Reply from the Authors

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Overview of Complement Activation and Regulation

SummaryComplement is an important component of the innate immune system that is crucial for defense from microbial infections and for clearance of immune complexes and injured cells. In normal conditions complement is tightly controlled by a number of fluid-phase and cell surface proteins to avoid injury to autologous tissues. When complement is hyperactivated, as occurs in autoimmune diseases or in subjects with dysfunctional regulatory proteins, it drives a severe inflammatory response in numerous organs. The kidney appears to be particularly vulnerable to complement-mediated inflammatory injury. Injury may derive from deposition of circulating active complement fragments in glomeruli, but complement locally produced and activated in the kidney also may have a role. Many kidney disorders have been linked to abnormal complement activation, including immune-complex–mediated glomerulonephritis and rare genetic kidney diseases, but also tubulointerstitial injury associated with progressive proteinuric diseases or ischemia-reperfusion

Medicine and art: one culture?

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Renoprotection: Clues from knockout models of rare diseases

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Acute Kidney Injury in Poor Countries Should No Longer Be a Death Sentence: The ISN '0 by 25' Project.

Acute kidney injury (AKI) is a common disorder throughout the world that is associated with severe morbidity, mortality and cost. Although deaths due to AKI occur in both high- and low- and middle-income countries (LMIC), the majority of avoidable deaths occur in LMIC nations. If managed adequately and in a timely fashion, the majority of these cases of AKI are preventable, treatable and often reversible with simple measures. AKI also has a major economic impact on healthcare expenditure. This is particularly true in poor countries where AKI especially impacts young productive people, imposing severe penury on their families. The International Society of Nephrology (ISN) has launched a long-term program, the '0 by 25' project, which advocates that zero people should die of untreated AKI in the poorest part of Africa, Asia and Latin America by 2025. The mission is to eventually lessen the high burden in terms of deaths consequent to this disorder in resource-poor regions worldwide. This is a challenging but potentially feasible and productive initiative that requires a broad vision about how the public and private sectors can work in partnership with the governments of the LMIC countries and leading nongovernmental organizations operating locally, to ensure sustainability of the 0 by 25 program and save many lives

Acute kidney injury in low-income and middle-income countries: no longer a death sentence

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CD133+ renal stem cells always co-express CD24 in adult human kidney tissue

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Effect of inborn pancreatic islet deficit in the Munich Wister Frömter rat

The total mass of pancreatic islet cells is a critical factor in glucose metabolic control. The aim of the present study was to investigate whether in the Munich Wistar Frömter (MWF) rat, beside a reduction in the number of nephrons, there are also alterations in the number of pancreatic islets and of β cell mass. We also examined glucose metabolism, both in normal conditions and following intravenous glucose injection. The number of islets per pancreas, estimated by morphometrical analysis, was significantly lower in MWF rats than in Wistar rats (3,501±1,285 vs. 7,259±2,330 islet/rat, respectively). Also the mean number of islets per gram of body weight was significantly lower in MWF rats than in Wistar rats (18±7 in MWF rats vs. 28±10 islets/g bw in Wistar rats). Morphometric analysis of β cell mass showed an average of 77.1±7% islet cells staining for insulin in MWF rats and 83.9±2.1% in the control Wistar rats. Despite the lower number of islets and β cells, MWF and Wistar rats had comparable fasting blood glucose levels but significant differences in blood glucose following an intraperitoneal glucose tolerance test. In summary, pancreatic islets of MWF and Wistar rats showed a marked difference in morphometrical characteristics. While this difference is not associated with blood glucose levels, glucose metabolism after IPGTT between MWF and Wistar rats is significantly different. These data suggest that an inborn deficit in β cell mass of about 60% is responsible for altered glucose metabolism and could favor the development of diabetes