Marcadores biológicos para necrose tubular aguda em pacientes com doença glomerular / Biological markers for acute tubular necrosis in patients with glomerular disease

INTRODUCTION: Acute kidney injury (AKI) is a common complication in patients with nephrotic syndrome (NS), and it is reported in 34% of adults with idiopathic nephrotic syndrome. Emergence of AKI in the course of nephrotic syndrome requires a prompt differential diagnosis between acute tubular necrosis (ATN) and proliferative glomerular lesions leading to rapidly progressive glomerulonephritis. Although clinical and conventional laboratory clues can be decisive in many cases, sometimes such distinctions rely on renal biopsy, which is an invasive procedure and is not available in many centers. Several new biomarkers have emerged, increasing the perspective on early diagnosis and the prognostic prediction of AKI. OBJECTIVES: In this work, we studied the use of tests based on the urinary concentrations of kidney injury molecule-1 (KIM-1)...

INTRODUÇÃO: A lesão renal aguda (LRA) é uma complicação frequente em pacientes com glomerulopatias, acomentendo até 34% dos adultos com síndrome nefrótica (SNO) idiopática. O diagnóstico diferencial de necrose tubular aguda (NTA) de glomeulonefrite proliferativa ou crescêntica em pacientes com SNO e LRA é fundamental, visto que a NTA pode mimetizar quadro de glomerulonefrite rapidamente progressiva. Dados clínicos e laboratoriais podem ser úteis no diagnóstico diferencial da LRA na SNO, entretanto a distinção entre NTA e glomerulonefrite proliferativa ou crescêntica é feito pela biópsia renal, procedimento invasivo e que não está disponível amplamente. Novos biomarcadores para diagnóstico precoce e preditores diagnósticos na LRA têm sido identificados. OBJETIVOS: Neste trabalho nós avaliamos o uso de testes baseados nas concentrações urinárias de kidney injury molecule-1 (KIM-1)...

Marcadores de necrose tubular aguda e lesão inflamatória glomerular no sedimento urinária de pacientes com síndrome / Acute tubular necrosis markers and inflammatory glomerular injury urinary sediment syndrome patients

Necrose tubular aguda (NTA) é a causa mais frequente de lesão renal aguda (LRA) em pacientes hospitalizados. Em pacientes com síndrome nefrótica (SNO), a NTA mimetiza, por vezes, quadro de glomerulonefrite rapidamente progressiva e requer instituição precoce de imunossupressores. A análise do sedimento urinário é uma ferramenta não invasiva, de baixo custo e ampla disponibilidade. O achado de células epiteliais no sedimento urinário de pacientes com LRA foi associado ao diagnóstico de NTA. Entretanto, estudos em pacientes com SNO associada são escassos. Técnicas de diagnóstico utilizando sedimento urinário corado normalmente não são utilizadas nesses casos. Além do mais, o sedimento urinário é uma importante fonte de proteínas; estudos proteômicos do sedimento urinário revelaram importantes frações de proteínas não encontradas em sobrenadante, que pode ser usado como potencial biomarcador de LRA. Nosso objetivo é identificar alterações citológicas e protéicas no sedimento urinário que permitam o diagnóstico diferencial entre NTA ou lesão inflamatória-proliferativa glomerular (INF) em pacientes com SNO. Trata-se de um estudo de corte transversal, onde foram incluídos 32 pacientes: 5 pacientes normais (grupo controle), 10 com NTA, 9 sem NTA e 8 com glomerulonefrites exsudativas. As células do sedimento urinário foram contadas, citocentrifugadas, coradas em hematoxilina/eosina ou Papanicolaou e contadas diferencialmente como pequenas (<30μm de diâmetro), médias (30-48μm)...

Acute tubular necrosis (ATN) is the most frequent cause of acute kidney injury (AKI) in hospitalized patients. In patients with nephrotic syndrome (NS), acute tubular necrosis mimic, sometimes, rapidly progressive glomerulonephritis and requires premature institution of immunosuppressive treatment. The analysis of urinary sediment is a noninvasive tool, low cost and wide availability. The found of epithelial cells in the urinary sediment of patients with AKI was associated to ATN diagnosis. However, studies in patients with AKI in the set of NS are scarce. Diagnostics techniques using stained urinary sediment are not ordinarily used in these cases. Furthermore, urinary sediment is an important source of proteins; proteomic studies revealed important fractions of proteins not found in urinary supernatant that could be used as potential biomarkers for AKI. Our goal is identify cytological alterations and protein in urinary sediment which allow the differential diagnosis between ATN and inflammatory-proliferative glomerular lesion (INF) in patients with NS. This is a cross sectional study, in which 32 patients were included: 5 normal patients (control group), 10 with ATN, 9 without ATN and 8 with exudative glomerulonephritis. The cells of urinary sediment were counted, cytocentrifuged, stained of hematoxylin/eosin or Papanicolaou and differentially counted as small (<30μm of diameter), medium (30-48μm)...

[Protective effect of Captopril and Allopunnol against renal warm ischemia reperfusion injury in dogs]

Captopril and Allopurinol have protective effect against renal warm ischemia with different mechanisms. The aime of this study was to evaluate this protective effect against induced 1 hour warm ischemia in dog's kidneys. This experimental study was done in the year 2006. We performed the operation on 15 healthy dogs. During these procedures both kidneys were clamped for 1 hour, then left kidney was removed for pathologic evaluation and right kidney remained insitue for functional assessment. Five random dogs received 1 [mg/kg]d[day] Captopril orally before and after surgery [captopril group]; another five dogs received 10 [mg/kg]/day Allopurinol orally before and after surgery [allopurinol group]. Five dogs of control group received no drugs. Serum urea and creatinine were measured preoperatively and on postoperative days of 1, 3, 5, 10 and 16 in all groups. Serum levels of urea and creatinine elevated in all groups but in Captopril group maximum levels of urea and creatinine were significantly lower than control [P<0.05]. In Allopurinol group the maximum rise of creatinine was significantly lower in comparison to control group [p< 0.05], but the maximum levels of urea in this group had no significant difference when compared with control values [p< 0.05]. There was no significant difference in pathologic changes in the three groups. One hour warm ischemia results in ATN so it is not safe for dog's kidneys. Althogh Captopril and Allopurinol do not prevent ATN after one hour warm ischemia; they can reduce its severity and improve renal function after warm ischemia