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Dive into the research topics where Sunil V. Badve is active.

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Featured researches published by Sunil V. Badve.


Nephrology Dialysis Transplantation | 2014

Effects of uric acid-lowering therapy on renal outcomes: a systematic review and meta-analysis.

Bhadran Bose; Sunil V. Badve; Swapnil Hiremath; Neil Boudville; Fiona G. Brown; Alan Cass; Janak de Zoysa; Robert G. Fassett; Randall Faull; David C.H. Harris; Carmel M. Hawley; John Kanellis; Suetonia C. Palmer; Vlado Perkovic; Elaine M. Pascoe; Gopala K. Rangan; Robert J. Walker; Giles Walters; David W. Johnson

BACKGROUND Non-randomized studies suggest an association between serum uric acid levels and progression of chronic kidney disease (CKD). The aim of this systematic review is to summarize evidence from randomized controlled trials (RCTs) concerning the benefits and risks of uric acid-lowering therapy on renal outcomes. METHODS Medline, Excerpta Medical Database and Cochrane Central Register of Controlled Trials were searched with English language restriction for RCTs comparing the effect of uric acid-lowering therapy with placebo/no treatment on renal outcomes. Treatment effects were summarized using random-effects meta-analysis. RESULTS Eight trials (476 participants) evaluating allopurinol treatment were eligible for inclusion. There was substantial heterogeneity in baseline kidney function, cause of CKD and duration of follow-up across these studies. In five trials, there was no significant difference in change in glomerular filtration rate from baseline between the allopurinol and control arms [mean difference (MD) 3.1 mL/min/1.73 m2, 95% confidence intervals (CI) -0.9, 7.1; heterogeneity χ2=1.9, I2=0%, P=0.75]. In three trials, allopurinol treatment abrogated increases in serum creatinine from baseline (MD -0.4 mg/dL, 95% CI -0.8, -0.0 mg/dL; heterogeneity χ2=3, I2=34%, P=0.22). Allopurinol had no effect on proteinuria and blood pressure. Data for effects of allopurinol therapy on progression to end-stage kidney disease and death were scant. Allopurinol had uncertain effects on the risks of adverse events. CONCLUSIONS Uric acid-lowering therapy with allopurinol may retard the progression of CKD. However, adequately powered randomized trials are required to evaluate the benefits and risks of uric acid-lowering therapy in CKD.


Journal of the American College of Cardiology | 2011

Effects of beta-adrenergic antagonists in patients with chronic kidney disease: A systematic review and meta-analysis

Sunil V. Badve; Matthew A. Roberts; Carmel M. Hawley; Alan Cass; Amit X. Garg; Henry Krum; Andrew Tonkin; Vlado Perkovic

OBJECTIVES The aim of this systematic review was to study the benefits and risks of beta-adrenergic antagonists (beta-blockers) in patients with chronic kidney disease (CKD). BACKGROUND There is an excess burden of cardiovascular disease and death in people with CKD. Despite their potential benefits, the effects of beta-blockers in this population are uncertain. METHODS CENTRAL (Cochrane Central Register of Controlled Trials), Medline (Medical Literature Analysis and Retrieval System Online), and Embase (Excerpta Medical Database) were searched for randomized controlled trials with at least 3 months of follow-up in patients with CKD stages 3 to 5 that reported mortality outcomes. Summary estimates of effect were obtained using a random effects model. RESULTS Eight trials met criteria for review: 6 placebo-controlled trials involving 5,972 participants with chronic systolic heart failure and 2 angiotensin-converting enzyme inhibitor-comparator trials involving 977 participants not known to have heart failure. In CKD patients with heart failure, compared with placebo, beta-blocker treatment reduced the risk of all-cause (risk ratio [RR]: 0.72, 95% confidence interval [CI]: 0.64 to 0.80) and cardiovascular mortality (RR: 0.66, 95% CI: 0.49 to 0.89), but increased the risk of bradycardia (RR: 4.92, 95% CI: 3.20 to 7.55) and hypotension (RR: 5.08, 95% CI: 3.48 to 7.41). Quantitative meta-analysis was not performed for the non-heart failure studies due to substantial clinical diversity or lack of informative data. CONCLUSIONS Treatment with beta-blockers improved all-cause mortality in patients with CKD and chronic systolic heart failure. There is insufficient evidence to conclude whether people with CKD who are not known to have heart failure derive benefit from beta-blockers.


Journal of Clinical Pathology | 2009

Oestrogen-receptor-positive breast cancer: towards bridging histopathological and molecular classifications

Sunil V. Badve; Harikrishna Nakshatri

The oestrogen receptor (ER) pathway is key for survival and progression in a significant proportion of breast cancers. The ER can be activated by oestrogen or activated due to “crosstalk” with growth factor receptor pathways. Activated ER signals through transcriptional and non-transcriptional mechanisms. Immunohistochemistry (IHC), in spite of the shortcomings, remains the method of choice as it provides for in situ assessment of ER expression within the tumour cells. This capability is lost in tissue grinding methods that assess oestrogen-binding activity or messenger RNAs in tumours. IHC is also not influenced by the presence of non-tumoural cells or low amounts of tumour cells within samples examined. It is clear that ER-positive tumours do not represent a single entity. Irrespective of the terminology used, low-grade ER-positive (also known as luminal A) tumours need to be differentiated from high-grade/highly proliferative ER-positive tumours. This can be done in a variety of ways including but not limited to analysis of FOXA1 and GATA-3 by IHC, and limited molecular profiling by Oncotype DX, MGH2-gene signature, intrinsic gene signature or MapQuant Dx. Several areas of ER biology are still poorly understood; these include: its function in the cytoplasm/plasma membrane, its role in the differentiation to proliferation switch, and pathways associated with resistance to hormonal therapy. A detailed understanding of these areas will permit better classification and a personalised approach to management of ER-positive breast cancers.


Proceedings of the National Academy of Sciences of the United States of America | 2006

A cancer-associated PCNA expressed in breast cancer has implications as a potential biomarker

Linda H. Malkas; Brittney Shea Herbert; Waleed Abdel-Aziz; Lacey E. Dobrolecki; Yang Liu; Beamon Agarwal; Derek J. Hoelz; Sunil V. Badve; Lauren Schnaper; Randy J. Arnold; Yehia Mechref; Milos V. Novotny; Patrick J. Loehrer; Robert J. Goulet; Robert J. Hickey

Two isoforms of proliferating cell nuclear antigen (PCNA) have been observed in breast cancer cells. Commercially available antibodies to PCNA recognize both isoforms and, therefore, cannot differentiate between the PCNA isoforms in malignant and nonmalignant breast epithelial cells and tissues. We have developed a unique antibody that specifically detects a PCNA isoform (caPCNA) associated with breast cancer epithelial cells grown in culture and breast-tumor tissues. Immunostaining studies using this antibody suggest that the caPCNA isoform may be useful as a marker of breast cancer and that the caPCNA-specific antibody could potentially serve as a highly effective detector of malignancy. We also report here that the caPCNA isoform functions in breast cancer-cell DNA replication and interacts with DNA polymerase δ. Our studies indicate that the caPCNA isoform may be a previously uncharacterized detector of breast cancer.


Molecular and Cellular Biology | 2008

AKT Alters Genome-Wide Estrogen Receptor α Binding and Impacts Estrogen Signaling in Breast Cancer

Poornima Bhat-Nakshatri; Guohua Wang; Hitesh Appaiah; Nikhil Luktuke; Jason S. Carroll; Tim R. Geistlinger; Myles Brown; Sunil V. Badve; Yunlong Liu; Harikrishna Nakshatri

ABSTRACT Estrogen regulates several biological processes through estrogen receptor α (ERα) and ERβ. ERα-estrogen signaling is additionally controlled by extracellular signal activated kinases such as AKT. In this study, we analyzed the effect of AKT on genome-wide ERα binding in MCF-7 breast cancer cells. Parental and AKT-overexpressing cells displayed 4,349 and 4,359 ERα binding sites, respectively, with ∼60% overlap. In both cell types, ∼40% of estrogen-regulated genes associate with ERα binding sites; a similar percentage of estrogen-regulated genes are differentially expressed in two cell types. Based on pathway analysis, these differentially estrogen-regulated genes are linked to transforming growth factor β (TGF-β), NF-κB, and E2F pathways. Consistent with this, the two cell types responded differently to TGF-β treatment: parental cells, but not AKT-overexpressing cells, required estrogen to overcome growth inhibition. Combining the ERα DNA-binding pattern with gene expression data from primary tumors revealed specific effects of AKT on ERα binding and estrogen-regulated expression of genes that define prognostic subgroups and tamoxifen sensitivity of ERα-positive breast cancer. These results suggest a unique role of AKT in modulating estrogen signaling in ERα-positive breast cancers and highlights how extracellular signal activated kinases can change the landscape of transcription factor binding to the genome.


Modern Pathology | 2011

Atypical ductal hyperplasia: interobserver and intraobserver variability

Rohit K. Jain; Rutika Mehta; Rosen K. Dimitrov; Lisbeth G Larsson; Paul M Musto; Kurt B. Hodges; Thomas M. Ulbright; Eyas M. Hattab; Narasimhan P. Agaram; Muhammad T. Idrees; Sunil V. Badve

Interobserver reproducibility in the diagnosis of benign intraductal proliferative lesions has been poor. The aims of the study were to investigate the inter- and intraobserver variability and the impact of the addition of an immunostain for high- and low-molecular weight keratins on the variability. Nine pathologists reviewed 81 cases of breast proliferative lesions in three stages and assigned each of the lesions to one of the following three diagnoses: usual ductal hyperplasia, atypical ductal hyperplasia and ductal carcinoma in situ. Hematoxylin and eosin slides and corresponding slides stained with ADH-5 cocktail (cytokeratins (CK) 5, 14. 7, 18 and p63) by immunohistochemistry were evaluated. Concordance was evaluated at each stage of the study. The interobserver agreement among the nine pathologists for diagnosing the 81 proliferative breast lesions was fair (κ-value=0.34). The intraobserver κ-value ranged from 0.56 to 0.88 (moderate to strong). Complete agreement among nine pathologists was achieved in only nine (11%) cases, at least eight agreed in 20 (25%) cases and seven or more agreed in 38 (47%) cases. Following immunohistochemical stain, a significant improvement in the interobserver concordance (overall κ-value=0.50) was observed (P=0.015). There was a significant reduction in the total number of atypical ductal hyperplasia diagnosis made by nine pathologists after the use of ADH-5 immunostain. Atypical ductal hyperplasia still remains a diagnostic dilemma with wide variation in both inter- and intraobserver reproducibility among pathologists. The addition of an immunohistochemical stain led to a significant improvement in the concordance rate. More importantly, there was an 8% decrease in the number of lesions classified as atypical ductal hyperplasia in favor of usual hyperplasia; in clinical practice, this could lead to a decrease in the number of surgeries carried out for intraductal proliferative lesions.


Journal of The American Society of Nephrology | 2012

Recent Peritonitis Associates with Mortality among Patients Treated with Peritoneal Dialysis

Neil Boudville; Anna Kemp; Philip A. Clayton; Wai H. Lim; Sunil V. Badve; Carmel M. Hawley; Stephen P. McDonald; Kathryn J. Wiggins; Kym M. Bannister; Fiona G. Brown; David W. Johnson

Peritonitis is a major complication of peritoneal dialysis, but the relationship between peritonitis and mortality among these patients is not well understood. In this case-crossover study, we included the 1316 patients who received peritoneal dialysis in Australia and New Zealand from May 2004 through December 2009 and either died on peritoneal dialysis or within 30 days of transfer to hemodialysis. Each patient served as his or her own control. The mean age was 70 years, and the mean time receiving peritoneal dialysis was 3 years. In total, there were 1446 reported episodes of peritonitis with 27% of patients having ≥ 2 episodes. Compared with the rest of the year, there were significantly increased odds of peritonitis during the 120 days before death, although the magnitude of this association was much greater during the 30 days before death. Compared with a 30-day window 6 months before death, the odds for peritonitis was six-fold higher during the 30 days immediately before death (odds ratio, 6.2; 95% confidence interval, 4.4-8.7). In conclusion, peritonitis significantly associates with mortality in peritoneal dialysis patients. The increased odds extend up to 120 days after an episode of peritonitis but the magnitude is greater during the initial 30 days.


Journal of the American College of Cardiology | 2011

Clinical ResearchCardiovascular PharmacologyEffects of Beta-Adrenergic Antagonists in Patients With Chronic Kidney Disease: A Systematic Review and Meta-Analysis

Sunil V. Badve; Matthew A. Roberts; Carmel M. Hawley; Alan Cass; Amit X. Garg; Henry Krum; Andrew Tonkin; Vlado Perkovic

OBJECTIVES The aim of this systematic review was to study the benefits and risks of beta-adrenergic antagonists (beta-blockers) in patients with chronic kidney disease (CKD). BACKGROUND There is an excess burden of cardiovascular disease and death in people with CKD. Despite their potential benefits, the effects of beta-blockers in this population are uncertain. METHODS CENTRAL (Cochrane Central Register of Controlled Trials), Medline (Medical Literature Analysis and Retrieval System Online), and Embase (Excerpta Medical Database) were searched for randomized controlled trials with at least 3 months of follow-up in patients with CKD stages 3 to 5 that reported mortality outcomes. Summary estimates of effect were obtained using a random effects model. RESULTS Eight trials met criteria for review: 6 placebo-controlled trials involving 5,972 participants with chronic systolic heart failure and 2 angiotensin-converting enzyme inhibitor-comparator trials involving 977 participants not known to have heart failure. In CKD patients with heart failure, compared with placebo, beta-blocker treatment reduced the risk of all-cause (risk ratio [RR]: 0.72, 95% confidence interval [CI]: 0.64 to 0.80) and cardiovascular mortality (RR: 0.66, 95% CI: 0.49 to 0.89), but increased the risk of bradycardia (RR: 4.92, 95% CI: 3.20 to 7.55) and hypotension (RR: 5.08, 95% CI: 3.48 to 7.41). Quantitative meta-analysis was not performed for the non-heart failure studies due to substantial clinical diversity or lack of informative data. CONCLUSIONS Treatment with beta-blockers improved all-cause mortality in patients with CKD and chronic systolic heart failure. There is insufficient evidence to conclude whether people with CKD who are not known to have heart failure derive benefit from beta-blockers.


Kidney International | 2013

The impact of neutral-pH peritoneal dialysates with reduced glucose degradation products on clinical outcomes in peritoneal dialysis patients

Yeoungjee Cho; David W. Johnson; Sunil V. Badve; Jonathan C. Craig; Giovanni F.M. Strippoli; Kathryn J. Wiggins

Neutral-pH peritoneal dialysates, with reduced glucose degradation products (GDPs), have been developed to reduce peritoneal membrane damage. Here our review evaluated the impact of these solutions on clinical outcomes using data from The Cochrane CENTRAL Registry, MEDLINE, Embase, and reference lists for randomized trials of biocompatible solutions. Summary estimates of effect were obtained using a random-effects model of 20 eligible trials encompassing 1383 patients. The quality of studies was generally poor, such that 13 studies had greater than a 20% loss to follow-up and only 3 trials reported adequate concealment of allocation. Use of neutral-pH dialysates with reduced GDPs resulted in larger urine volumes (7 trials; 520 patients; mean difference 126 ml/day, 95% CI 27-226), improved residual renal function after 12 months (6 trials; 360 patients; standardized mean difference 0.31, 95% confidence interval 0.10-0.52), and a trend to reduced inflow pain (1 trial; 58 patients; relative risk 0.51, 95% CI 0.24-1.08). However, there was no significant effect on body weight, hospitalization, peritoneal solute transport rate, peritoneal small-solute clearance, peritonitis, technique failure, patient survival, or adverse events. No significant harms were identified. Thus, based on generally poor quality trials, the use of neutral-pH peritoneal dialysates with reduced GDPs resulted in greater urine volumes and residual renal function after 12 months, but without other clinical benefits. Larger, better-quality studies are needed for accurate evaluation of the impact of these newer dialysates on patient-level hard outcomes.


Nephrology Dialysis Transplantation | 2013

Impact of icodextrin on clinical outcomes in peritoneal dialysis: a systematic review of randomized controlled trials

Yeoungjee Cho; David W. Johnson; Sunil V. Badve; Jonathan C. Craig; Giovanni Fm Strippoli; Kathryn J. Wiggins

BACKGROUND Although icodextrin has been shown to augment peritoneal ultrafiltration in peritoneal dialysis (PD) patients, its impact upon other clinical end points, such as technique survival, remains uncertain. This systematic review evaluated the effect of icodextrin use on patient level clinical outcomes. METHODS The Cochrane CENTRAL Registry, MEDLINE, Embase and reference lists were searched (last search 13 September 2012) for randomized controlled trials of icodextrin versus glucose in the long dwell exchange. Summary estimates of effect were obtained using a random effects model. RESULTS Eleven eligible trials (1222 patients) were identified. There was a significant reduction in episodes of uncontrolled fluid overload [two trials; 100 patients; relative risk (RR) 0.30, 95% confidence interval (CI) 0.15-0.59] and improvement in peritoneal ultrafiltration [four trials; 102 patients; mean difference (MD) 448.54 mL/day, 95% CI 289.28-607.80] without compromising residual renal function [four trials; 114 patients; standardized MD (SMD) 0.12, 95% CI -0.26 to 0.49] or urine output (three trials; 69 patients; MD -88.88, 95% CI -356.88 to 179.12) with icodextrin use for up to 2 years. There was no significant effect on peritonitis incidence (five trials; 607 patients; RR 0.97, 95% CI 0.76-1.23), peritoneal creatinine clearance (three trials; 237 patients; SMD 0.36, 95% CI -0.24 to 0.96), technique failure (three trials; 290 patients; RR 0.58, 95% CI 0.28-1.20), patient survival (six trials; 816 patients; RR 0.82, 95% CI 0.32-2.13) or adverse events. CONCLUSIONS Icodextrin prescription improved peritoneal ultrafiltration, mitigated uncontrolled fluid overload and was not associated with increased risk of adverse events. No effects of icodextrin on technique or patient survival were observed, although trial sample sizes and follow-up durations were limited.

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David W. Johnson

Princess Alexandra Hospital

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Neil Boudville

University of Western Australia

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Alan Cass

Charles Darwin University

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Yeoungjee Cho

Princess Alexandra Hospital

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