Tumor lysis syndrome

A síndrome da lise tumoral é caracterizada por complicações metabólicas e desenvolvimento de insuficiência renal aguda, em geral ocorrendo em pacientes com neoplasias linfoproliferativas e após o início do tratamento quimioterápico. A hiperuricemia é o distúrbio metabólico mais característico, ocorrendo também hiperfosfatemia, hipocalcemia e hipercalemia. A insuficiência renal é decorrente principalmente da deposição de urato nos túbulos renais. Hidratação vigorosa e administração de alopurinol constituem o manejo principal da síndrome. Identificação precoce e instituição de medidas preventivas são importantes para que se evite o desenvolvimento de dano renal.Tumor lysis syndrome is characterized by metabolic derangements and development of acute renal failure, generally occurring in patients with lymphoproliferative malignancies after chemotherapy initiation. Hyperuricemia is the most characteristic metabolic abnormality, with presence of hyperphosphatemia, hypocalcemia and hyperkalemia as well. Renal failure mainly results from urate deposition on renal tubules. Vigorous hydration and allopurinol administration are the main management options. Early recognition and institution of preventive measures are important to avoid renal impairment

Acute renal failure : review

A insuficiência renal aguda é um problema clínico freqüente em pacientes hospitalizados (5%), principalmente em unidades de terapia intensiva. Apesar dos avanços na medicina, a insuficiência renal aguda ainda está associada a uma mortalidade que pode variar de 50 a 80%. Esta revisão aborda os aspectos relevantes quanto ao diagnóstico, patogênese, prevenção e tratamento da insuficiência renal aguda.Acute renal failure is a common clinical problem in hospitalized patients (5%), particularly in intensive care units. Despite the advances in medical care, acute renal failure is still associated with a mortality rate ranging from 50 to 80%. This review discusses diagnosis, pathogenesis, prevention and treatment of acute renal failure

Clinical treatment of chronic renal failure

A insuficiência renal crônica é um diagnóstico sindrômico, causado por inúmeras doenças. Independente da causa básica, a perda de um certo número de néfrons funcionantes desencadeia processos comuns, envolvendo fatores hemodinâmicos glomerulares, fatores de crescimento, mediadores inflamatórios e outros, que levam à esclerose glomerular e à fibrose intersticial, num ciclo progressivo de deterioração da filtração glomerular. Os médicos freqüentemente subestimam as conseqüências e as implicações terapêuticas deste processo que inicia quando a bioquímica e a clínica ainda são aparentemente normais. Quase metade dos pacientes que chega à insuficiência renal terminal não teve acompanhamento médico ou mesmo conhecimento prévio da sua situação. O encaminhamento tardio ao nefrologista tem sido muito discutido como um problema que aumenta a morbi-mortalidade dos pacientes urêmicos antes e depois do início do tratamento dialítico e eleva custos. O objetivo desta revisão é dar orientações gerais sobre o manejo conservador da insuficiência renal crônica, sugerindo atitudes que devam ser tomadas em conjunto com o nefrologista ou a este referenciadas. O manejo destes pacientes inclui abordagem da doença renal básica e de danos renais agudos adicionais; prevenção da progressão da insuficiência renal; manejo de co-morbidades; tratamento de complicações da uremia; monitorização da função renal e do estado nutricional; educação do paciente e preparo para diálise e transplante. A terapia nutricional e o controle da hipertensão são medidas importantes para prevenir perda de função renal, mas outros fatores devem ser reconhecidos.Chronic renal failure is a syndromic diagnosis caused by various diseases. Regardless of the etiology, the loss of a certain number of functioning nephrons triggers common processes involving glomerular hemodynamics and growth factors, inflammatory mediators, and others that lead to glomerular sclerosis and interstitial fibrosis in a rogressive cycle of deterioration of the glomerular filtration. Physicians often underestimate the prognostic and therapeutic consequences of this process, which begins when biochemical and clinical findings are still apparently normal. Almost half of the patients who reach end-stage renal disease did not have proper medical assistance or even previous knowledge of the situation. Late referral to a nephrologist has been widely discussed as it increases the morbi-mortality of uremic patients, before andafter the beginning of dialysis, and as it increases treatment costs. Our objective is to provide general guidelines regarding the conservative treatment of chronic renal failure, suggesting measures that should be understood and carried out by, or together with, those indicated by a nephrologist. The treatment of end-stage renal disease patients includes: an approach to the primary renal disease and to additional acute renal damages; preventing the progression of renal failure; treatment of comorbidities; treatment of uremia complications; monitoring of renal function and nutritional status; patient education and preparation for dialysis and transplantation. Nutritional therapy and control of arterial hypertension are important measures in order to prevent loss of renal function; however, other factors should also be considered

Proteinuria : clinical and laboratory evaluation

Neste artigo, apresentamos uma revisão geral dos aspectos clínicos e laboratoriais do paciente com proteinúria. A proteinúria reflete um aumento na permeabilidade do capilar glomerular. São descritos três tipos básicos de proteinúria: glomerular, tubular ou por aumento da produção. A proteinúria assintomática também pode ser dividida em três categorias: transitória, ortostática e persistente. A avaliação desses pacientes com proteinúria deve começar com o exame comum de urina, repetido pelo menos duas vezes. O sedimento urinário também deve ser feito, procurando-se sinais de comprometimento glomerular, como: hematúria dismórfica, cilindros hemáticos ou lipidúria. Uma cuidadosa história médica é importante, buscando-se a presença de hipertensão, diabetes melito, insuficiência cardíaca congestiva ou história prévia de doença renal. A proteinúria persistente pode ser avaliada através da medida na urina de 24 horas ou medindo-se a proteinúria e a creatinina em amostra isolada de urina. A amostra de urina aleatória é um método simples, rápido e com boa correlação com a urina de 24 horas. A quantidade de proteinúria excretada é importante, do ponto de vista prognóstico, nos pacientes com doença glomerular primária, tais como: glomerulonefrite membranosa, glomerulonefrite por IgA, glomeruloesclerose segmentar e focal. Nesses pacientes, quanto maior for a proteinúria, maior será o risco de lesão renal.In this paper, we present a general review of clinical and laboratory approaches to patients with proteinuria. Proteinuria reflects an increase in glomerular capillary permeability. There are three basic types of proteinuria: glomerular, tubular, and overflow. Asymptomatic proteinuria can also be divided into three categories: transient or intermittent, orthostatic, and persistent. The evaluation of patients with proteinuria should begin by testing the urine on at least two different occasions. The urine sediment should also be examined, searching for other signs of glomerular disease, such as dysmorphic hematuria, red cell casts or lipiduria. A careful medical history is also indicated, searching for hypertension, diabetes mellitus, congestive heart failure or previous history of renal disease. Persistent proteinuria can be evaluated by a 24-hour urine collection or a random urine protein-to-creatinine ratio. The random urine sample can be simply and quickly obtained and presents good correlation with the 24-hour urine evaluation. The degree of proteinuria is prognostically important in patients with primary glomerular disease, such as membranous glomerulonephritis, IgA glomerulonephritis or focal and segmental glomerulosclerosis. The higher the proteinuria, the higher the risk of renal injury for these patient

Proteinuria : clinical and laboratory approach

Proteinúria é um forte indicador de doença renal, e está presente em diversas síndromes. No presente artigo, os mecanismos fisiopatológicos que levam à proteinúria foram revisados, assim como os métodos disponíveis para sua detecção e quantificação, incluindo a fita reagente, proteinúria de 24 horas e o índice proteína/creatinina na urina. Atenção especial é dada à avaliação clínica dos pacientes com proteinúria, abordando os exames disponíveis e as situações em que são indicados. Um fluxograma para a investigação de pacientes com proteinúria é apresentado. Também ressaltamos a importância da proteinúria persistente na sua relação com a progressão de doenças renais.Proteinuria is a strong indicator of renal disease and it is present in many syndromes. Our objective is to review the pathophysiological mechanisms that lead to proteinuria, as well as the available methods for its detection and quantitation, including the dipstick, 24-hour proteinuria, and the urinary protein-creatinine ratio. We gave special attention to clinical evaluation of proteinuric patients, including the available exams and the situations in which they are indicated. An algorithm for the investigation of patients with proteinuria is presented. We also emphasized the importance of persistent proteinuria in its relation with the progression of renal diseases

Renal artery stenosis

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The spectrum of biopsy-proven glomerular diseases in a tertiary Hospital in Southern Brazil

Background: The prevalence and distribution of glomerular diseases difer among countries, and the indication to perform a kidney biopsy varies among centres. In this study, we assessed the prevalence of primary and secondary glomerulopathies based on histological diagnoses, and the correlation between glomerulopathies and demographic and clinical data was evaluated. Methods: In this study, 1051 kidney biopsies were retrospectively reviewed between 2000 and 2018. Patient demographic, clinical and laboratory data were assessed. The prevalence of primary glomerulonephritis (PG) and secondary glomerulopathies (SG), as well as tubulointerstitial diseases (TIDs), hereditary nephropathies (HNs) and other diagnoses, were determined. The frequency of primary and secondary glomerulopathies was evaluated by age group, and the temporal variation in frequencies across three time periods (2000-2005, 2006-2011, and 2012-2018) was reported. Results: The prevalence of SG predominated (52.4%), followed by PG (29.6%), other diagnoses (10.7%), TID (6.6%) and HN (1.1%). Among the primary forms of glomerular disease, focal segmental glomerulosclerosis (FSGS) was the most common (37.3%), followed by IgA nephropathy (IgAN, 24.4%), membranous nephropathy (MN, 18.6%) and minimal change disease (MCD, 8.4%). Lupus nephritis (LN, 41.1%) was most common in patients with SG, followed by diabetic kidney disease (DKD, 17.8%), systemic vasculitis (SV, 10.2%) and secondary FSGS (2nd FSGS, 10%). Nephrotic syndrome was the most common clinical presentation in patients with PG and also in patients with DRD and 2nd FSGS, whereas in patients with IgAN and SV, nephritic syndrome was the main presentation. For the age group between 18 and 50 years, LN, FSGS and IgAN predominated; for patients aged between 51 and 65 years, the proportion of DKD and 2nd FSGS increased, and SV was more common in patients >65 years. The temporal variation in PG across the three time periods showed a statistically signifcant increase in IgAN (p =0.001) and a reduction in FSGS over time (p <0.001). In SG, there was a reduction in LN (p =0.027) and an increase in DKD (p <0.001) over time, with a tendency for 2nd FSGS to decrease over time (p =0.053). Conclusions: In the studied kidney biopsy registry, FSGS and IgAN were the most prevalent diagnoses in patients with PG, and LN and DKD were the most prevalent in patients with SG. Nephrotic syndrome was the major indication for biopsy. When comparing the temporal variation in glomerulopathies, there was a reduction in FSGS and an increase in IgAN in patients with PGs over time, and for patients with SGs, there was a reduction in LN with an increase in cases of DKD over time