to therapeutic overlap when used with certain drug combinations. Rituximab is a novel treatment that provides a clear alternative for patients in different clinical situations, and allows for customization of therapy. However, much remains to be understood as to how best to use it in a cost-effective manner, when not to use it, and what the long-term impact of therapy may be.

Background: Acute kidney injury (AKI) is common in hospitalised patients and is associated with adverse long-term consequences. There is an urgent need to understand these sequelae in general hospitalised patients utilising a prospective cohort-based approach. We aimed to test the feasibility of study methodology prior to commencing a large-scale study and investigate the effects of AKI on chronic kidney disease (CKD) progression and proteinuria.

Methods: Pilot study testing novel methodology for remote patient recruitment within a prospective case-control design. 300 cases (hospitalised patients with AKI) and controls (hospitalised patients without AKI) were matched 1:1 for age and baseline estimated glomerular filtration rate (eGFR). 70% of cases had AKI stage 1, 16% AKI stage 2 and 14% AKI stage 3. Renal function and proteinuria were measured 3 and 12 months after hospital admission.

Results: The study met pre-defined recruitment, withdrawal and matching criteria. Renal function was worse in the AKI group at 3 (eGFR 61 ± 20 vs. 74 ± 23 ml/min/1.73 m(2), p < 0.001) and 12 months (eGFR 64 ± 23 vs. 75 ± 25 ml/min/1.73 m(2), p < 0.001). More cases than controls had CKD progression at 3 months (14 vs. 0.7%, p < 0.001). This difference persisted to 12 months, but there was no significant change between 3 and 12 months. Proteinuria and albuminuria were more prevalent in the AKI group and associated with CKD progression.

Conclusions: We describe a method of remote patient recruitment which could be employed more widely for prospective observational studies. Even mild AKI is associated with long-term renal dysfunction. Further investigation using this methodology is now underway.

Nearly all body organs and systems are affected by the toxicity of uremic compounds retained in the course of renal dysfunction. Knowledge about the origin, chemical structure and composition of the retained endogenous substances responsible for these symptoms is far from complete. Organic retention solutes present a great variety of properties which makes their accurate classification extremely difficult. Their potential toxicity remains to be elucidated with meticulous observation of clearly formulated rules guiding the process. Toxicity assessment is a complex process because not just one but several retained compounds may be simultaneously involved in the same biological and metabolic processes. The search for new uremic compounds and combining them into panels of substances involved in the same pathophysiological processes seems to offer a novel approach to identifying and explaining any so far unexplored specific effects of endogenous compounds on the body organs and systems.