A mutation, c.1370A > T was found in exon 8 in family 4, which caused a glutamate substitution for valine at nucleotide 457 (E457V) in the tail domain. Analysis of nucleotide sequences of the desmin gene in family 5 revealed a c.1064G > C mutation in exon 5. This mutation resulted in a replacement of arginine with proline (R355P) in the helix 2B domain. In sporadic case 1, a c.338–339delA_G deletion mutation was identified in exon 1. This mutation caused a truncated protein at codon 115 (Q113fsX115) in the helix 1A domain. In sporadic case 2, a c.1333A > G

mutation in exon 8 resulted in a replacement BMS-777607 of threonine with alanine (T445A) in the tail domain. The affected members from different families had the same mutation as the respective Paclitaxel chemical structure index case, but these mutations did not appear in unaffected family members and in 100 control samples. The analysis provides strong evidence that the above described mutations are responsible for the disease and not a coincidental polymorphism. First, we confirmed that a vector containing wild-type desmin produced functional desmin protein capable of building a cytoplasmic network in C2C12 (Figure 5A) and SW13 (Figure 5B) cells. Then we investigated the ability of these disease-associated mutations

(S12F, L274P, L274R, R355P, T445A, E457V and Q113fsX115) to form extended filamentous networks in C2C12 and SW13 cells. Immunofluorescence analysis of the SW13 cells transfected with mutant vectors showed completely disorganized coarse aggregates and clumps scattered throughout the cytoplasm (Figure 5D,F,H,J,L,P). The C2C12 cells transfected with

mutant desmin revealed a disturbed endogenous intermediate filament structure and multiple desmin-positive clumps or abnormal solid large aggregates (Figure 5C,E,G,I,K,O). However, the E457V mutant in the tail domain did not form a cytoplasmic network like the wild-type desmin in the C2C12 and SW13 cells, but it did not cause obvious desmin aggregation (Figure 5M,N). We have identified five novel mis-sense mutations and one novel deletion mutation distributed along the desmin gene in five unrelated Chinese families and two sporadic cases with cardiac and skeletal myopathy. Prominent cardiac disorders were the major clinical characteristics in this cohort these of patients and other reported Asian patients [20–22]. The prevalence was more than 95% in our patients, but only 60% [3] to 70% [12] in Caucasian patients. Although dilated or restrictive cardiomyopathy has been considered as the most common forms of cardiac abnormalities in desminopathy patients [12], the present observations suggest that various forms of conduction block are most prominent in Chinese desminopathy patients. Kostera-Pruszczyk et al. summarized that all 47 patients examined by echocardiography in a cohort of 92 cases with desminopathy exhibited structural cardiomyopathy [12], while only six out of 25 patients presented with cardiomyopathy in our study.

11 The human DRPLA gene spans approximately 20 kbp and consists of 10 exons, with the CAG repeats located in exon 5.12 The number of CAG repeats in normal chromosomes and DRPLA patients range from 6 to 35 and from 54 to 79, respectively.13 It is characteristic that there is anticipation in DRPLA.9,10,14 Paternal transmission results in more

prominent anticipation (26–29 years/generation) than does maternal transmission (14–15 years/generation). There is an inverse correlation between the size of expanded CAG repeats and age at onset, and also a correlation between clinical features and the repeat selleckchem size.13 DRPLA patients with longer CAG repeats show a more early onset and severer phenotypes. The physiological functions of DRPLA protein remain to this website be elucidated. It is generally accepted that mutant

DRPLA proteins with expanded polyglutamine stretches are toxic to neuronal cells (“gain of toxic functions”). The discovery of neuronal intranuclear inclusions (NIIs) in transgenic mice for Huntington’s disease15 triggered new development of neuropathology in polyglutamine diseases, including DRPLA. NIIs are eosinophilic round structures, and easily detectable by ubiquitin immunohistochemistry (Fig. 3c). In DRPLA, they are also immunoreactive for expanded polyglutamine stretches (Fig. 3d) as well as for atrophin-1, the DRPLA gene product.16,17 Ultrastructurally, NIIs are non-membrane bound, heterogeneous in composition, and contain a mixture of granular and filamentous structures,

approximately 10–20 nm in diameter. NIIs were initially thought to be toxic structures responsible for neuronal cell death in affected brain regions; however, subsequent Tryptophan synthase investigations raised the possibility that NII formation itself might be a cellular reaction designed to reduce the acute toxic effect of the mutant proteins.18–20 In DRPLA, NIIs were detectable in multiple brain regions far beyond the dentatorubral and pallidoluysian systems, suggesting that neurons are affected much more widely than was recognized previously, although the incidences of NIIs were very low even in the affected regions.21 In 2001, it became apparent that diffuse intranuclear accumulation of the mutant DRPLA protein affects many neurons in wide area of the CNS, including the cerebral cortex (Fig. 3e–g), and that the prevalence of this pathology changes dynamically in relation to CAG repeat size. The results suggest that the novel lesion distribution revealed by the diffuse nuclear labeling may be responsible for a variety of clinical features, such as dementia and epilepsy in DRPLA.22 In addition to NIIs, skein-like inclusions were also detectable in DRPLA brains, although their appearances were restricted in the cerebellar dentate nucleus (Fig. 3h).23 To elucidate the molecular mechanisms of neuronal degeneration in DRPLA, transgenic mice harboring a single copy of a full-length human mutant DRPLA gene with 76 or 129 CAG repeats have been generated.

Fourteen patients (23.3%) developed Pneumocystis pneumonia. Eleven patients had a positive IFA but only nine were positive by cytological staining. Sixteen patients had a positive detection of P. jiroveci by PCR and nested-PCR. Thirteen of these patients were considered as having a definite Pneumocystis pneumonia and one patient with a probable Torin 1 mw Pneumocystis pneumonia. Five other patients had a positive detection only by nested-PCR. These patients were classified as no Pneumocystis pneumonia. PCR

detection of P. jiroveci is a very sensitive test and will offer a powerful technique in clinical laboratories for the routine diagnosis of Pneumocystis pneumonia. Using the nested-PCR, additional clinical cases can be diagnosed, but there is then an

obvious risk of detecting subclinical colonisation by P. jiroveci. “
“Since two large-scale, randomised studies on posaconazole prophylaxis have demonstrated a clear benefit for patients at high risk for contracting invasive fungal disease (IFD), posaconazole prophylaxis has been adopted as standard of care for this patient collective. Several years on from implementation at our institution, we wanted to evaluate its impact on the incidence and use of empirical antifungal therapy in a real-life setting. We analysed retrospectively incidence and severity of IFD in high-risk patients with prophylaxis, using a historical cohort as comparator. A total of 200 patients had either received the extended spectrum triazole posaconazole in prophylactic dosage of 200 mg tid or empirical antifungal therapy. Disease events were analysed by application of the revised EORTC/MSG definitions for IFD. Z-VAD-FMK solubility dmso Before posaconazole prophylaxis, we recorded 57/100 cases of IFD which was reduced to 28/100 with prophylaxis. The empirical use of antifungal drugs was reduced to 41% from 91% in the non-prophylaxis

cohort. Furthermore, we observed a shift in the categorisation of IFD according to EORTC/MSG criteria. Our data suggest that posaconazole was effective in reducing the rate and probability of invasive fungal disease in high-risk patients. “
“Ultraviolet-C irradiation as a method to induce the production of plant compounds with antifungal properties was investigated in the leaves of 18 plant species. A susceptibility assay Tyrosine-protein kinase BLK to determine the antifungal susceptibility of filamentous fungi was developed based on an agar dilution series in microtiter plates. UV irradiation strongly induced antifungal properties in five species against a clinical Fusarium solani strain that was responsible for an onychomycosis case that was resistant to classic pharmacological treatment. The antifungal properties of three additional plant species were either unaffected or reduced by UV-C irradiation. This study demonstrates that UV-C irradiation is an effective means of modulating the antifungal activity of very diverse plants from a screening perspective.

This process ensures the preservation of the benefits of randomization and avoids the introduction of bias during analysis. As-treated analysis may sometimes be used to test the robustness of findings but should rarely be used to replace the

use of intention-to-treat analysis. In the study by Obeticholic Acid Suki et al.,1 as almost half of the study participants discontinued the study for a range of reasons such as non-compliance, loss to follow-up and adverse events, it was particularly important to include this proportion in the analyses so as to prevent overestimation of the treatment effect. Based on the results presented in the article, you are confident that the study has undertaken analyses according to the original randomization of participants, BGB324 mw that is, by intention-to-treat. Questions: What were the results? What was the size and precision of the effect? When considering the results of a study, an assessment of the precision is essential. The exact ‘true’ effect of an intervention is never known. However, it is possible to estimate this effect.

When we consider the precision of a study, we are considering the proximity of an estimate to the ‘true’ effect. The interval, enclosed by the extremes at which the estimate may possibly lie, is known as the 95% confidence intervals (CIs). By accepting the 95% CI, one is accepting that the true effect lies within that range 95% of the time, in other words, the estimate will lie outside the interval 5% of the time. The precision of a study ultimately depends on the number of events, and therefore its sample size. As a general rule of thumb, the larger the proportion of participants who experience the outcome, the greater the precision, that is, total number of events drives the power of the study whilst the sample size and event rate determines Acyl CoA dehydrogenase the total number of events. A larger sample size will produce more outcomes

and therefore narrower CIs, allowing one to be more confident that the estimate is closer to the true effect. The results of a study can be expressed in a number of different ways and it is important to understand and interpret the significance of such results. Some examples include differences in a continuous factor (e.g. effects of sevelamer on serum phosphate levels), a dichotomous outcome (e.g. relative risk of hyperphosphataemia or risk of cardiovascular events) or as time-to-event analyses, comparing the length of time taken for a particular event of interest to occur between the two groups, thus providing additional information and statistical power.8 The results of time-to-event analyses are often expressed by hazard ratios.9 Perhaps the most important method for presenting the results of dichotomous outcomes is the absolute risk difference, which describes the proportion of individuals prevented from having an event, and can be used to calculate numbers needed to treat.

Among them, the most significant inhibition was observed in DC-FcγRIIb (Fig. 5B). Similarly, natural IC/Ig pretreatment significantly inhibited the LPS-induced TNF-α secretion from the three types of DCs. Among them, the most significant inhibition was observed in DC-FcγRIIb (Fig. 5B). Therefore, the results indicated that DC-FcγRIIb display more potent tolerogenic properties once stimulated with IC/Ig. Since IC could inhibit the maturation of FcγRIIb-overexpressing immature DCs, we further observed the effect of IC on DC-mediated T-cell proliferation. IC-stimulated DCs or GFP-expressing DCs (DC-GFP) significantly induced the proliferation of antigen-specific

T cells; in contrast, IC-stimulated DC-FcγRIIb significantly inhibited the proliferation of antigen-specific T cells (Fig. 6A). Furthermore, IC stimulation could promote DC-FcγRIIb to Venetoclax in vitro produce more PGE2 than DCs or DC-GFP (Fig. 6B). Interestingly, the hyporesponsiveness of CD4+ T cells disappeared when IC-stimulated DC-FcγRIIb were pretreated by celecoxib. Addition of exogenous PGE2 together with celecoxib Selleck AUY-922 significantly restored the response of CD4+KJ1.26+ T cells in this system (Fig. 6C). Thus, IC-stimulated DC-FcγRIIb induce T-cell hyporesponsiveness more significantly via more induction of PGE2. Considering that

high level of circulating IC are present in lupus-prone MRL/lpr mice, we wondered whether in vivo infusion with DC-FcγRIIb could attenuate lupus progression. We observed that adoptively transferred DCs had a rapid reduction after 2 wk of injection, then decreased slowly, and could be detectable even after 4 wk in B6/lpr mice (Supporting Information Fig. 4). MRL/lpr mice (4-wk-old) were i.p. administered with a single dose of 2×106 DCs, DC-GFP or DC-FcγRIIb respectively. At the age of 12 wk, serum autoantibodies, including ANAs, anti-DNA, and anti-chromatin

histones, were evaluated. MRL/lpr mice that received DC-GFP or DCs had significant increases in serum ANA, anti-dsDNA, Sucrase anti-ssDNA, anti-chromatin histone 1, 2A and 2B than MRL/lpr mice that received DC-FcγRIIb (Fig. 7A and B). We also measured the levels of Ig subclasses in these mice, however, no significant differences of serum IgG1, IgG2a and IgM were found (data not shown). Thus, infusion with DC-FcγRIIb markedly inhibited production of autoantibodies in MRL/lpr mice. The mortality caused by lupus is a result of renal failure caused by IC deposition. The kidney sections were prepared from MRL/lpr mice at the age of 30 wk for measurement of IC deposition and histological evaluation. MRL/lpr mice received DC-GFP or DCs had obviously IC deposition in the kidneys, whereas MRL/lpr mice received DC-FcγRIIb had minimal IC deposition (Fig. 7C).

Studying hormonal effects on systemic immune cells may selleck inhibitor not be an appropriate system for defining the responses of FRT mucosal immune cells. Immune cells in the FRT have a different phenotype from those in systemic circulation.79 For example, uterine NK cells

express higher levels of specific markers and have greater anti-HIV activity than blood NK cells.80 Neutrophils and macrophages also possess distinct characteristics from their counterparts in the blood. FRT neutrophils have lower levels of lactoferrin and matrix metaloproteinase-9, but appear to be primed for a more rapid induction of innate immune defense.81 Typically, levels of antimicrobials in mucosal fluids are measured by ELISA. Nutlin-3a molecular weight In some cases, antimicrobial levels correlate with biologic activity while others do not.82 As discussed elsewhere, molecules in CVL may be quantitatively detected in an ELISA, but might not be biologically active, depending on the local environment in FRT secretions.83 Several factors determine biologic activity of antimicrobials in the FRT. Female reproductive tract secretions contain both proteases and protease inhibitors, many of which are hormonally regulated.69 For example, several proteases with trypsin-like

activity in cervical vaginal secretions are regulated throughout the menstrual cycle with levels highest at ovulation and during the secretory phase. Families of proteases include cathepsins, kallikreins, MMPs, CD26, and others, all of which are responsible anti-PD-1 antibody for activating and/or deactivating a variety of antimicrobial peptides.84 In addition, antimicrobials

such as SLPI and Elafin are themselves protease inhibitors and can therefore regulate the endogenous proteases. Factors such as pH, salt, serum, and presence of sperm can affect biologic activity of antimicrobials. For example, the activity of the antimicrobial LL-37 is altered in the presence of sperm. LL-37 is processed and activated by prostate-derived protease gastricsin in a pH-dependent manner.26 Many antimicrobials are sensitive to salt as well as the presence of serum. The activity and efficacy of defensins have been shown to change with pH and salt concentration.85 Daher et al.16 showed that the addition of serum inhibited neutralization of HSV by HNPs. More recently, Mackewicz et al.86 demonstrated that HIV inhibition by alpha defensins was almost completely abrogated by the presence of 10% fetal calf serum. Many antimicrobials present in mucosal fluids can act in synergy. Lactoferrin and lysozyme have been shown to be synergistic against Gram-negative bacteria.87 HBD2 and LL-37 also show synergistic effects.10 Singh et al.11 has shown that SLPI, lactoferrin, and lysozyme, in combination, have significantly higher antimicrobial activity than each of the molecules individually. Van Wetering et al.

It arose in the left anterior cingulate cortex with a pseudo-polycystic appearance on neuroimaging. Histological features contained the “specific glioneuronal element” mimicking DNT Selleckchem Roxadustat and the components of distinct neurocytic rosettes with a center of neuropil islands and pilocytic astrocytoma resembling RGNT. Although the mechanisms of mixed glioneuronal tumor are far from being well-known, their co-existence might suggest a possible etiologic relationship between DNT and RGNT. “
“C. Soler-Martín, Ú. Vilardosa, S. Saldaña-Ruíz, N. Garcia and J. Llorens (2012) Neuropathology and Applied Neurobiology38, 61–71 Loss of neurofilaments in the neuromuscular junction

in a rat model of proximal axonopathy Aims: Rodents exposed to 3,3′-iminodipropionitrile (IDPN) develop an axonopathy similar to that observed in amyotrophic lateral sclerosis motor neurones, in which neurofilaments accumulate in swollen proximal axon segments. This study addressed the hypotheses that this proximal axonopathy is associated with loss of neurofilament proteins in the neuromuscular GS-1101 ic50 junctions and a progressive loss of neurofilaments

advancing in a distal-proximal direction from the distal motor nerve. Methods: Adult male Long-Evans rats were exposed to 0 or 15 mM of IDPN in drinking water for 1, 3 or 5 weeks, and their distal axons and neuromuscular junction organization studied by immunohistochemistry. Quantitative data were obtained by confocal microscopy on whole mounts of the Levator auris longus. Results: Benzatropine Muscles showed no change in the distribution of acetylcholine receptor

labelling in the neuromuscular junctions after IDPN. In contrast, the amount of neurofilament labelling in the junctions was significantly reduced by IDPN, assessed with two different anti-neurofilament antibodies. In preterminal axons and in more proximal axon levels, no statistically significant reductions in neurofilament content were observed. Conclusions: The proximal neurofilamentous axonopathy induced by IDPN is associated with an abnormally low content of neurofilaments in the motor terminals, with a potential impact in the function or stability of the neuromuscular junction. In contrast, neurofilaments are significantly maintained in the distal axon. “
“We report clinicopathological features of a 23-year-old woman with Down syndrome (DS) presenting with subacute myelopathy treated with chemotherapy, including intravenous and intrathecal administration of methotrexate (MTX), and with allogenic bone-marrow transplantation for B lymphoblastic leukemia. Autopsy revealed severe demyelinating vacuolar myelopathy in the posterior and lateral columns of the spinal cord, associated with macrophage infiltration, marked axonal loss and some swollen axons.

This was not the case: infants took an average of 15.6 (SD = 5.07) trials to reach habituation criterion in Experiment 3, while they averaged 16.6 (SD = 6.37) trials in Experiment 1 and 17.6 (SD = 6.02) in Experiment 2. Note that as trials were not terminated

due to lack of attention, this means that infants in Experiment 3 averaged 15.6 × 7 = 109.2 tokens of the words compared with 116.2 in Experiment 1 and 123.2 in Experiment 2. These differences were not significant (F < 1), and if anything the infants in Experiments 1 and 2 received more exposure. Consequently, the learning observed here can not be attributed to the number of words heard by the infants. Instead, it must be that the acoustic variability along noncriterial dimensions affected infants’ learning. A second concern was that we operationally defined the contrastive cues for voicing as the absolute VOT, Dabrafenib in vivo rather than the relative duration of the aspiration and voiced period. As a timing cue, VOT varies as a function of the speaking rate, which can be approximated as the duration of the vowel. If infants perceive voicing using VOT relative to the vowel length, then there may be some contrastive variability embedded in this set. Any effect of speaking rate (vowel length) will

be necessarily small: a 100-msec difference in vowel can only shift the VOT boundary by 5–10 msec in synthetic speech (McMurray, check details Clayards, Tanenhaus, & Aslin, 2008; Summerfield, 1981), and barely at all in natural speech Selleck MK-3475 (Toscano & McMurray, 2010b; Utman, 1998). Moreover, McMurray et al. (2008) demonstrate that listeners are capable of using VOT before they have heard the vowel length, suggesting the two function as independent cues to voicing, not as a

single relative cue (see Toscano & McMurray, 2010a). Nonetheless, it is important to determine whether, even when VOT is treated as a relative cue, we reduced the variability in contrastive cues from Rost and McMurray (2009). One way to operationalize this relative measure is the ratio of VOT to vowel length. Analysis of the relationship between the original items reported in Rost and McMurray (2009) and the modified versions of those stimuli used in the experiment reported here indicated that our stimulus construction minimized, rather than contributed to, variability in this measure. For reference purposes, this measure lead to a mean ratio of .012 for /b/ in the modified set (.063 in the original), and .45 for /p/ (.51 original). Computing the standard deviations of this ratio measure of voicing showed a substantial decrement between the experiments for both /buk/ (SDoriginal = .027, SDmodified = .0085) and /puk/ (SDoriginal = .227; SDmodified = .18).3 We can also operationalize this relative measure by using linear regression to partial out the effect of vowel length from VOT. An analysis of these residuals after linear regression also showed that the present stimuli have lower variance by an order of magnitude.

Thus, adverse events associated with immunosuppressive therapy and complications of Tx were analyzed in The Nationwide Retrospective Cohort

Study in IgAN in Japan. Methods: Study subjects were all IgAN patients diagnosed by the first renal biopsy in 42 collaborating hospitals during 2002 to 2004. Patients under 18 years old were excluded. Data at the time of renal biopsy ZVADFMK and during the follow-up were collected, including death, complications of Tx and the following adverse events requiring specific treatment; infection, psychiatric disorder, aseptic necrosis, peptic ulcer, de novo diabetes, osteoporosis and others. We analyzed 1,082 cases which have sufficient data for the analysis. Results: The median observation period was 5.4 years. Choice of therapy was as follows; conservative therapy (Cons) see more 534, oral steroids (Oral) 208, pulse methylprednisolone (mPSL) 123,

and Tx with pulse methyprednisone (Tx+mPSL) 217. In this period, 9 patients died (5 malignancy, 2 CVD, 1 COPD, 1 drug-induced lung injury), and death cases were not obviously association with immunosuppressive therapy. Adverse event rates were significantly lower in Cons (1.5%) and in Tx+mPSL (1.38%) groups compared to Oral (5.29%) and mPSL (4.88%) groups. Complication of Tx was occurred in 7 out of 327 (2.1%) cases. Conclusion: Adverse event rate was PLEK2 low in Cons and Tx+mPSL groups and complication of Tx was 2.1% among Japanese IgAN patients. FUSHIMA TOMOFUMI1, OE YUJI1,2, IWAMORI SAKI1, SATO EMIKO1, SUZUKI YUSUKE3, TOMINO YASUHIKO3, ITO SADAYOSHI2, SATO HIROSHI1,2, TAKAHASHI NOBUYUKI1,2 1Div. of Clinical Pharmacology and Therapeutics, Grad Sch of Pharmaceutical Sciences and Faculty

of Pharmaceutical Sciences, Tohoku Univ., Sendai Japan; 2Div. of Nephrology, Endocrinology and Vascular Medicine, Dept. of Medicine, Tohoku Univ., Sendai, Japan; 3Div. of Nephrology, Dept. of Int. Med. Juntendo Univ., Tokyo, Japan Introduction: IgA nephropathy is the most common form of progressive primary glomerulonephritis, exhibiting mesangial IgA and IgG co-deposition. Endothelin (ET) plays a pivotal role in progressing IgA nephropathy. When cells are stimulated by ET, ADP ribosyl cyclase (ADPRC) produces cyclic ADP-ribose (cADPR), which mediates an increase in cytosolic Ca. Nicotinamide, an amide of vitamin B3, is a potent inhibitor of ADPRC. The aim of the present study is to test whether nicotinamide has beneficial effects on IgA nephropathy using grouped ddY mice. Method: Male grouped ddY mice 5 weeks of age were divided into two groups that were administered orally either nicotinamide (500 mg/kg/day) or water daily using gavage.

In some genetic conditions, combined organ transplantation (e.g. liver–kidney transplantation) should be considered as the treatment of choice. Additional factors that may impact on paediatric recipient suitability are discussed in more

detail below. Transplantation is the primary goal for children with end stage kidney disease and results in improvements in growth, physical and intellectual development. Data from a number of case series show that there is no younger age limit to transplantation, although it is recommended that transplantation of Epacadostat solubility dmso infants under 1 year of age be performed in highly specialized units with extensive experience in paediatric transplantation. While poor adherence remains a significant cause of graft failure in the adolescent age group, delaying transplantation may be associated with poorer outcomes and is not recommended. Children with urological abnormalities require careful pretransplant assessment with consideration

given selleck screening library to correction of bladder abnormalities prior to transplantation. Other comorbid conditions such as obesity, mental retardation and haemostatic defects should not be considered a contraindication to transplantation. *Explanation of grades The evidence and recommendations in this KHA-CARI guideline have been evaluated and graded following the approach detailed by the GRADE working group (http://www.gradeworkinggroup.org). A description of the grades and levels assigned to recommendations is provided in Tables 1 and 2. High quality of evidence. We are confident that the true effect lies close to that of the estimate of the effect. Moderate quality of evidence. The true effect is likely to be close to the estimate of the effect, but there is a possibility that it is substantially Thiamine-diphosphate kinase different. Low quality of evidence. The true effect may be substantially different from the estimate of the effect. Very low quality of evidence. The estimate of effect is very

uncertain, and often will be far from the truth. **Access to the full text version For a full-text version of the guideline, readers need to go to the KHA-CARI website (go to the Guidelines section (http://www.cari.org.au)). “
“Date written: August 2009 Final submission: June 2009 No recommendations possible based on Level I or II evidence (Suggestions are based primarily on Level III and IV evidence) An accurate assessment of the glomerular filtration rate (GFR) should be undertaken in all potential donors. The benefit of obtaining a directly measured GFR (thought to be more accurate) over an estimated GFR, has not been proven in live donors (refer to CARI guidelines titled ‘Use of estimated glomerular filtration rate to assess level of kidney function’ and ‘Direct measurement of glomerular filtration rate’). 1 Ensure all donors are followed and results submitted to the Donor Registry.