Navegando por Palavras-chave "insuficiência renal"
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- ItemAcesso aberto (Open Access)Anemia crônica e glomerulopatia secundárias à Doença de Depósito das Cadeias Leves(Associação Brasileira de Hematologia e Hemoterapia e Terapia Celular, 2004-01-01) Silveira, Ítala P.; Jerônimo, Antonio L. C.; Silva, Herivaldo F.; Nogueira, José O. L.; Correia, José W.; Moura, Luiz Antonio Ribeiro de [UNIFESP]; Hospital Geral Dr. César Cals Departamento de Clínica Médica; Universidade Federal de São Paulo (UNIFESP)The authors present a case of a 65-year-old female patient, with chronic anemia associated with glomerulopathy manifested as proteinuria, cylindruria and renal failure. There were high serum and urinary levels of light chains and the diagnosis was performed by renal biopsy, examined using immunofluorescence and by electron microscopy that showed light chain paraproteins. Nephropathy of light-chain deposition disease occurs due to an over-production of light chains from immunoglobulins produced by B lymphocytes with a deposit in tubular and glomerular membranes.
- ItemSomente MetadadadosEfeito da administração da n-acetilcisteína na reposição volêmica sobre a lesão renal induzida por choque hemorrágico em ratos(Universidade Federal de São Paulo (UNIFESP), 2014-08-27) Moreira, Miriam Aparecida [UNIFESP]; Martins, Jose Luiz Martins [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Objective: To evaluate the effect of N-acetylcysteine on renal injury due to controlled hemorrhagic shock in rats. Method: hemorrhagic shock was induced in Wistar rats by withdrawing blood to reach mean arterial blood pressure to 35 ± 5 mmHg for 60 minutes blood. After this period, the animals were distributed randomly into two groups according to treatment: Ringer lactate group (RL), resuscitated with Ringer's lactate 33mL/Kg and N-acetylcysteine group (NAC), resuscitated with Ringer's lactate and 150mg/Kg of N-acetylcysteine and 50% of blood drawn for both groups. A third group of animals (control group) was submitted of catheterization procedure without inducing shock. After fluid resuscitation, the animals were observed for 120 minutes and euthanized. Results: NAC attenuated renal dysfunction, indicated by lower plasma creatinine in the group of animals treated with NAC compared to the RL group (0.39±0.1 vs 2.9±1.6 mg/dL, P<0.0001). The animals treated with NAC had less oxidative stress with lower values of TBARS tissue, nitric oxide and superoxide anion when compared with the RL group (0.60± 0.05 vs 1.3±0.2 nmol/mL protein,.184.7±20 vs 381.3±93 nM and 4.3±0.4 vs 18.2 ± 3.1%, P<0.0001, respectively) and apoptosis observed by the lower expression of Bax, cytochrome c and caspase 3 proteins in animals treated with NAC as compared to animals of RL group (0,9±0.06 vs 7.1±1.3; 0.3±0.3 vs 17.8±2.8; 3.8±0.4 vs. 10.0±1.5%, P<0.0001; respectively). NAC attenuated the morphological changes that were induced by the shock and larger diameter of the glomeruli when compared to the other two groups. Conclusion: NAC associated with fluid resuscitation attenuated renal injury in rats previously submitted to controlled hemorrhagic shock. NAC promotes improvement of morphological and functional changes and decreased oxidative stress and apoptosis of the kidney.
- ItemAcesso aberto (Open Access)Manifestações renais na síndrome de Joubert(Sociedade de Pediatria de São Paulo, 2009-06-01) Weiss, Ana Paula [UNIFESP]; Andrade, Maria Cristina de [UNIFESP]; Carvalhaes, João Tomás de Abreu [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)OBJECTIVE:To describe the case of a patient with Joubert syndrome associated with renal impairments. CASE DESCRIPTION: A 2 month-old patient was admitted with hypotonia and hyperpneia. At the physical exam, besides irregular breathing pattern, abnormal eye movements and arterial hypertension without abnormalities in cardiac or pulmonary sounds were observed. At the initial clinical and laboratorial investigations, cardiac and pulmonary causes were excluded. The diagnostic hypothesis was: neurological illness associated with renal disease. Laboratorial analysis showed respiratory alkalosis, metabolic acidosis and hyperkalemia, with normal renal function. In the magnetic resonance, images of neurological alterations were compatible with the molar tooth sign, frequently associated with Joubert syndrome. Renal investigation was performed and cystic images in renal parenchyma were found. COMMENTS: Cardiac and pulmonary illness are frequently associated with clinical manifestations such as tachypnea and metabolic alterations. Nevertheless, neurological investigation may be necessary, since some diseases that affect the central nervous system may manifest these signs and symptoms. Association between renal alterations and central nervous system malformations are frequent in several diseases and should be investigated. Joubert syndrome and its associated disorders are characterized by aplasia of the cerebellar vermis, ataxia, abnormal eye movements and irregular breathing pattern with psychomotor and mental delay. The most frequent renal problems associated with the disease are renal cysts and nephronophtisis that can progress to end-stage renal failure.
- ItemAcesso aberto (Open Access)Microangiopatias trombóticas: púrpura trombocitopênica trombótica e síndrome hemolítico-urêmica(Sociedade Brasileira de Nefrologia, 2010-09-01) Polito, Maria Goretti [UNIFESP]; Mastroianni Kirsztajn, Gianna [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Thrombotic microangiopathies (TMAs) are pathological conditions characterized by generalized microvascular occlusion by platelet thrombi, thrombocytopenia, and microangiopathic hemolytic anemia. Two typical phenotypes of TMAs are hemolytic- uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP). Other disorders occasionally present with similar manifestations. Depending on whether renal or brain lesions prevail, two pathologically indistinguishable but somehow clinically different disorders have been described: HUS and TTP. Injury to the endothelial cell is the central and likely inciting factor in the sequence of events leading to TMA. Loss of physiological thromboresistance, leukocyte adhesion to damaged endothelium, complement consumption, abnormal von Willebrand factor release and fragmentation, and increased vascular shear stress may then sustain and amplify the microangiopathic process. Intrinsic abnormalities of the complement system and of the von Willebrand factor pathway may account for a genetic predisposition to the disease that may play a paramount role in particular in familial and recurrent forms. In the case of diarrhea-associated HUS (D+HUS), renal endothelial damage is mediated (at least in large part) by the bacterial agent Shigatoxin (Stx), which is actually a family of toxins elaborated by certain strains of Escherichia coli and Shigella dysenteriae. Outcome is usually good in childhood, Shiga toxin-associated HUS, whereas renal and neurological sequelae are more frequently reported in adult, atypical, and familial forms of HUS and in TTP. Recent studies have demonstrated that deficiency in the von Willebrand factor cleaving protease ADAMTS13, due to deficiency of ADAMTS13 can be genetic or more common, acquired, resulting from autoimmune production of inhibitory anti-ADAMTS13 antibodies, that causes TTP. During the last decade, atypical HUS (aHUS) has been demonstrated to be a disorder of the complement alternative pathway dysregulation, as there is a growing list of mutations and polymorphisms in the genes encoding the complement regulatory proteins that alone or in combination may lead to aHUS. Approximately 60% of aHUS patients have so-called 'loss-of-function' mutations in the genes encoding the complement regulatory proteins, which normally protect host cells from complement activation: complement factor H (CFH), factor I (CFI) and membrane cofactor protein (MCP or CD46), or have 'gain-of-function' mutations in the genes encoding the complement factor B or C3. In addition, approximately 10% of aHUS patients have a functional CFH deficiency due to anti-CFH antibodies. Although TMAs are highly heterogeneous pathological conditions, one-third of TMA patients have severe deficiency of ADAMTS13. Platelet transfusions are contraindicated. Plasma infusion or exchange (PE) is the only treatment of proven efficacy.