Bleeding complications after transcutaneous kidney biopsy in patients with systemic amyloidosis: single-center experience in 101 patients.

BACKGROUND: Bleeding is one of the most common complications after kidney biopsy. Amyloidosis is thought to be 1 of the risk factors, but this has not been confirmed in a large study. We performed this study to assess the risk of bleeding after kidney biopsy in patients with amyloidosis. STUDY DESIGN: Retrospective study. SETTINGS & PARTICIPANTS: 101 patients with and 188 patients without amyloidosis undergoing outpatient percutaneous kidney biopsy at a major medical center in the absence of abnormal partial thromboplastin time, prothrombin time international normalized ratio, or platelet count and/or uncontrolled hypertension. PREDICTOR: Clinical diagnosis of amyloidosis. OUTCOMES & MEASUREMENTS: Post-kidney biopsy bleeding confirmed by means of imaging. Bleeding was defined as major if it required blood transfusion, hospital admission, or other invasive procedures and minor if none of these interventions were needed. RESULTS: Post-kidney biopsy bleeding was observed in 9.9% of patients with amyloidosis and 10.6% of controls (P = 0.8). Bleeding was major in 4% of patients with amyloidosis and 2.1% of controls (P = 0.4). Three patients from each group required blood transfusions and selective renal angiography. All except 1 patient from the control group underwent embolization. LIMITATIONS: Retrospective data analysis and overall low event rate did not allow for independent risk-factor analysis. CONCLUSIONS: The present study suggests that in the absence of a hematostatic disorder and/or uncontrolled hypertension, bleeding risk during kidney biopsy is not increased in patients with systemic amyloidosis. Kidney biopsy can be performed safely using the same screening criteria as for patients without amyloidosis.

Potential role of the ubiquitin-proteasome system in atherosclerosis: aspects of a protein quality disease.

Misfolded or damaged proteins are recognized intracellularly by protein quality mechanisms. These include chaperones and the ubiquitin-proteasome system, which aim at restoration of protein function and protein removal, respectively. A number of studies have outlined the functional significance of the ubiquitin-proteasome system for the heart and, as of recently, for the vascular system. This review summarizes these recent findings with a focus on atherosclerosis. In particular, this paper reflects on the viewpoint of atherosclerosis as a protein quality disease.

The enzyme CD38 (a NAD glycohydrolase, EC 3.2.2.5) is necessary for the development of diet-induced obesity.

Obesity is one of the major health problems of our times. Elucidating the signaling mechanisms by which high-fat caloric diet induces obesity is critical for the understanding of this condition and for the development of therapeutic strategies for its treatment. Here, we demonstrate a novel role for protein CD38 as a regulator of body weight during a high-fat diet. CD38 is a ubiquitous enzyme that catalyzes the synthesis of second messengers and has been implicated in the regulation of a wide variety of signaling pathways. We report that CD38-deficient mice are protected against high-fat diet-induced obesity owing to enhanced energy expenditure. In fact, calorimetric studies indicate that CD38-deficient animals have a higher metabolic rate compared to control mice. Analysis of the mechanism revealed that this resistance to diet-induced obesity is mediated at least in part via a NAD-dependent activation of SIRT-PGC1alpha axis, a well-established cascade, involved in the regulation of mitochondrial biogenesis and energy homeostasis. Thus, together these results identify a novel pathway regulating body weight and clearly show that CD38 is a nearly obligatory component of the cellular cascade that led to diet-induced obesity.

A proliferative glomerulonephritis secondary to a monoclonal IgA.

A distinct entity mimicking immune-complex-mediated glomerulonephritis characterized by a proliferative glomerulonephritis with monoclonal immunoglobulin G (IgG) deposits recently was described. We now report a case of a 35-year-old woman who presented with sudden onset of edema, proteinuria, hematuria, and hypertension. Renal biopsy showed diffuse endocapillary proliferation, mesangial cellularity, and amorphous material in the mesangium. Immunofluorescence examination showed mesangial and capillary wall staining for IgA (2+), C3 (2+), fibrinogen (2+), and lambda (2+). Congo red stain was negative. Electron microscopy showed mesangial and subendothelial deposits with a paracrystalline lattice-like substructure forming parallel linear arrays. Extensive laboratory evaluation showed a small population of monoclonal plasma cells with lambda restriction. The present case suggests that monoclonal IgA deposits also can cause proliferative glomerulonephritis. However, the presence of paracrystalline deposits in association with monoclonal IgA deposits has not been described previously.

Role of the second-messenger cyclic-adenosine 5'-diphosphate-ribose on adrenocorticotropin secretion from pituitary cells.

We examined the role of the second-messenger cyclic-ADP-ribose (cADPR) on the regulation of ACTH secretion using AtT20 corticotroph tumor cell line. We found that the cADPR antagonist, 8-Br-cADPR, substantially diminished the secretion of ACTH induced by CRH and potassium in these cells, whereas xestospongin C, an inositol 1,4,5-triphosphate receptor antagonist, had no effect. In addition, the cADPR agonist, 3-deaza-cADPR, augmented ACTH secretion. The presence of the components of the cADPR system, namely ryanodine receptor, CD38, and cADPR itself, was determined in AtT20 cells. Furthermore, we observed that antagonists of the ryanodine channel and cADPR system can decrease the potassium-induced Ca2+ transients in these cells. These results suggest that cADPR is a second messenger in pituitary cells and regulates ACTH secretion by a mechanism dependent on activation of the ryanodine channel by extracellular Ca2+.

Perfil dos pacientes participantes do Clube da Amizade do Servico de Saude Mental Melanie Klein: Hospital Psiquiatrico Sao Pedro - POA/RS

Os autores se propoem a tracar o perfil dos portadores de doenca mental que frequentam o Clube da Amizade, bem como o numero de reinternacoes pos-ingresso nessa modalidade de tratamento. Para tanto, foi selecionada uma amostra de 35 pacientes que apresentaram 80 por cento ou mais de frequencia ao Clube da Amizade no periodo de agosto de 95 a agosto de 96. Para tal, foi realizada consulta ao livro de presenca do Clube, questionario e consulta ao prontuario medico. O aspecto mais relevante obtido nesse levantamento e analise descritiva dos dados e de que 57,14 por cento dos pacientes nao internaram apos o ingresso no Clube da Amizade. Sugerem-se novos procedimentos para enriquecer os resultados.