– This PowerPack requires Agentil SAP ProMonitor or later. It requires ProMonitor SAP Connector to be installed on all collectors configured with ProMonitor Plugin.
– When installing the PowerPack for the first time or after any database schema changes, the post_ script will need to be run on all collectors monitoring SAP. The post_ script can be found in the content library on the collector under the directory: /var/lib/em7/content/agentil.
– EM7 collector upgrades may override database changes made by Agentil SAP ProMonitor . In these cases, the post_ script will need to be re-run after an EM7 upgrade. The post_ script can be found in the content library on the collector under the directory: /var/lib/em7/content/agentil.
It has been known since 1980s that an increase in phosphate excretion per nephron induces renal tubular damage and interstitial fibrosis in rats [ 27 ]. Haut et al. [ 27 ] manipulated phosphate excretion per nephron by placing partially nephrectomized rats on a diet containing different amounts of phosphate for 18 weeks and then scored the histological kidney damage. Their conclusion was that the severity of renal tubular damage and interstitial fibrosis was positively correlated with phosphate excretion per nephron. A plausible mechanism was that an increase in phosphate excretion per nephron could increase the phosphate concentration of the renal tubular fluid, which likely exceeded the solubility limit and triggered precipitation of calcium–phosphate (CaPi) in the lumen [ 28 ]. CaPi nanocrystals were reported to induce cellular damage when applied to cultured renal proximal tubular cells through a mechanism yet to be identified [ 29 ]. Persistent CaPi-induced renal tubular damage can result in interstitial fibrosis and eventually decrease the nephron number, which may further increase phosphate excretion per nephron and thus promote CaPi precipitation unless phosphate intake is reduced, thereby triggering a vicious cycle leading to progressive nephron loss. This hypothetical mechanism is supported by the fact that the kidney damage induced by a high-phosphate diet in rats was alleviated by administration of bisphosphonate, which can prevent formation of CaPi crystals [ 27 ]. Although the FGF23–αKlotho endocrine axis had not been discovered at that time, if FGF23 had been measured in this study, FGF23 would have been positively correlated with the histological kidney damage. Provided that the FGF23 increase in CKD patients is a sign of excess phosphate intake relative to the residual nephron number, it can be a reason for phosphate restriction, even when serum phosphate levels are within normal range. The FGF23 increase may also be regarded as a risk for renal tubular damage and interstitial fibrosis [ 30 ]. This notion needs to be verified in future clinical studies.