Acute kidney injury (AKI) is a complex disorder for which currently there is no accepted definition. Having a uniform standard for diagnosing and classifying AKI would enhance our ability to manage these patients. Future clinical and translational research in AKI will require collaborative networks of investigators drawn from various disciplines, dissemination of information via multidisciplinary joint conferences and publications, and improved translation of knowledge from pre-clinical research. We describe an initiative to develop uniform standards for defining and classifying AKI and to establish a forum for multidisciplinary interaction to improve care for patients with or at risk for AKI. Members representing key societies in critical care and nephrology along with additional experts in adult and pediatric AKI participated in a two day conference in Amsterdam, The Netherlands, in September 2005 and were assigned to one of three workgroups. Each group's discussions formed the basis for draft recommendations that were later refined and improved during discussion with the larger group. Dissenting opinions were also noted. The final draft recommendations were circulated to all participants and subsequently agreed upon as the consensus recommendations for this report. Participating societies endorsed the recommendations and agreed to help disseminate the results. The term AKI is proposed to represent the entire spectrum of acute renal failure. Diagnostic criteria for AKI are proposed based on acute alterations in serum creatinine or urine output. A staging system for AKI which reflects quantitative changes in serum creatinine and urine output has been developed. We describe the formation of a multidisciplinary collaborative network focused on AKI. We have proposed uniform standards for diagnosing and classifying AKI which will need to be validated in future studies. The Acute Kidney Injury Network offers a mechanism for proceeding with efforts to improve patient outcomes.

Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury

Sidney C. Smith, Jr, MD, FACC, FAHA, FESC, Chair; Alice K. Jacobs, MD, FACC, FAHA, Vice-Chair; Cynthia D. Adams, MSN, APRN-BC, FAHA; Jeffery L. Anderson, MD, FACC, FAHA; Elliott M. Antman, MD, FACC, FAHA[‡][1]; Jonathan L. Halperin, MD, FACC, FAHA; Sharon Ann Hunt, MD, FACC, FAHA; Rick Nishimura,

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ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society

http://hwmaint.circ.ahajournals.org/cgi/reprint/110/9/e82.pdf

ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction

Since its introduction as a clinical entity in 1992, the Brugada syndrome has progressed from being a rare disease to one that is second only to automobile accidents as a cause of death among young adults in some countries Electrocardiographically characterized by a distinct ST-segment elevation in the right precordial leads, the syndrome is associated with a high risk for sudden cardiac death in young and otherwise healthy adults, and less frequently in infants and children Patients with a spontaneously appearing Brugada ECG have a high risk for sudden arrhythmic death secondary to ventricular tachycardia/fibrillation The ECG manifestations of Brugada syndrome are often dynamic or concealed and may be unmasked or modulated by sodium channel blockers, a febrile state, vagotonic agents, α-adrenergic agonists, β-adrenergic blockers, tricyclic or tetracyclic antidepressants, a combination of glucose and insulin, hypo- and hyperkalemia, hypercalcemia, and alcohol and cocaine toxicity In recent years, an exponential rise in the number of reported cases and a striking proliferation of articles defining the clinical, genetic, cellular, ionic, and molecular aspects of the disease have occurred The report of the first consensus conference, published in 2002, focused on diagnostic criteria The present report, which emanated from the second consensus conference held in September 2003, elaborates further on the diagnostic criteria and examines risk stratification schemes and device and pharmacological approaches to therapy on the basis of the available clinical and basic science data

Brugada Syndrome: Report of the Second Consensus Conference Endorsed by the Heart Rhythm Society and the European Heart Rhythm Association

1999 update: ACC/AHA guidelines for the management of patients with acute myocardial infarction: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute Myocardial Infarction)

A case report of a patient with frequent ventricular premature beats but with an otherwise normal ECG and no structural heart disease. Propafenone in therapeutical doses unmasked the ECG picture of the Brugada phenomenon.

Unmasking effect of propafenone on the concealed form of the Brugada phenomenon.

We analysed frequencies of two single-nucleotide polymorphisms (SNP) in the interferon-γ (IFN-γ) receptor-1 (IFNGR1) gene promoter (G-611A, T-56C) in tuberculosis patients (n = 244) and compared them with controls (n = 521). These frequencies were not significantly different, whether analysed independently or as haplotypes. Because these SNP affect transcription, the results suggest that the expression of the IFNGR1 gene does not confer susceptibility to disease in patients from Croatia. Further analysis revealed a significant association between the protective (CA)n polymorphism (22 repeats, 192 FA1), located in the fifth intron of the IFNGR1 gene (+16682), and GT promoter haplotype (−611; −56) that showed the strongest expression capacity. In addition to this cis relationship, the (CA)22 allele was correlated in trans with an IFN-γ SNP (IFNG G + 2109A), which might affect the transcription of the IFNG gene. These results suggest that a particular combination of IFNG and IFNGR1 SNP might offer a better protection against tuberculosis in this population.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-3083.2005.01694.x

Interferon‐γ Receptor‐1 Gene Promoter Polymorphisms (G‐611A; T‐56C) and Susceptibility to Tuberculosis

Prognostic significance of complete atrioventricular block in patients with acute inferior myocardial infarction with and without right ventricular involvement

Background. To establish the baseline cutoff value of C-reactive protein (CRP) that would predict increased overall and cardiovascular mortality in patients with end-stage renal disease (ESRD). Methods. A cohort of 270 prevalent hemodialysis patients treated at Rijeka University Hospital was eligible for the study. Monthly CRP measurements were performed for three consecutive months. Only the patients with CRP values varying 10.0 mg/L. The survival was evaluated by Kaplan-Meier curve. Results. During the two-year follow-up, 59 patients died. The major cause of death was cardiovascular disease (64%). Significantly higher overall and cardiovascular mortality was observed in group 3 when compared with groups 1 and 2 (χ2=11.97; P < 0.001) and in group 4 when compared with groups 1 and 2 (χ2=14.40; P<0.001). Compared with survivors, non-survivors had a higher median CRP value (19.0 [1.5–99.7] mg/L vs. 2.3 [0.1–49.1] mg/L, respectively; P<0.001). Conclusion. Serum concentration of CRP above 6.2 mg/L is a strong predictor of overall and cardiovascular mortality in patients with ESRD.

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C-reactive Protein Is a Strong Predictor of Mortality in Hemodialysis Patients

Zinc is necessary for growth and cells’ division. Its deficiency may seriously affect antioxidant defense system and is usually related to renal failure, gastrointestinal diseases and alcoholism. It is very important to know zinc status in dialyzed patients and to prevent hypo- or hyperzincemia. Serum samples from 89 patients with chronic terminal renal failure on regular hemodialysis were withdrawn for the estimation of zinc concentrations immediately before and after dialysis. Serum zinc concentrations showed to be highly dependent on hemodialysis. In 57 (64%) patients, serum zinc concentrations
decreased, sometimes from very high to normal values. In remaining 32 (36%) patients serum zinc concentrations tended to increase, but remained within normal range. Zinc supplementation may be recommended only in the patients with proven zinc deficiency, but for all chronic renal failure patients it is questionable.

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Luka Zaputović

Papers

Unmasking effect of propafenone on the concealed form of the Brugada phenomenon.

Interferon‐γ Receptor‐1 Gene Promoter Polymorphisms (G‐611A; T‐56C) and Susceptibility to Tuberculosis

Prognostic significance of complete atrioventricular block in patients with acute inferior myocardial infarction with and without right ventricular involvement

C-reactive Protein Is a Strong Predictor of Mortality in Hemodialysis Patients

Serum zinc concentrations in the maintenance hemodialysis patients.