Subject(s)
Atherosclerosis/physiopathology , Back Pain/etiology , Renal Dialysis , Abscess/etiology , Abscess/surgery , Aged , Amputation, Surgical , Atherosclerosis/surgery , Humans , Leg , Magnetic Resonance Imaging , Male , Pulmonary Embolism/pathology , Spinal Diseases/pathology , Treatment OutcomeABSTRACT
Studies on living donor kidney transplantation primarily address the recipients; few publications focus on kidney donors. The aim of the present study was to detect changes in and compensations of defined parameters of anemia and inflammation in the immediate postnephrectomy period. We included six living kidney donors who underwent an open anterior-extraperitoneal nephrectomy. We excluded donors with complications, such as significant blood loss or infection. Blood samples were taken before nephrectomy as well as on postoperative days 1, 3, 5, and 7, and at discharge for measurements of hemoglobin (Hb), serum erythropoietin (Epo), reticulocytes (Reti), pentraxin 3 (PTX3), and C-reactive protein (CRP). There was a significant decrease in Hb (>3 g/dL), reaching a maximum on day 3 followed by a significant threefold increase in Epo levels on day 5 and a nonsignificant elevation of Reti count. CRP increased approximately 80-fold on day 3. PTX3 showed a similar course, peaking on day 3 with an approximate 70-fold increase. After living donor nephrectomy, there was an unexpectedly pronounced inflammatory reaction in the absence of any signs of bacterial infection simultaneous with a significant decrease in Hb. These parameters improved during the hospital stay, in some cases they achieved the prenephrectomy level at discharge. These data may assist in interpreting laboratory results after nephrectomy among living kidney donors.
Subject(s)
Inflammation/physiopathology , Kidney , Living Donors , Nephrectomy/adverse effects , Postoperative Complications/physiopathology , Aged , C-Reactive Protein/metabolism , Creatinine/blood , Erythropoietin/blood , Female , Hemoglobins/metabolism , Humans , Male , Middle Aged , Postoperative Period , Tissue and Organ Procurement , Treatment OutcomeABSTRACT
Development of micro- and macrovascular disease in diabetes mellitus (DM) warrants a thorough investigation into the repertoire of endothelial cell (EC) responses to diabetic environmental cues. Using human umbilical vein EC (HUVEC) cultured in three-dimensional (3-D) native collagen I (NC) or glycated collagen I (GC), we observed capillary cord formation that showed a significant reduction in branching when cells were cultured in GC. To gain insight into the molecular determinants of this phenomenon, HUVEC subjected to GC vs. NC were studied using a PCR-selected subtraction approach. Nine different genes were identified as up- or downregulated in response to GC; among those, plasminogen activator inhibitor-1 (PAI-1) mRNA was found to be upregulated by GC. Western blot analysis of HUVEC cultured on GC showed an increase in PAI-1 expression. The addition of a neutralizing anti-PAI-1 antibody to HUVEC cultured in GC restored the branching pattern of formed capillary cords. In contrast, supplementation of culture medium with the constitutively active PAI-1 reproduced defective branching patterns in HUVEC cultured in NC. Ex vivo capillary sprouting in GC was unaffected in PAI-1 knockout mice but was inhibited in wild-type mice. This difference persisted in diabetic mice. In conclusion, the PCR-selected subtraction technique identified PAI-1 as one of the genes characterizing an early response of HUVEC to the diabetic-like interstitial environment modeled by GC and responsible for the defective branching of endothelial cells. We propose that an upregulation of PAI-1 is causatively linked to the defective formation of capillary networks during wound healing and eventual vascular dropout characteristic of diabetic nephropathy.
Subject(s)
Endothelium, Vascular/physiology , Plasminogen Activator Inhibitor 1/biosynthesis , Animals , Antibodies/immunology , Aorta , Blotting, Northern , Blotting, Western , Capillaries/physiology , Cell Division , Cells, Cultured , Collagen/analogs & derivatives , DNA, Complementary/analysis , Diabetes Mellitus, Experimental/physiopathology , Diabetic Nephropathies/physiopathology , Endothelium, Vascular/ultrastructure , Glycosylation , Mice , Mice, Knockout , Neovascularization, Physiologic , Plasminogen Activator Inhibitor 1/genetics , Plasminogen Activator Inhibitor 1/immunology , Time Factors , Umbilical VeinsABSTRACT
We have developed a new 'glycoprotein lectin immunosorbent assay' (GLIA) which permits the obstetrician to identify accurately pregnant women at risk for preterm delivery. This GLIA uses two lectins for the quantitative detection of glycosylation variants of fibronectins, namely, Maackia amurensis lectin (MAA) for the detection of fetal fibronectin (fFN), and Sambucus nigra lectin (Elderberry bark lectin; SNA). Fibronectin was quantitated in cervicovaginal secretions, amniotic fluid, and plasma of pregnant women. Detection of fFN in cervicovaginal secretions was considered to indicate a high risk of imminent delivery. The results were as follows: (1) The GLIA could differentiate between pregnant women after the onset of labour and/or with rupture of membranes and women without any signs of an imminent delivery (sensitivity 94%, specificity 96%, p < 0.001). (2) Differentiation was possible between asymptomatic pregnant women delivering within 10 days of sampling or after more than 10 days (sensitivity 93%, specificity 99%; p < 0.001). (3) If fFN was present in the cervicovaginal secretions, delivery occurred within 10 days of sampling irrespective of preterm delivery or delivery at term (p < 0.001). Thus, this GLIA is a useful assay for identifying those asymptomatic pregnant women who will deliver within 10 days of sampling.
