Search

Myeloablative (m-allo) hematopoietic stem cell transplantation (SCT) involves a great risk of acute kidney injury (AKI). We assessed whether or not early elevation of urinary biomarkers is useful for identifying high-risk patients for AKI.A prospective cohort study was conducted in 40 patients (46.0+/-12.5 years, eGFR 96.1 +/- 25.3 mL/min/1.73 m2) who received m-allo SCT in our hospital. We measured urinary biomarkers such as N-acetyl-beta -glucosaminidase (NAG), beta2 microglobulin (beta 2M), alpha microglobulin ( alpha1M) before conditioning therapy, on the day of SCT and both days 7 and 14 after SCT. AKI was defined as a decrease in eGFR within 100 days after SCT, and classified based on the RIFLE criteria. Discriminative sensitivity of urinary biomarkers was estimated using area under receiver operating characteristic (AuROC) curve analysis.AKI occurred in 28 cases(70 %): risk was 25.0 %, injury was 17.5 %, failure was 22.5 % and loss was 5.0 %, respectively. Only 4 cases with AKIor = injury that occurred less than 40 days after SCT died within 100 days after SCT. Thus, this level of AKI was denoted as"severe AKI"and targeted for early identification. Values of all urinary biomarkers increased gradually after the conditioning therapy, and both NAG and alpha 1M values at day 7 became significantly higher in the severe AKI group than in the opposite group. The AuROC showed that both NAG and alpha 1M values at day 7 had moderate discriminative sensitivity for predicting severe AKI (NAG : 0.783, 95 % confidence interval [CI] 0.611-0.966 ; and alpha 1M: 0.807, 95 % CI 0.647-0.956, respectively). Multivariate logistic regression showed that only alpha 1M at day 7 was significantly associated with the occurrence of severe AKI(odds ratio 18.4, 95 % CI 1.210-736, p=0.035).Consecutive monitoring of urinary alpha 1M after SCT is likely to be useful for early identification of patients at risk for severe AKI, leading to early death.

A 38-year-old male with impaired renal function and serious anemia was admitted to our hospital. He had suffered from a disorder of urination since early childhood and been diagnosed as having neurogenic bladder by an urologist when he was 20 years old. Since February 2007, general fatigue emerged and gradually worsened. In addition, he began to feel nauseous around February 2008. He visited a family doctor and was diagnosed with renal failure and anemia both of which were serious. H e was referred t o our office and admitted immediately because his blood test showed a serum creatinine level of 4.4 mg/dL and hemoglobin of 3.1 g/dL. The initial study with ultrasonograhy suggested that both kidneys contained multiple cysts for the most part, likely due to hereditary polycystic kidney disease. However, a subsequent series of diagnostic imaging tests, including computed tomography and magnetic resonance urography, determined that the cause of renal failure was most likely reflux nephropathy due to secondary vesicouretral reflux induced by the chronic neurogenic bladder. Moreover, the upper gastrointestinal endoscopic examination showed that the cause of anemia was probably the persistent bleeding from gastric antral vascular ectasia. Reflux nephropathy emerges in early childhood and slowly progresses to chronic renal failure in some cases. According to the literature, it is not rare as a cause of end-stage kidney failure even among adult populations. Diagnostic imaging of severe reflux nephropathy is apparently similar to that of polycystic kidney disease. We herein present an adult male with chronic renal failure due to reflux nephropathy, the images of which were similar to polycystic kidney disease.