As the organ shortage increases, inherently the demand for donor kidneys continues to rise. Thus, live kidney donation is essential for increasing the donor pool. In order to create successful expansion, extended criteria live kidney donors should be considered. This review combines current guidelines with all available literature in this field, trying to seek and establish the optimal extended criteria. Comprehensive searches were carried out in major databases until November 2013 to search for articles regarding older age, overweight and obesity, hypertension, vascular anomalies/multiplicity, nulliparous women, and minors as donors. Of the 2079 articles found, 152 fell within the scope of the review. Five major guidelines were included and reviewed. Based on the literature search, live kidney donation in older donors (up to 70 years of age) seems to be safe as outcome is comparable to younger donors. Obese donors have comparable outcome to lean donors, in short- and mid-term follow-up. Since little literature is available proving the safety of donation of hypertensive donors, caution is advised. Vascular multiplicity poses no direct danger to the donor and women of childbearing age can be safely included as donors. Although outcome after donation in minors is shown to be comparable to adult donors, they should only be considered if no other options exist. We conclude that the analyzed factors above should not be considered as absolute contraindications for donation.

BackgroundSUMOylation involves the attachment of small ubiquitin-like modifier (SUMO) proteins to specific lysine residues on thousands of substrates with target-specific effects on protein function. Sentrin-specific proteases (SENPs) are proteins involved in the maturation and deconjugation of SUMO. Specifically, SENP7 is responsible for processing polySUMO chains on targeted substrates including the heterochromatin protein 1α (HP1α).MethodsWe performed exome sequencing and segregation studies in a family with several infants presenting with an unidentified syndrome. RNA and protein expression studies were performed in fibroblasts available from one subject.ResultsWe identified a kindred with four affected subjects presenting with a spectrum of findings including congenital arthrogryposis, no achievement of developmental milestones, early respiratory failure, neutropenia and recurrent infections. All died within four months after birth. Exome sequencing identified a homozygous stop gain variant inSENP7c.1474C>T; p.(Gln492*) as the probable aetiology. The proband’s fibroblasts demonstrated decreased mRNA expression. Protein expression studies showed significant protein dysregulation in total cell lysates and in the chromatin fraction. We found that HP1α levels as well as different histones and H3K9me3 were reduced in patient fibroblasts. These results support previous studies showing interaction between SENP7 and HP1α, and suggest loss of SENP7 leads to reduced heterochromatin condensation and subsequent aberrant gene expression.ConclusionOur results suggest a critical role for SENP7 in nervous system development, haematopoiesis and immune function in humans.