A finger systolic blood pressure (FSBP) cooling test was introduced in 1977 and standardized during the following years for the optimal provocation and best characterization of an attack of vasospastic Raynaud's phenomenon (RP). The purpose of the present review is to compare and analyse some different techniques used in FSBP cooling tests from different countries and described in the final draft of the international standard, ISO/DIS 14835-2 (2004). The selected FSBP test results indicate to some extent that the tests are reliable and have acceptable diagnostic values despite the use of different techniques to obtain them. However, only a few studies used a zero-pressure FSBP%(0) to verify an ongoing attack of vasospastic RP. Most studies used an abnormal cold reaction FSBP%(A) located below the lower limit of controls, to make the anamnestic diagnosis of RP probable. According to the ISO draft, different types of finger cooling and body thermostating can be used together in the seated or supine position, and FSBP%(A) is indicated to be used for diagnostic purposes. Further studies are recommended to solve future standardization problems not included in the upcoming ISO standard. An international agreement on the presentation and comparison of test results is needed as a supplement to ISO/DIS 14835-2.

Kidneys are sensitive to disturbances in oxygen homeostasis. Hypoxia and activation of the hypoxia-inducible factor (HIF) pathway alter the expression of genes involved in the metabolism of renal and immune cells, interfering with their functioning. Whether the transcriptional activity of HIF protects the kidneys or participates in the pathogenesis of renal diseases is unclear. Several studies have indicated that HIF signaling promotes fibrosis in experimental models of kidney disease. Other reports showed a protective effect of HIF activation on kidney inflammation and injury. In addition to the direct effect of HIF on the kidneys, experimental evidence indicates that HIF-mediated metabolic shift activates inflammatory cells, supporting the HIF cascade as a link between lung or gut damage and worsening of renal disease. Although hypoxia and HIF activation are present in several scenarios of renal diseases, further investigations are needed to clarify whether interfering with the HIF pathway is beneficial in different pathological contexts.