Background. To date, there have been no studies reliably showing an influence of the kidney on the concentration of troponins. We therefore analysed the concentration curves in patients after ...coronary artery bypass grafting (CABG) according to their dependence on renal function. Methods. We determined cardiac troponin I (cTnI), cardiac troponin T (cTnT) and creatinine in plasma in 28 patients after CABG. Discrimination into patients with normal (n = 13) and impaired (n = 15) renal function was based on creatinine clearance (Crea-Clear). The curves for cTnI and cTnT, as recorded by post-operative measurements, were approximated using mathematical functions. The curve parameters peak maximum (Pmax), peak position (Ppos), half-height breadth (HHB) and area under the curve (AUC) were established after this. Assuming an exponential function, the half-life (t1/2) of cTnI was determined from the declining part of the curve. Results. For both, cTnI and cTnT, significant differences in Pmax, Ppos, HHB and AUC were detected after curve approximation. The t1/2 values of cTnI were 25.1 h (22.0–35.3) for the group with normal renal function and 38.4 h (35.9–51.9) for patients with impaired renal function (P = 0.001). An influence of diabetes mellitus (Dm), renal replacement therapy or the age of the patients could not be verified. Conclusion. The results of this study clearly demonstrate that kidney function has an impact on plasma troponin concentrations. In everyday clinical practice this has to be considered when interpreting elevated plasma troponin concentration in patients with impaired renal function.
Purpose
Systemic heparin administration during laparoscopic donor nephrectomy (LDN) may prevent microvascular thrombus formation following warm ischemia. We herein present our experience with and ...without systemic heparinization during LDN.
Methods
We retrospectively reviewed donor complications and graft outcomes in 119 consecutive live donor kidney transplantations between January 2005 and December 2009. Systemic heparin was administered to the first 65 donors. LDN was carried out by 2 surgeons using a pure laparoscopic technique.
Results
Total operating time for LDN was significantly longer in the heparin group (202 vs. 157 min). The incidence of renal artery multiplicity was significantly higher in the heparin group. Mean warm ischemia time was 160 s, and mean hospital stay was 5 days with no differences between groups. Postoperative hemorrhage occurred in 3 donors with systemic heparinization and in 1 without heparinization. Two donors received blood transfusions, and 2 underwent laparoscopic reexploration. Three grafts were lost in the heparin group and 1 in the non-heparin group. Graft loss was due to early vascular thrombosis (
n
= 3) and due to acute rejection (
n
= 1). Overall, 1-year graft survival was 96.6%, and 1-year serum creatinine was 1.41 mg/dl (
P
= n. s. between groups).
Conclusions
Abandoning systemic donor heparinization in LDN with short warm ischemia has a low complication rate without adverse effects on short- and long-term graft outcomes.
Objectives To evaluate the functional outcomes and complications after allogeneic kidney transplantation into recipients with a urinary conduit using ureteroureterostomy between the transplant and ...native ureter. Methods We performed a retrospective study of 6 patients with a pre-existing urinary conduit undergoing kidney transplantation at a single tertiary academic center from May 1982 to February 2007. Results The study included 1 female and 5 males aged 16 to 65 years. Two patients received a living donor transplant. The indications for pretransplant conduit formation were neurogenic bladder in 3 and bladder contraction with vesicoureteral reflux in 3. One patient received a colon conduit. All patients underwent kidney transplantation into a urinary conduit using ureteroureterostomy between the transplant ureter and the ipsilateral native ureter. The average interval between conduit formation and kidney transplantation was 83.5 months and the average time of requiring hemodialysis was 56.3 months. The mean follow-up was 5.3 years. The patient and graft survival rate was 100% and 83.3%, respectively. The 3-year serum creatinine averaged 1.4 mg/dL. One graft was lost because of chronic rejection. Transplant ureter obstruction occurred in 2 patients and required endoscopy or open revision. Four patients underwent post-transplant native nephrectomy for recurrent pyelonephritis. Three patients were hospitalized for treatment of graft pyelonephritis. Conclusions In our experience, ureteroureterostomy between the transplant and native ureter is technically feasible and provides good functional results despite a high incidence of urinary tract infection. We recommend this approach in renal transplant recipients with a short contracted conduit or in those in whom the donor ureter is too short to warrant a tension-free ureteroileal anastomosis.
Cardiovascular mortality is remarkably high in patients who are on hemodialysis. Soluble CD154 (sCD154), a protein that belongs to the TNF receptor superfamily, has been implicated in the ...pathogenesis of atheromatous plaque destabilization and thrombotic events. The predictive value of sCD154 as a marker for clinical outcome in patients with ESRD was investigated. A total of 232 patients were prospectively followed for 52 mo. At study entry, clinical characteristics were documented and plasma concentrations of sCD154 and those of conventional risk predictors were analyzed. The time and cause of any hospitalization and death were documented during the entire follow-up. Survival rates were compared by Kaplan-Meier and Cox regression analyses. A total of 122 patients died, 64 of cardiovascular disease, including 20 cases of fatal atherothrombotic diseases (myocardial infarction, stroke, mesenteric ischemia). All 20 cases of fatal atherothrombotic events had high sCD154 plasma levels (cutoff >6.42 ng/ml) at study entry. The total number of fatal and nonfatal atherothrombotic events was 66. Only five atherothrombotic nonfatal events occurred in patients with sCD154 <6.42 ng/ml, whereas 61 fatal and nonfatal events were seen in patients with sCD154 > or =6.42 ng/ml (P < 0.005). This was confirmed by Kaplan-Meier curves for fatal atherothrombotic events (P = 0.0214) and the combined end point fatal and nonfatal atherothrombotic events (P = 0.0039). Cox regression analysis revealed that high sCD154 is an independent predictor (relative risk 6.80; 95% confidence interval 1.64 to 28.26; P = 0.008) for the combined end point death or hospitalization as a result of atherothrombotic events. Death or hospitalizations as a result of any other reason (arrhythmia, heart failure, infectious diseases, and cancer) were not linked to sCD154 plasma concentrations. In conclusion, sCD154 predicts nonfatal and fatal atherothrombotic events (myocardial infarction, stroke, mesenteric ischemia) but not death and hospitalization as a result of any other reason in stable patients who have ESRD and are on hemodialysis.
Abstract With cross-over living donor kidney transplantation, immunologic incompatibilities within the original donor/recipient pair can be overcome. As minimal invasive techniques for organ recovery ...are increasingly applied, this should also be performed in a cross-over kidney transplantation. We present the first report of a successful simultaneous laparoscopic kidney recovery for cross-over kidney transplantation as well as a review of the international practice of cross-over kidney transplantation in the context of national laws. Cross-over kidney transplantation should be encouraged. A databank on pairs willing to participate in organ exchange programs should be created.
Platelet inhibition limits TGF-β overexpression and matrix expansion after induction of anti-thy1 glomerulonephritis.
Although a role of platelets is well established in atherosclerosis, only little ...is known about their contribution to pathologic renal matrix expansion. The present study analyzes the effect of the platelet inhibitor clopidogrel on the early injury and subsequent repair phase of experimental anti-thy1 glomerulonephritis.
In male Sprague-Dawley rats, acute anti-thy1 glomerulonephritis was induced by intravenous injection of OX-7 antibody. In protocol 1 (injury), clopidogrel was given starting 5days before antibody injection. One day after disease induction, parameters of mesangial cell injury (glomerular cell number, inducible NO synthesis, and macrophage infiltration) were analyzed. In protocol 2 (repair), clopidogrel treatment was started one day after antibody injection. On day 6, parameters of glomerular repair glomerular matrix score, expression of transforming growth factor (TGF)-β1, fibronectin, and plasminogen activator inhibitor (PAI)-1 and thrombosis (aneurysm formation and fibrinogen deposition) were determined. In both protocols, an additional group of rats was treated with the angiotensin-converting enzyme (ACE) inhibitor enalapril.
In the injury protocol, platelet inhibition did not affect mesangial cell lysis, glomerular NO production, and macrophage infiltration, while ACE inhibition was protective. In the repair protocol, clopidogrel significantly limited aneurysm formation and fibrinogen deposition, as well as glomerular matrix expansion, TGF-β1, fibronectin, and PAI-1 expression. In comparison, enalapril was less effective in preventing glomerular thrombosis, but was significantly superior to clopidogrel in limiting matrix protein expression and accumulation.
The present study shows that platelets play a significant role in the sequence from mesangial cell injury to renal matrix expansion in anti-thy1 glomerulonephritis. The results, directly comparing renin-angiotensin-system and platelet inhibition, suggest that platelets contribute less than angiotensin II to TGF-β overexpression and matrix accumulation in this model of acute glomerular wound repair.
NO mediates antifibrotic actions of L-arginine supplementation following induction of anti-thy1 glomerulonephritis.
L-Arginine plays a complex role in renal matrix expansion, involving endogenous ...metabolism into nitric oxide (NO), polyamines, L-proline and agmatine. Supplementing dietary L-arginine intake has been shown to limit transforming growth factor (TGF)-β1 overproduction and matrix accumulation in rats with induced anti-thy1 glomerulonephritis (GN). The present study tests the hypothesis that this beneficial effect on in vivo TGF-β overexpression is mediated via the generation of NO.
One day after induction of anti-thy1 GN, male Wistar rats fed a normal protein diet were assigned to the following groups: (1) normal controls; (2) GN; (3) GN-Arg (plus 500mg L-arginine/day); (4) GN-Arg-NAME plus 500mg L-arginine/day and 75mg/L of the NO synthase inhibitor nitro-L-arginine-methyl ester (L-NAME) in the drinking water; and (5) GN-Molsi (10mg/day of the NO donor molsidomine). In protocol 1, treatment lasted until day 7, and in protocol 2, until day 12 after disease induction, respectively. Analysis included systolic blood pressure, a glomerular histologic matrix score, and the glomerular mRNA and protein expression of the key fibrogen TGF-β1, the matrix protein fibronectin, and the protease inhibitor plasminogen activator inhibitor type 1 (PAI-1).
Blood pressure was normal in untreated anti-thy1 animals and not significantly affected by any of the treatments. Compared to untreated nephritic rats, administration of both L-arginine and molsidomine reduced glomerular TGF-β1 overexpression significantly and to a similar degree in both protocols, while the beneficial effect of L-arginine was abolished by concomitant NO synthesis inhibition. Glomerular matrix accumulation, fibronectin and PAI-1 mRNA and protein expression closely followed the expression of TGF-β1.
The present study shows that L-arginine's antifibrotic action in normotensive anti-thy1 GN is mainly mediated by endogenous production of NO. The data suggest that NO limits in vivo TGF-β overexpression in a pressure-independent manner and that NO donors may be of benefit in the treatment of human fibrotic renal disease.
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