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Kidney disease is a worldwide threat to public health and has a risk-multiplier effect on major non-communicable diseases, including cardiovascular diseases. More than 322 million individuals are currently affected by chronic kidney disease (CKD) worldwide, and the number of patients with end-stage kidney disease (ESKD) treated with renal replacement therapy with dialysis or transplantation globally exceeds 2.6 million people. In the past 20 years, age-standardized death rate from CKD increased by 15% whereas rates for other non-communicable disease declined, including major vascular diseases, pulmonary disorders, most forms of cancer and liver cirrhosis. Independent of the initial insult, the progression to ESKD is relatively common in chronic nephropathies.
Huge numbers of experimental studies and pivotal clinical trials in the nephrology areas efficiently demonstrated the renoprotective effects of treatment with renin-angiotensin system inhibitors in patients with diabetic and non-diabetic proteinuric nephropathies. However, a significant cohort of patients treated with renin-angiotensin system blockers shows only partial response, eventually heralding a progressive loss of renal function in most cases. Also, primary immune diseases of the kidney require a paradigm shift in their current non-specific and toxic immunosuppressive regimes toward more pathophysiological rationale for interventions that specifically target B-cell lineages to prevent antibody production. Moreover, despite renal transplantation being the renal replacement modality of choice for suitable candidates with ESKD, unfortunately it remains plagued by the need for immunosuppressants that are associated with numerous toxicites, including nephrotoxicities. Even long-surviving grafts are haunted by the specter of chronic allograft nephropathy. Reducing morbidity and mortality in transplantation requires novel approaches to reduce the burden of pharmacologic immunosuppression. Efforts to dissect in more depth the mechanisms and mediators underling disease progression in nephropathies as well as loss of kidney graft function in the long-term are of the utmost importance to help designing novel medications and tools for further improving the efficacy of current renoprotective interventions.
This implies, however, to concieve and explore innovative therapeutic strategies which take into account individual variability in genetic and other molecular measurements, environmental exposures, and lifestyle. The development and availability of genetic and other molecular profiling technologies provide an unprecedented opportunity to apply this precision medicine in nephrology research for diseases with unmet needs.
Thus, Renal Pharmacology, a specialty section of Frontiers in Pharmacology, is willing to consider high quality experimental and clinical articles of evidence-based studies on genetic and cell-based pharmacology for acute and chronic renal disease as well as kidney transplantation. The focus will be, but not limited to, i) silencing of protein coding genes by the help of small interfering RNAs (siRNAs) or antisense oligonucleotides and advancing their delivery systems vivo, ii) gene editing of animal models and human DNA defects getting rid of mutations that cause renal disease by the use of CRISPR/Cas9 technology, iii) safety and pharmacodynamics of novel cell-based therapies for immune modulation and tissue regeneration processes, iv) safety and pharmacodynamics of innovative biologics including IgG-endopeptidase to unhinge pathogenic antibodies, and v) molecular epigenetic targets for histone modifications and abnormal changes in the genomic architecture.
Overall the areas covered by Renal Pharmacology are expected to be those that would allow medical breakthroughs to arrive at a meaningful, innovative, pharmacological solution to tackle the present day scenario of renal diseases and kidney transplantation.
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