Background In 2004, researchers reported that the number of nephrology clinical trials was low and that the reporting quality of such trials was suboptimal. Furthermore, the number or quality of preclinical kidney-related studies has not been systematically evaluated. Methods We performed a systematic review of randomized clinical trials published in 1966-2017 (listed in the Cochrane Library) and preclinical studies published in 1945-2017 (listed in PubMed). For reporting quality analysis, we evaluated the final main paper of 118 clinical trial reports and 135 preclinical studies published in leading journals in 1996, 2006, and 2016 on the basis of criteria from the widely used CONSORT and ARRIVE guidelines. Results The annual number of reports of clinical kidney-related trials more than doubled between 2004 and 2014 along with reports in other medical disciplines. Hypertension remains the dominant focus of study, but ongoing trials also center on CKD, ESRD, and AKI. The reporting quality analysis revealed improvements, but deficits in reporting of clinical trial design, mode of randomization, and intention-totreat analysis remain. Annual numbers of kidney-related preclinical studies remained low between 1945 and 2017 compared with other disciplines. Reporting quality analysis of preclinical studies revealed substantial reporting deficits across all leading journals, with little improvement over the last 20 years, especially for group size calculations, defining primary versus secondary outcomes, and blinded analysis. Conclusions Nephrology studies keep increasing in number but still lag behind other medical disciplines, and the quality of data reporting in kidney research can be further improved.

Renal and immune systems maintain body homoeostasis during physiological fluctuations and following tissue injury. The immune system plays a central role during acute kidney injury (AKI), adapting evolutional systems programmed for host defence and minimizing unnecessary collateral damage. Indeed, depending upon the disease context, the impact of the immune system upon the manifestations and consequences of AKI can be quite different. Here we provide an overview of the known and unknown involvement of the immune system within the wide range of different forms of AKI, to oppose oversimplification and to endorse deeper insights into the pathogenesis of the different diseases causing kidney injury. This approach may help to overcome some of the current hurdles in translational AKI research and the development of specific treatments for the different diseases, all presenting with an acute increase in serum creatinine or decline in urinary output. One concept does not fit all.