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Objectives. The purpose of the present study is to verify if the degree of immunological response against metastatic tumors, measured by the number of CD57+ NK-cells in the tissue of a brain metastasis, influences the later development of new brain metastases or tumor recurrence. Patients and Methods. CD57+ NK-cells were immunohistochemically identified in the resected tumor, in a series of twenty patients operated on by a single brain metastasis secondary to lung adenocarcinoma. In each case, the degree of CD57+ NK-cells infiltration within the tumor tissue and the period free of new intracranial disease after brain surgery were recorded. Results. All the studied tumors showed variable number of CD57+ NK-cells (mean ± standard deviation: 8.4 ± 4.8 per microscopical field, at 200x). The period free of intracranial disease ranged between 10 and 52 weeks (mean ± standard deviation: 22.7 ± 11.9). Statistical analysis showed that there was no correlation between the degree of NK-cells infiltration within the resected tumor and the period free of intracranial disease after surgery (P > 0.05). Conclusion. This finding supports that clinical behavior in metastatic brain disease is not influenced by the immunological response mediated by CD57+ NK-cells. [ABSTRACT FROM AUTHOR]

BACKGROUND: The prevalence of elderly individuals continues to increase over time, as does the incidence of acute kidney injury (AKI). However, it is not known whether age is an important prognostic predictor for renal recovery after an episode of AKI. STUDY DESIGN: Systematic review of MEDLINE and EMBASE databases and meta-analysis of pooled data using random-effect models. SETTING & POPULATION: Adults with AKI, not including kidney transplant recipients. SELECTION CRITERIA FOR STUDIES: Studies published in English between 2000 and 2007 were eligible for this analysis if they met the following inclusion criteria: (1) clear definition of AKI and recovery of kidney function, (2) assessment of kidney function recovery as the primary or secondary outcome, and (3) participant age reported. We contacted the investigators of studies and requested data for recovery of kidney function by patient age. PREDICTOR: Patient age of 65 years and older and younger than 65 years. OUTCOMES: Recovery of kidney function defined as independence from dialysis therapy, decrease in serum creatinine level to less than a defined threshold, or return to baseline kidney function. RESULTS: We obtained data for recovery of kidney function by age from 17 studies of patients with AKI. Overall, 31.3% of surviving elderly patients did not recover kidney function compared with 26% of younger patients (pooled relative risk, 1.28, 95% confidence interval, 1.06 to 1.55; P < 0.05). The increased risk of nonrecovery in the elderly remained greater in several subgroups examined through sensitivity analyses, including those stratified by type of dialysis support, time of assessment of recovery (short versus long term), and definition of renal recovery. LIMITATIONS: There was significant heterogeneity among studies with respect to comorbid factors, definition of AKI, and study design. CONCLUSIONS: There is impaired recovery of kidney function after AKI in aged individuals. Future studies should be cognizant of 'age' as a potential effect modifier in the prognosis after AKI, and clinical trials should focus on improving outcomes in the elderly cohort. Copyright © 2008 National Kidney Foundation, Inc. [ABSTRACT FROM AUTHOR]

The diagnosis of acute kidney injury (AKI) is usually based on changes in serum creatinine, but such measurements are a poor marker of acute deterioration in kidney function. We performed a systematic review of publications that evaluated the accuracy and reliability of serum and urinary biomarkers in human subjects when used for the diagnosis of established AKI or early AKI, or to risk stratify patients with AKI. Two reviewers independently searched the MEDLINE and EMBASE databases (January 2000–March 2007) for studies pertaining to biomarkers for AKI. Studies were assessed for methodologic quality. In total, 31 studies evaluated 21 unique serum and urine biomarkers. Twenty-five of the 31 studies were scored as having ‘good’ quality. The results of the studies indicated that serum cystatin C, urine interleukin-18 (IL-18), and urine kidney injury molecule-1 (KIM-1) performed best for the differential diagnosis of established AKI. Serum cystatin C and urine neutrophil gelatinase-associated lipocalin, IL-18, glutathione-S-transferase-π, and γ-glutathione-S-transferase performed best for early diagnosis of AKI. Urine N-acetyl-β-D-glucosaminidase, KIM-1, and IL-18 performed the best for mortality risk prediction after AKI. In conclusion, published data from studies of serum and urinary biomarkers suggest that biomarkers may have great potential to advance the fields of nephrology and critical care. These biomarkers need validation in larger studies, and the generalizability of biomarkers to different types of AKI as well as the incremental prognostic value over traditional clinical variables needs to be determined.Kidney International (2008) 73, 1008–1016; doi:10.1038/sj.ki.5002729; published online 19 December 2007 [ABSTRACT FROM AUTHOR]

Summary ¶Background. Cell apoptosis in solid tumours has been related to immunological attack by NK-cells. The purpose of the present study is to verify in the tissue of brain metastases a possible relationship among the degree of NK-cell infiltration and the number of apoptotic tumour cells. Methods. Twenty brain metastases whose tumour cells expressed CD95 (Fas/APO1) have been studied. NK-cells were identified by using the monoclonal antibody to CD57, and apoptotic tumour cells by means of the immunostain with the anti-ssDNA monoclonal antibody F7-26. The Spearman rank correlation test was used to study the relationship between the degree of CD57-NK-cell infiltration and the apoptosis labelling-index. Findings. Positivity to F7-26 was present in all tumour samples, but the number of immunostained cells showed a wide variability, with a mean apoptosis labelling-index of 11.48%. All the studied tumours showed CD57 immunostained cells, with a number that ranged between 4 and 20 per microscopical field at 200× (mean±standard deviation: 8.4±3.7). Statistical studies showed that there was no correlation between the number of CD57 immunostained NK-cells and the apoptosis labelling-index (p>0.05). Interpretation. These findings suggest that in brain metastases, apoptosis related to immune r esponse is mainly mediated by activated tumour-infiltrating mononuclear cells other than CD57+ NK-cells. [ABSTRACT FROM AUTHOR]