The early identification of renal transplant recipients at enhanced risk of developing acute and subclinical rejection would allow individualized adjustment of immunosuppression before functional graft injury occurs and would exclude these patients from drug-weaning studies. Protein and reverse transcriptase-polymerase chain reaction-based analyses of candidate markers in urine open the opportunity to closely monitor kidney-transplanted patients non-invasively. The chemokine interferon-inducible protein 10 (IP-10; CXCL10) might be an interesting candidate to uncover ongoing immune processes within the graft. Urine samples from kidney-transplanted recipients were retrospectively analyzed for IP-10 mRNA and protein expression. IP-10 levels were correlated with the incidence of acute rejection episodes proven by histology and long-term graft function assessed by the glomerular filtration rate 6 months post transplantation. IP-10 expression in urine identified patients with ongoing acute rejection episodes several days before a biopsy was indicated by rising serum creatinine levels. Most importantly, elevated levels of urinary IP-10 protein within the first four postoperative weeks were predictive of graft function at 6 months even in the absence of acute rejection. These data reveal a correlation between elevated IP-10 expression in urine at early time points post-transplantation and intragraft immune activation that leads to acute rejection and compromised long-term graft function.
The authors' data illustrate that the noninvasive kinetic mRNA expression measurement of defined markers in urinary cells of renal allograft recipients allows the early noninvasive detection of ongoing aRx.
Summary:logous progenitor cells from the bone marrow or peripheral blood, nephrotoxicity is one of the most frequent and often dose-limiting toxicities from this treatment. 2,4,5 Yet, the High-dose carboplatin, etoposide and ifosfamide (CEI) is an active chemotherapy regimen (HDCT) in solid incidence of this side-effect varied considerably in a large number of trials and the implications on hematologic recovtumors and lymphomas. In patients with previous exposure to cisplatin, its nephrotoxicity is dose-limiting.ery and clinical outcome in patients with germ-cell tumors who suffer from nephrotoxicity remain largely unknown. in consecutive phase I/II and phase III trials with high-dose (29%) patients, particularly at doses of carboplatin carboplatin, etoposide and ifosfamide followed by autolog-Ͼ1500 mg/m 2 . Hemodialysis was required in 12/150 ous stem cell rescue (ASCR). The details of these trials (8%) patients, but could be discontinued until discharge have been reported. 5,6 Patients were eligible having failed in all except two survivors. Nephrotoxicity did not delay at least one cisplatin and etoposide combination regimen. hematologic recovery when adjusted for the use of Overall 15 patients (10%) had failed one regimen, 106 PBPC and hematopoietic growth factors by multivariate (71%) patients had failed two, and 29 (19%) patients had analysis, but resulted in higher transfusion requirefailed more than two regimens prior to HDCT. Pretreatment ments, more overall toxicities and a longer hospital stay.characteristics were similar in patients with and without There were no differences in the response rates or surnephrotoxicity after HDCT. Details of the patient charactervival in patients with or without nephrotoxicity. Acute istics are shown in Table 1. As part of the protocols a nephrotoxicity is a frequent and clinically relevant commedian of two (range, 1-3) conventional-dose treatment plication of CEI in germ cell tumors. The acute sidecycles, each consisting of cisplatin 100 mg/m 2 , etoposide effects from CEI are reversible in the majority of 500 mg/m 2 and ifosfamide 6 g/m 2 were used prior to HDCT patients.in order to assess tumor response to conventional-dose salKeywords: antineoplastic agents therapeutic use; antivage treatment, and to maintain tumor control until HDCT neoplastic agents toxicity; bone marrow transplantation; could be given. This conventional-dose salvage treatment hematopoietic stem cell transplantation; prognosis; testicuwas followed by one cycle of high-dose CEI. lar neoplasms TreatmentThe high-dose combination of carboplatin, etoposide andThe details of the dose escalation and supportive care have ifosfamide (CEI) represents an active and potentially curabeen previously reported. 5 Carboplatin and etoposide were tive chemotherapy regimen (HDCT) in a number of solid administered as a short infusion over 1 h in divided doses tumors and lymphomas.1-6 Whereas substantial hematolover 3 and 4 days, respectively. Ifosfamide was given as a ogic toxicity can be fully reversed by the reinfu...
The sequential application of double-balloon catheter and vaginal PGE2 is as effective as the sole use of vaginal PGE2 with less applications and total amount of PGE2.
Alterations in the metabolism of glycosaminoglycans (GAG) may play a role in the pathogenesis of diabetic-associated microangiopathy. Consequently, the relationship between diabetic nephropathy and retinopathy and urinary GAG distribution was assessed in 96 IDDM patients in comparison to 103 healthy controls. GAG concentration in 24h urine samples was determined by precipitation with cetylpyridinium chloride and potassium acetate in ethanol followed by a colorimetric test with carbazole. A marked difference (P = 0.0008) in urinary GAG excretion between patients (24.3 +/- 1.5 mg/24 h, mean +/- SEM) and controls (16.2 +/- 0.75 mg/24 h) could be detected. In patients with IDDM of longer duration, GAG excretion was increased (< or = 10 yr: 20.8 +/- 2.1 vs > 10 yr: 27.4 +/- 2.1 mg/24 h; P = 0.03). Furthermore, IDDM patients with class 4 nephropathy and retinopathy exhibited a markedly higher GAG excretion compared to those without nephropathy (33.1 +/- 3.0 vs 22.6 +/- 1.7 mg/24 h, P = 0.005) or retinopathy (29.7 +/- 2.8 vs 21.2 +/- 1.7 mg/24 h, P = 0.009). An increased urinary GAG concentration was detected in IDDM patients with albuminuria (> 300 mg/24 h: 29.9 +/- 3.3 vs < 30 mg/24 h: 23.0 +/- 1.7 mg/24 h; P = 0.048), proteinuria (> 0.5 g/24 h: 30.3 +/- 3.7 vs < 0.05 g/24 h: 22.7 +/- 1.6 mg/24 h) and in patients with augmented serum creatinine in comparison to those with normal values (> 0.12 mg/L: 34.9 +/- 2.3 vs < 0.12 mg/L: 22.4 +/- 1.6 mg/24 h; P = 0.01). The results demonstrate a close relationship renal GAG excretion and the presence of microangiopathy in IDDM patients.
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