Recessive Mutations in ACP4 Cause Amelogenesis Imperfecta.

Amelogenesis imperfecta (AI) is an innate disorder that affects the formation and mineralization of the tooth enamel. When diagnosed with AI, one's teeth can be hypoplastic (thin enamel), hypomature (normal enamel thickness but discolored and softer than normal enamel), hypocalcified (normal enamel thickness but extremely weak), or mixed conditions of the above. Numerous studies have revealed the genes that are involved in causing AI. Recently, ACP4 (acid phosphatase 4) was newly found as a gene causing hypoplastic AI, and it was suggested that mutant forms of ACP4 might affect access to the catalytic core or the ability to form a homodimer. In this study, a Korean and a Turkish family with hypoplastic AI were recruited, and their exome sequences were analyzed. Biallelic mutations were revealed in ACP4: paternal (NM_033068: c.419C>T, p.(Pro140Leu)) and maternal (c.262C>A, p.(Arg88Ser)) mutations in family 1 and a paternal (c.713C>T, p.(Ser238Leu)) mutation and de novo (c.350A>G, p.(Gln117Arg)) mutation in the maternal allele in family 2. Mutations were analyzed by cloning, mutagenesis, immunofluorescence, immunoprecipitation, and acid phosphatase activity test. Comparison between the wild-type and mutant ACP4s showed a decreased amount of protein expression from the mutant forms, a decreased ability to form a homodimer, and a decreased acid phosphatase activity level. We believe that these findings will not only expand the mutational spectrum of ACP4 but also increase our understanding of the mechanism of ACP4 function during normal and pathologic amelogenesis.

Peri-ampullary duodenal diverticulum: effect on extrahepatic bile duct dilatation after cholecystectomy.

AIM: To investigate the effect of peri-ampullary duodenal diverticula (PAD) on extrahepatic bile duct (EHBD) dilatation before and after cholecystectomy. MATERIALS AND METHODS: During a 5-year period, a total of 860 consecutive patients with prior cholecystectomy were examined using abdominal computed tomography (CT). After exclusion of those with other obstructive EHBD lesions, 61 patients with PAD were recruited for evaluation of EHBD dilatation before and after cholecystectomy and were compared with a randomly sampled control group (n=113) without PAD. EHBD diameter was measured on coronal reconstruction CT using electronic callipers on the picture archiving and communication system monitors by two reviewers in consensus. RESULTS: There was no significant difference in EHBD diameter between PAD and non-PAD groups (8.2±2.8 versus 7.8±2.3 mm; p=0.276) before cholecystectomy. Compared with preoperative diameter, EHBD was significantly dilated after cholecystectomy (7.9±2.5 versus 9.8±3.4 mm, p<0.001), regardless of the presence of PAD; the degree of change was more prominent in the PAD group than in the non-PAD group (3.3±2.4 versus 1.1±1.6 mm; p<0.001) after surgery. The size of PAD did not affect the degree of EHBD dilatation after cholecystectomy (p=0.522). In the non-PAD group, the degree of EHBD dilatation was positively correlated with the follow-up interval after cholecystectomy (r=0.298; p=0.002), while the PAD group showed no significant correlation (r=-0.036; p=0.797). In patients with ≥2 mm postoperative EHBD dilatation, PAD incidence was higher than that in other patients (odds ratio, 8.739; p<0.001). CONCLUSION: Regardless of their size or postoperative follow-up duration, PAD induce marked post-cholecystectomy biliary dilatation.

Role of PIN1 on in vivo periodontal tissue and in vitro cells.

BACKGROUND: Although expression of peptidyl-prolyl cis/trans isomerase NIMA-interacting 1 (PIN1) was reported in bone tissue, the precise role of PIN1 in periodontal tissue and cells remain unclear. MATERIAL & METHODS: To elucidate the roles of PIN1 in periodontal tissue, its expression in periodontal tissue and cells, and effects on in vitro 4 osteoblast differentiation and the underlying signaling mechanisms were evaluated. RESULTS: PIN1 was expressed in mouse periodontal tissues including periodontal ligament cells (PDLCs), cementoblasts and osteoblasts at the developing root formation stage (postnatal, PN14) and functional stage of tooth (PN28). Treatment of PIN1 inhibitor juglone, and gene silencing by RNA interference promoted osteoblast differentiation in PDLCs and cementoblasts, whereas the overexpression of PIN1 inhibited. Moreover, osteogenic medium-induced activation of AMPK, mTOR, Akt, ERK, p38 and NF-jB pathways were enhanced by PIN1 siRNA, but attenuated by PIN1 overexpression. Runx2 expressions were induced by PIN1 siRNA, but downregulated by PIN1 overexpression. CONCLUSION: In summary, this study is the first to demonstrate that PIN1 is expressed in developing periodontal tissue, and in vitro PDLCs and cementoblasts. PIN1 inhibition stimulates osteoblast differentiation, and thus may play an important role in periodontal regeneration.

Wnt activity is associated with cementum-type transition.

BACKGROUND AND OBJECTIVE: Cellular and acellular cementum and the cells that form them are postulated to have different characteristics, and the relationship between these two tissues is not well understood. Based on the hypothesis that Wnt signaling is involved in the determination of cementum type, we examined Wnt activity along the tooth root and analyzed cementum formation in genetic mutant models. MATERIAL AND METHODS: We generated mutant models with Wnt signaling upregulation (OC Catnblox(ex3)/+ ), downregulation (OC Wlsfl/fl ), and a compound mutant (Enpp1asj/asj ;OC Catnblox(ex3)/+ ) to compare cementum apposition patterns of ectonucleotide diphosphatase/phosphodiesterase (Enpp1) mutant (Enpp1asj/asj ). The analysis of structural morphology and histology was performed with hematoxylin and eosin and immunohistochemical staining and scanning electron microscopy. RESULTS: The cementum type of upper apical region of tooth roots in the molar is altered from the cellular form at the initial stage to the acellular form at the late stage of cementum formation. However, the basal part of this apical region is not altered and retains cellular cementum characters with strong Wnt activity. In the genetic mutant models for Wnt upregulation, cellular cementum is formed at the cervical region instead of acellular cementum. However, Enpp1 mutant mice have clearly different characteristics with cellular-type cementum even with dramatically increased cervical cementum matrix. In addition, we found that acellular-type formation could be altered into cellular-type formation by analyzing Wnt upregulation and compound mutant models. CONCLUSIONS: Cementum type is not determined by its specific location and could be transformed with Wnt activity during cementum formation.

High-flow haemangiomas versus hypervascular hepatocellular carcinoma showing "pseudo-washout" on gadoxetic acid-enhanced hepatic MRI: value of diffusion-weighted imaging in the differential diagnosis of small lesions.

AIM: To validate the usefulness of diffusion-weighted imaging (DWI) in the differentiation of high-flow haemangiomas showing pseudo-washout appearance on gadoxetic acid-enhanced hepatic MRI from small hypervascular hepatocellular carcinomas (HCCs). MATERIALS AND METHODS: DWI (b=50, 800 s/mm2) with apparent diffusion coefficient (ADC) maps for 50 haemangiomas (6.4±2.9 mm) showing intense enhancement on arterial dominant phase imaging and hypointensity on transitional and/or hepatobiliary phase imaging during gadoxetic acid-enhanced MRI were retrospectively analysed and compared with that of 113 hypervascular HCCs (12.8±3.7 mm). In addition to measurement of mean ADC values on DWI and contrast-to-noise ratio (CNR) on corresponding T2-weighted imaging, qualitative analysis of DWI was performed for each lesion by two independent observers using a five-point scale. RESULTS: Both of mean ADC value (1.902 versus 0.997×10-3 mm2/s) and mean CNR (119.2 versus 36.9) for haemangioma were significantly larger than for HCC (p<0.001). On receiver operating characteristic (ROC) analysis, an area under the curve (AUC) of 0.995 for ADC values was significantly larger than 0.915 for CNRs (p=0.002). When the ADC value of 1.327×10-3 mm2/s was used as the threshold for the diagnosis of haemangioma, the sensitivity and specificity were 98% and 97.3%, respectively. The mean sensitivity and specificity of qualitative analysis for the differentiation of haemangioma from HCC were 92% and 99.1%, respectively. CONCLUSION: For high-flow small haemangiomas showing pseudo-washout appearance during gadoxetic acid-enhanced hepatic MRI, high b-factor DWI including an ADC map may provide additional information to enhance the confidence to exclude small hypervascular HCCs.

Effects of oxygenated or hydrogenated water on growth performance, blood parameters, and antioxidant enzyme activity of broiler chickens.

This study was conducted to investigate the effects of providing oxygenated and hydrogenated water on the growth performance, blood biochemical parameters, and immunoglobulin concentrations and antioxidant enzyme activity of broiler chickens. In our investigation, 144 Ross × Ross broiler chicks were randomly allotted to three different treatment groups with four replicates (treatment × replicate × bird = 3 × 4 × 12). All chicks were given one of the following types of water for five weeks: tap water (CON), hydrogenated water (HNW), and oxygenated water (ONW). ONW supplementation increased the final body weight and weight gain and also improved both feed intake and feed conversion of broiler chickens as compared to those of CON broiler chickens (P < 0.05). The abdominal fat and its ratio to the final body weight showed that fat accumulation in the broiler chicken abdomen was reduced when broiler chickens drank only ONW for five weeks (P < 0.05). ONW supplementation improved blood parameters, including triacylglyceride, total cholesterol, and low-density lipoprotein-cholesterol. Additionally, in accordance with a globulin increase in broiler chickens, both IgG and IgM generation were significantly enhanced when ONW was supplied to broiler chickens (P < 0.05) but only a numerical advance was observed in the HNW group (P > 0.05). Both oxygenated and hydrogenated water supplementation significantly improved the antioxidant effects (P < 0.05), and it seems that superoxide dismutase refinement was completed due to oxygen and/or hydrogen enhancement of drinking water. These results indicate that oxygen enhancement of drinking water may be recommended to improve growth performance by increasing immunoglobulins mainly IgG and IgM.

Smad4 in osteoblasts exerts a differential impact on HSC fate depending on osteoblast maturation stage.

Osteoblasts (OBs) are indispensable for the maintenance of hematopoietic stem cells (HSCs) in the bone marrow microenvironment. Here we investigated how Smad4 modulates HSC fate at distinct stages of OB development. For this, we conditionally knocked out Smad4 in cells expressing type I collagen (Col1a1) and osteocalcin (OC), respectively. Col1a1-expressing OBs were widely present in both the trabecular and cortical compartment, whereas OC-expressing OBs were predominantly located in the cortical compartment. HSCs from Col1a1 mutants displayed senescence-associated phenotypes. OC mutants did not exhibit HSC senescence-related phenotypes, but instead showed preferential HSC death. Of note, stromal cell-derived factor 1 expression was lower in Col1a1 mutants than control littermates, suggesting potential impairment of CXCR4-CXCL12-mediated HSC retention. Disruption of the CXCR4-CXCL12 axis by AMD3100 administration led to an increase in the senescence-associated ß-galactosidase activity and low competitive potential. Collectively, our findings indicate that deletion of Smad4 in OBs differentially modulates HSC fate in a stage-dependent manner.

Novel SNPs in the growth arrest and DNA damage-inducible protein 45 alpha gene (GADD45A) associated with meat quality traits in Berkshire pigs.

This study was conducted to evaluate the porcine gene GADD45A (growth arrest and DNA-damage-inducible protein 45 alpha) as a positional candidate controlling quantitative trait loci (QTL) for meat quality traits on chromosome 6 (SSC6). Four exons of the porcine GADD45A gene were defined from cDNA and BAC clone sequences. A total of 4 single nucleotide polymorphisms (SNPs) were identified in porcine GADD45A. The association of these SNPs (g.196A>G, g.392C>A, g.955T>C and g.3247A>T) with meat quality traits was evaluated in 678 Berkshire pigs. The genotype distribution of only one SNP (g.3247A>T) conformed to Hardy Weinberg equilibrium in the pig population analyzed in this study, and the other SNPs were not in Hardy-Weinberg equilibrium. All four SNPs were significantly associated with meat quality traits. Three SNPS (g.196A>G, g.392C>A, and g.955T>C) showed similar significant association patterns for drip loss, cooking loss, meat color (lightness; MC_L and yellowness; MC_B), shear force and water-holding capacity traits. By contrast, g.3247A>T had a different association pattern with other traits such as intramuscular fat content (IMF) and backfat thickness (BF), drip loss, MC_L, and moisture. These findings will provide useful information for genetic characterization or association studies in other pig populations. Additionally, these markers can potentially be applied in pig breeding programs to improve meat quality traits, including IMF and BF.

Disruption of Tgfbr2 in odontoblasts leads to aberrant pulp calcification.

Transforming growth factor ß (TGF-ß) signaling has been implicated in dentin formation and repair; however, the molecular mechanisms underlying dentin formation remain unclear. To address the role of TGF-ß signaling in dentin formation, we analyzed odontoblast-specific Tgfbr2 conditional knockout mice. The mutant mice had aberrant teeth with thin dysplastic dentin and pulpal obliteration, similar to teeth from human patients with dentinogenesis imperfecta type II and dentin dysplasia. In mutant, the odontoblasts lost their cellular polarity, and matrix secretion was disrupted after mantle dentin formation. As a consequence, the amount of predentin decreased significantly, and an ectopic fibrous matrix was formed below the odontoblast layer. This matrix gradually calcified and obliterated the pulp chamber with increasing age. Immunohistochemistry revealed decreased expression of alkaline phosphatase in mutant odontoblasts. In mutant dentin, Dsp expression was reduced, but Dmp1 expression increased significantly. Collagen type I, biglycan, and Dsp were expressed in the ectopic matrix. These results suggest that loss of responsiveness to TGF-ß in odontoblasts results in impaired matrix formation and pulpal obliteration. Our study indicates that TGF-ß signaling plays an important role in dentin formation and pulp protection. Furthermore, our findings may provide new insight into possible mechanisms underlying human hereditary dentin disorders and reparative dentin formation.

Osterix regulates tooth root formation in a site-specific manner.

Bone and dentin share similar biochemical compositions and physiological properties. Dentin, a major tooth component, is formed by odontoblasts; in contrast, bone is produced by osteoblasts. Osterix (Osx), a zinc finger-containing transcription factor, has been identified as an essential regulator of osteoblast differentiation and bone formation. However, it has been difficult to establish whether Osx functions in odontoblast differentiation and dentin formation. To understand the role of Osx in dentin formation, we analyzed mice in which Osx was subjected to tissue-specific ablation under the control of either the Col1a1 or the OC promoter. Two independent Osx conditional knockout mice exhibited similar molar abnormalities. Although no phenotype was found in the crowns of these teeth, both mutant lines exhibited short molar roots due to impaired root elongation. Furthermore, the interradicular dentin in these mice showed severe hypoplastic features, which were likely caused by disruptions in odontoblast differentiation and dentin formation. These phenotypes were closely related to the temporospatial expression pattern of Osx during tooth development. These findings indicate that Osx is required for root formation by regulating odontoblast differentiation, maturation, and root elongation. Cumulatively, our data strongly indicate that Osx is a site-specific regulator in tooth root formation.

Wntless regulates dentin apposition and root elongation in the mandibular molar.

Wnt signaling plays an essential role in the dental epithelium and mesenchyme during tooth morphogenesis. However, it remains unclear if Wnt ligands, produced from dental mesenchyme, are necessary for odontoblast differentiation and dentin formation. Here, we show that odontoblast-specific disruption of Wntless (Wls), a chaperon protein that regulates Wnt sorting and secretion, leads to severe defects in dentin formation and root elongation. Dentin thickness decreased remarkably and pulp chambers enlarged in the mandibular molars of OC-Cre;Wls(CO/CO) mice. Although the initial odontoblast differentiation was normal in the mutant crown, odontoblasts became cuboidal and dentin thickness was reduced. In immunohistochemistry, Wnt10a, ß-catenin, type I collagen, and dentin sialoprotein were significantly down-regulated in the odontoblasts of mutant crown. In addition, roots were short and root canals were widened. Cell proliferation was reduced in the developing root apex of mutant molars. Furthermore, Wnt10a and Axin2 expression was remarkably decreased in the odontoblasts of mutant roots. Deletion of the Wls gene in odontoblasts appears to reduce canonical Wnt activity, leading to inhibition of odontoblast maturation and root elongation.

Alteration of conserved alternative splicing in AMELX causes enamel defects.

Tooth enamel is the most highly mineralized tissue in vertebrates. Enamel crystal formation and elongation should be well controlled to achieve an exceptional hardness and a compact microstructure. Enamel matrix calcification occurs with several matrix proteins, such as amelogenin, enamelin, and ameloblastin. Among them, amelogenin is the most abundant enamel matrix protein, and multiple isoforms resulting from extensive but well-conserved alternative splicing and postsecretional processing have been identified. In this report, we recruited a family with a unique enamel defect and identified a silent mutation in exon 4 of the AMELX gene. We show that the mutation caused the inclusion of exon 4, which is almost always skipped, in the mRNA transcript. We further show, by generating and characterizing a transgenic animal model, that the alteration of the ratio and quantity of the developmentally conserved alternative splicing repertoire of AMELX caused defects in enamel matrix mineralization.

Effect of an organic buffer layer on the stability of zinc oxide thin-film transistors.

Compared with other materials, zinc oxide (ZnO) exhibits stability in air, high-electron mobility, transparency and low light sensitivity. We investigated these properties in ZnO thin-film transistors (TFTs) containing a cross-linked poly(vinyl alcohol) (C-PVA) (1:3) buffer layer stacked between the semiconductor and gate dielectric. We measured the impact of this C-PVA layer on gate bias stress. We measured the transfer characteristics of the saturation region to determine the threshold voltage and the field-effect mobility of the transistors. We recorded a threshold voltage of 11.53 V in the ZnO TFTs with the C-PVA buffer layer, the field-effect mobility was 0.2 cm2/Vs. There was a positive shift in the threshold voltage of deltaV(TH) approximately 10 V in response to the application of a gate bias stress of 20 V. The positive shift in the threshold voltage was lower than that in pristine ZnO TFTs. This finding suggests that the shift in threshold voltage was due to reduced charge trapping at the semiconductor-gate dielectric interface. Our report indicates that the organic buffer layer enhanced the stability of ZnO TFTs.

Protective effect of the roots extract of Platycodon grandiflorum on bile duct ligation-induced hepatic fibrosis in rats.

The aim of the present study was to evaluate the protective effect of aqueous extract from Platycodon grandiflorum (BC703) on bile duct ligation (BDL)-induced hepatic fibrosis in rats. BDL rats were divided into three groups, which orally received distilled water or BC703 (10 or 50 mg/kg/day) for consecutive 28 days. Antifibrotic effects of BC703 on BDL-induced hepatic fibrosis in rats were estimated by assessing serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL), blood urea nitrogen (BUN), transforming growth factor-beta 1 (TGF-ß1) and hepatic levels of malondialdehyde (MDA), glutathione (GSH), total superoxide dismutase (SOD) and nitric oxide (NO). The biochemical observations were supplemented by histopathological examination of liver samples stained with hematoxylin and eosin and Masson's trichrome stain. ALT, AST, TBIL and BUN were elevated in the group treated with BDL alone than in the sham-operated group. These elevations were significantly decreased by BC703 treatment. Hepatic GSH and SOD levels, depressed by BDL, were also increased in the BC703 group. In addition, increases in hepatic MDA and NO levels in the BDL-induced cholestasis were attenuated by BC703 treatment. Furthermore, BC703 treatment significantly reduced the serum level of fibrogenic cytokine, TGF-ß1. Histopathological studies further substantiated the protective effect of BC703 on BDL-induced hepatic fibrosis in rat. BC703 may have beneficial effects not only on hepatic fibrosis by cholestasis but also on hepatic fibrosis development in patients with chronic hepatic disease.

ß-catenin is required in odontoblasts for tooth root formation.

The tooth root is an important part of the tooth that works together with the surrounding periodontium to maintain the tooth in the alveolar socket. The root develops after crown morphogenesis. While the molecular and cellular mechanisms of early tooth development and crown morphogenesis have been extensively studied, little is known about the molecular mechanisms controlling tooth root formation. Here, we show that ß-catenin is strongly expressed in odontoblast-lineage cells and is required for root formation. Tissue-specific inactivation of ß-catenin in developing odontoblasts produced molars lacking roots and aberrantly thin incisors. At the beginning of root formation in the mutant molars, the cervical loop epithelium extended apically to form Hertwig's epithelial root sheath (HERS), but root odontoblast differentiation was disrupted and followed by the loss of some HERS inner layer cells. However, the outer layer of the HERS extended without the root, and the mutant molars finally erupted. The periodontal tissues extensively invaded the dental pulp. These results indicate that there is a cell-autonomous requirement for Wnt/ß-catenin signaling in the dental mesenchyme for root formation.

Excessive Wnt/ß-catenin signaling disturbs tooth-root formation.

BACKGROUND AND OBJECTIVE: Wingless-type MMTV integration site family (Wnt)/ß-catenin signaling plays an essential role in cellular differentiation and matrix formation during skeletal development. However, little is known about its role in tooth-root formation. In a previous study, we found excessive formation of dentin and cementum in mice with constitutive ß-catenin stabilization in the dental mesenchyme. In the present study we analyzed the molar roots of these mice to investigate the role of Wnt/ß-catenin signaling in root formation in more detail. MATERIAL AND METHODS: We generated OC-Cre:Catnb(+/lox(ex3)) mice by intercrossing Catnb(+/lox(ex3)) and OC-Cre mice, and we analyzed their mandibular molars using radiography, histomorphometry and immunohistochemistry. RESULTS: OC-Cre:Catnb(+/lox(ex3)) mice showed impaired root formation. At the beginning of root formation in mutant molars, dental papilla cells did not show normal differentiation into odontoblasts; rather, they were prematurely differentiated and had a disorganized arrangement. Interestingly, SMAD family member 4 was upregulated in premature odontoblasts. In 4-wk-old mutant mice, molar roots were about half the length of those in their wild-type littermates. In contrast to excessively formed dentin in crown, root dentin was thin and hypomineralized in mutant mice. Biglycan and dentin sialophosphoprotein were downregulated in root dentin of mutant mice, whereas dentin matrix protein 1 and Dickkopf-related protein 1 were upregulated. Additionally, ectonucleotide pyrophosphatase/phosphodiesterase 1 was significantly downregulated in the cementoblasts of mutant molars. Finally, in the cementum of mutant mice, bone sialoprotein was downregulated but Dickkopf-related protein 2 was upregulated. CONCLUSION: These results suggest that temporospatial regulation of Wnt/ß-catenin signaling plays an important role in cell differentiation and matrix formation during root and cementum formation.

The blood oxygen level-dependent functional MR imaging signal can be used to identify brain tumors and distinguish them from normal tissue.

BACKGROUND AND PURPOSE: In neuro-oncology, a major problem is clear identification of tumor from the surrounding normal tissue. We hypothesized that we could use the blood oxygen level-dependent functional MR imaging (BOLD fMRI) signals from tumors and normal brain to identify the tumors and distinguish them from the surrounding brain. MATERIALS AND METHODS: Fourteen patients with meningiomas, gliomas, and metastatic tumors were scanned before surgery. All subjects performed a motor task; 2 subjects were also scanned while in a resting state. The BOLD signals were taken from selected points within the tumor and from the surrounding normal brain and were analyzed by using correlation analysis to determine how closely they were related. RESULTS: The BOLD signals from all of the tumors were significantly different from those in the surrounding normal tissue. In meningiomas and gliomas, selection of a voxel in the tumor for signal-intensity analysis highlighted the entire tumor mass while excluding the normal tissue. The BOLD signal intensity was the same whether the subjects were motionless or finger tapping. CONCLUSIONS: Analysis of the BOLD signal intensity provides a relatively simple and straightforward method for identifying brain tumors and distinguishing them from normal tissue. This approach may be of use in neurosurgery.

Can machine perfusion decrease the likelihood of discard among biopsied kidneys?

Many factors, such as donor risk factors and renal function, have been shown to be associated with an increased likelihood of discard after recovering kidneys from deceased donors. When these factors are insufficient for assessment, renal biopsy is often performed at the time of harvest to assess suitability. Our aims were to identify factors that predict the discard of a biopsied kidney and to assess the impact of machine perfusion (MP) on kidney discard. We biopsied 678 kidneys from deceased donors aged >or=40 years from 2001 to 2006. We used a logistic regression model to estimate the adjusted odds ratios for kidney discard. Thirty-nine percent (n = 261) of biopsied kidneys were discarded. Kidneys with glomerulosclerosis (GS) > 20% had the highest likelihood of discard. Other significant predictors of discard included extreme donor age, final resistance (>40), atherosclerosis, interstitial fibrosis, arteriolosclerosis, and terminal serum creatinine value (SCr) > 1.5 mg/dL. MP kidneys (n = 69) were less likely to be discarded than cold storage (CS) kidneys after adjusting for other factors (adjusted odds ratio = .13, P < .001). In conclusion, abnormal biopsy findings were associated with the highest likelihood of discard. MP was used in only 10% of the cases; however, the use of MP was associated with a decreased likelihood of discard among biopsied kidneys.

Factors associated with discard of recovered kidneys.

We reviewed diseased donor (DD) kidney usage at a single Organ Procurement Organization in Southern California to more closely examine factors associated with discard. From 2001 to 2006, 3863 kidneys from 1959 DDs were recovered, but 454 (11.8%) were subsequently discarded. Among the discarded kidneys, 211 (46.5%) were discarded based upon biopsy findings, 19 (4.2%) due to anatomical abnormalities, 16 (3.5%) based on donor quality, and 14 (3.1%) because they were felt to be too old to be pumped. Multivariate logistic regression analysis was performed using significant prognostic factors upon univariate analyses. According to the magnitude of the adjusted odds ratio (AOR), significant prognostic factors for discard were extreme donor age (AOR = 24.1 of age 70-80 years, P < .001; AOR = 6.34 age 50-69 years, P < .001; AOR = 2.77 age 40-49 years, P < .001; and AOR = 3.09 age <10 years, P < .001 vs age 10-39 years), high final resistance (AOR = 8.86 of >40 vs others, P = .006), glomerulosclerosis (GS) > 20% (AOR = 5.94 vs GS 0%-5%/no biopsy, P < .001), severe atherosclerosis (AOR = 4.66, P = .003), abnormal anatomy (AOR = 2.7, P < .001), and moderate or severe arteriolosclerosis (AOR = 2.2 vs none/mild/no biopsy, P < .001). Among biopsy findings, the presence of GS > 20% was associated with the highest likelihood of discard. A high final resistance increased the likelihood of discard as well. In conclusion, these findings may help to set the groundwork toward a more uniform approach to organ utilization in donor service areas.