Redução da morbi-mortalidade na síndrome de hellp completa com o uso de altas doses de dexametasona

Objective: To determine the clinical maternal and neonatal outcomes in HELLP syndrome patients treated with dexamethasone who either developed renal injury or renal insufficiency and to identify predictive values of urea and creatinine for the identification of subjects with HELLP syndrome at risk of developing renal insufficiency. Methods: Non-radomized intervention study of dexamethasone use in HELLP syndrome. A total of 62 patients were enrolled at Maternidade Escola Januário Cicco (MEJC). Patients received a total of 30 mg of dexamethasone IV, in three doses of 10 mg every 12 hours. A clinical and laboratory follow up were performed at 24, 48 and 72 hours. Patients were followed up to 6 months after delivery. Patients were grouped in accordance to renal function, i.e, normal and some type of renal lesion. Renal lesion was considered when creatinine was equal or greater than 1.3 mg/dl and diuresis less than 100 ml in 4 hours period and renal insufficiency was defined when dialysis was needed. Results: A total of 1230 patients with preeclampsia were admitted at MEJC. Of those 62 (5%) developed HELLP syndrome. There was no statistical difference in the groups with renal involvement or normal renal function with respect to the demographics, type of anesthesia used and delivery, and weight of the newborn. An improvement in the AST, ALT, LDH, haptoglobine, antithrombine, fibrinogenen and platelets was observed within 72 hours after dexamethosone use. There was a significant increase in the diuresis within the interval of 6 hours before the delivery and 24 hours after it. Of the 62 patients, 46 (74. 2%) had normal renal function and 16 (25.8%) evolved with renal lesion, with 5 (8.1%) needing dialysis. These 5 patients who received dialysis recovered the xi renal function. The delay in administering dexamethasone increased in 4.6% the risk of development of renal insufficiency. Patients with renal insufficiency had received significantly more blood products than subjects without renal lesion (p=0.03). Diuresis, leukocytes, uric acid, urea, creatinine were significantly different between the groups with normal renal function, renal lesion and renal insufficiency. The levels of creatinine 1.2mg/dl and uric acid 51mg/dl, at admission are predictive of subjects who will evolve with renal lesion (p<0.001). Maternal mortality was 3.2%. None of the subjects with renal insufficiency evolved with chronic renal disease. Conclusions: Dexamethasone in patients with HELLP syndrome seems to reduce significantly the hepatic microthrombosis and normalize hemostasis as seen by improvement of liver function. Renal injury can be considered, in HELLP syndrome, when creatinine levels are greater than 1.3 mg/dl and diuresis less than 100 ml/h in interval of 4 hours. The level of creatinine greater than 1.2 mg/dl and urea greater than 51mg/dl are predictive of subjects with HELLP syndrome who will develop renal injury. Patients who receive more red cell packs develop renal insufficiency. Finally, the delay in administering dexamethasone increases the risk of developing renal insufficiency

Influence of educational level on myocardial hypertrophy of hemodialysis patients

Introduction: Chronic renal disease is associated with a high cardiovascular risk. Data from the general population associate cardiovascular diseases with low educational level, but no study has evaluated this association in patients on hemodialysis. Objective: This study aimed at evaluating the association between educational level, hypertension, and left ventricular hypertrophy in patients on chronic hemodialysis. Methods: A standard socioeconomic questionnaire was applied to 79 hemodialysis patients at the Hospital das Clínicas of Faculdade de Medicina de Botucatu, state of São Paulo. Clinical, laboratory and echocardiographic data were obtained from medical records. The patients were divided into two groups according to the median educational level, as follows: G1, patients with three or less years of schooling; G2, patients with more than three years of schooling. Results: Blood pressure, interdialytic weight gain, and variables statistically different in the two groups (p < 0.2) underwent multiple analysis. Independent associations were stated with p < 0.05 in multiple analysis. The mean age of patients was 57 ± 12.8 years, 46 were males (57%), and 53 white (67%). The variables selected for multiple analysis were: age (p = 0.004); educational level (p < 0.0001); body mass index (p = 0.124); left ventricular diameter (p = 0.048); and left ventricular mass index (p = 0.006). Antihypertensive drugs were similar in both groups. Systolic blood pressure (p = 0.006) and years of schooling (p = 0.047) had a significant and independent correlation with left ventricular mass index. Conclusion: In hemodialysis patients, left ventricular mass associated not only with blood pressure but also with educational level.

Panoramic radiography in the diagnosis of carotid artery atheromas and the associated risk factors

Atherosclerosis is a serious chronic disease, responsible for thousands of deaths worldwide and is characterized by thickening and loss of elasticity of the arterial walls, associated with the presence of atheromatous plaques. Various risk factors act directly on predisposition to the disease, among which the following are pointed out: diabetes mellitus, arterial hypertension and inadequate diet and eating habits. More recent researches have elucidated new risk factors acting in the development of this disease, such as, for example: periodontitis, chronic renal disease and menopause. The panoramic radiograph, commonly used in dental practice, makes it possible to see calcified atherosclerotic plaques that are eventually deposited in the carotid arteries. The aim of this review article was to emphasize the dentist's important role in the detection of carotid artery atheromas in panoramic radiographs and the immediate referral of patients affected by these calcifications to doctors. In addition, the study intended to guide the dentist, especially the dental radiologist, with regard to differential diagnosis, which should be made taking into consideration particularly the triticeal cartilage when it is calcified. © Henriques et al.

Unusually rapid growth of brown tumour in the mandible after parathyroidectomy associated with the presence of a supernumerary parathyroid gland

The aim of this study is to report the case of a quick growing brown tumour in the jaw after a parathyroidectomy due to the presence of a rare fifth parathyroid gland. The patient had chronic renal disease and the diagnosis was tertiary hyperparathyroidism. Thirty days after the parathyroidectomy, the patient returned with a significant increase in the tumour size. The suspicion of a supernumerary gland was confirmed by parathyroid scintigraphy. The treatment of brown tumour is dependent on the treatment of the hyperparathyroidism. However, curettage should be considered if a large lesion is disturbing mastication. In conclusion, this case should attract the attention of general practitioner dentists, since they may be the first professionals who have contact with the patient with a brown tumour in the jaws. Likewise, this case emphasises the importance of knowing the type of hyperparathyroidism involved to allow for effective treatment planning. © 2011 European Association for Cranio-Maxillo-Facial Surgery.

Associação entre atividade física e fatores de risco cardiovascular tradicionais e não tradicionais em pacientes em tratamento por hemodiálise

Pós-graduação em Fisiopatologia em Clínica Médica - FMB

Os efeitos do lupus eritematoso sistêmico no sistema urinário de pequenos animais

Systhemic lupus erythematous is a imunomediated disorder witch affects primarly dogs between two and nine years. Clinical manifestations are very diverse, including renal signs, that may lead to chronic renal disease, and dermatologic and joint sings. Systhemic lupus erythematous diagnostic is a challange to the clinician, due to its diverse list of differecial diagnoses and its low availability of specific tests. The treatment consists of corticosteroids and imunomodulators, and supportive therapy that inhibits the progression of the disease. Monitoring the animal with systhemic lupus erythematous is important, due to its recurrent caracteristic

Invariant Natural Killer T Cell Agonist Modulates Experimental Focal and Segmental Glomerulosclerosis

A growing body of evidence demonstrates a correlation between Th2 cytokines and the development of focal and segmental glomerulosclerosis ( FSGS). Therefore, we hypothesized that GSL-1, a monoglycosylceramide from Sphingomonas ssp. with pro-Th1 activity on invariant Natural Killer T ( iNKT) lymphocytes, could counterbalance the Th2 profile and modulate glomerulosclerosis. Using an adriamycin( ADM)-based model of FSGS, we found that BALB/c mice presented albuminuria and glomerular degeneration in association with a Th2-like pro-fibrogenic profile; these mice also expressed a combination of inflammatory cytokines, such as IL-4, IL-1 alpha, IL-1 beta, IL-17, TNF-alpha, and chemokines, such as RANTES and eotaxin. In addition, we observed a decrease in the mRNA levels of GD3 synthase, the enzyme responsible for GD3 metabolism, a glycolipid associated with podocyte physiology. GSL-1 treatment inhibited ADM-induced renal dysfunction and preserved kidney architecture, a phenomenon associated with the induction of a Th1-like response, increased levels of GD3 synthase transcripts and inhibition of pro-fibrotic transcripts and inflammatory cytokines. TGF-beta analysis revealed increased levels of circulating protein and tissue transcripts in both ADM- and GSL-1-treated mice, suggesting that TGF-beta could be associated with both FSGS pathology and iNKT-mediated immunosuppression; therefore, we analyzed the kidney expression of phosphorylated SMAD2/3 and SMAD7 proteins, molecules associated with the deleterious and protective effects of TGF-beta, respectively. We found high levels of phosphoSMAD2/3 in ADM mice in contrast to the GSL-1 treated group in which SMAD7 expression increased. These data suggest that GSL-1 treatment modulates the downstream signaling of TGF-beta through a renoprotective pathway. Finally, GSL-1 treatment at day 4, a period when proteinuria was already established, was still able to improve renal function, preserve renal structure and inhibit fibrogenic transcripts. In conclusion, our work demonstrates that the iNKT agonist GSL-1 modulates the pathogenesis of ADM-induced glomerulosclerosis and may provide an alternative approach to disease management.

Effetti dell'acido urico sulle cellule glomerulari mesangiali: meccanismi intracellulari di trasduzione del segnale e possibili implicazioni nella progressione del danno renale e nella sindrome infiammatoria in corso di nefropatie croniche

Uric acid is a major inducer of inflammation in renal interstitium and may play a role in the progression of renal damage in hyperuricemic subjects with primary nephropathies, renal vascular disease, and essential hypertension. At the same time, UA also acts as a water-soluble scavenger of reactive oxygen species. We evaluated the cellular effects of UA on cultured HMC as a potential interstitial target for abnormally elevated levels in acute and chronic renal disease. Intracellular free Ca2+ ([Ca2+]i) was monitored by microfluorometry of fura 2-loaded cells, while oxidation of intracellularly trapped non-fluorescent 2’,7’-dichlorofluorescein diacetate (DCFHDA, 20 uM) was employed to assess the generation of reactive oxygen species during 12-hr incubations with various concentrations of UA or monosodium urate. Fluorescent metabolites of DCFH-DA in the culture media of HMC were detected at 485/530 nm excitation/emission wavelengths, respectively. UA dose-dependently lowered resting [Ca2+]i (from 102±9 nM to 95±3, 57±2, 48±6 nM at 1-100 uM UA, respectively, p <0.05), leaving responses to vasoconstrictors such as angiotensin II unaffected. The effect was not due to Ca2+/H+ exchange upon acidification of the bathing media, as acetate, glutamate, lactate and other organic acids rather increased [Ca2+]i (to max. levels of 497±42 nM with 0.1 mM acetate). The decrease of [Ca2+]i was abolished by raising extracellular Ca2+ and not due to effects on Ca2+ channels or activation of Ca2+-ATPases, since unaffected by thapsigargin. The process rather appeared sensitive to removal of extracellular Na+ in combination with blockers of Na+/Ca2+ exchange, such as 2’,4’-dichlorobenzamil, pointing to a countertransport mechanism. UA dose-dependently prompted the extracellular release of oxidised DCFH (control 37±2 relative fluorescence units (RFU)/ml, 0.1uM 47±2, 1 uM 48±2, 10 uM 51±4, 0.1 mM 53±4; positive control, 10 uM sodium nitroprusside 92±5 RFU/ml, p<0.01). In summary, UA interferes with Ca2+ transport in cultured HMC, triggering oxidative stress which may initiate a sequence of events leading to interstitial injury and possibly amplifying renal vascular damage and/or the progression of chronic disease.

Glomerulonephropathy in Aged Captive Key Largo Woodrats (Neotoma floridana smalli)

A retrospective review of mortality records of Key Largo woodrats (Neotoma floridana smalli) in a captive breeding program revealed chronic renal disease in 5 of 6 woodrats older than 4 years of age. Two of the 5 woodrats with chronic renal disease also had clinical evidence of diabetes mellitus. Kidneys from all 5 woodrats were examined via light microscopy, histochemical staining, immunohistochemical staining, and transmission electron microscopy. The dietary histories of the affected animals were examined as well. The most striking histopathologic abnormality in the affected kidneys was the presence of large protein casts within cortical and medullary tubules in combination with lesions of membranous glomerulopathy and glomerulosclerosis. Transmission electron microscopy revealed thickening and undulation of the tubular and glomerular mesangial basement membranes with the variable presence of electron-dense deposits within the capillary endothelial basement membrane. Patchy glomerular immunoreactivity for IgG was noted in 2 cases, but IgA and IgM immunoreactivity were not present. The pathologic changes in the kidneys of the Key Largo woodrats mirrored many of the features of chronic progressive nephropathy commonly diagnosed in laboratory rats. Woodrats in the captive population were fed an ad libitum high-protein diet similar to diets that have been shown in laboratory rats to exacerbate the development and progression of chronic progressive nephropathy. It is concluded that Key Largo woodrats develop glomerulonephropathy with features similar to chronic progressive nephropathy described in laboratory rats. Age, concomitant disease, and dietary factors may contribute to the development and severity of this potentially age-limiting disease in Key Largo woodrats.

Physiologic and pathophysiologic fundamentals of proteinuria a review

The term proteinuria is taken to mean abnormally high protein excretion in the urine. Proteinuria is the consequence of glomerular filtration of plasma proteins, their subsequent reabsorption by the proximal tubular cells and secretion of protein by the tubular cells and distal urinary tract. In physiological conditions, the structural integry of the glomerular filtration barrier prevents the abnormal passage of albumin (molecular mass 66 kDa) and high-molecular-weight proteins (> 66 kDa), whereas the passage of low-molecular-weight proteins (< 66 kDa) is almost completely unrestricted. Proteins that arrive the tubular lumen are reabsorbed by endocytosis after binding to the megalin-cubilin complex. An increased load of proteins in the tubular lumen leads to the saturation of the reabsorptive mechanism and higher urinary protein excretion. Proteinuria can originate from prerenal, renal and postrenal causes. Elevated tubular protein concentrations have been recognized to be toxic to tubular cells and associated with the progression of chronic renal disease. Therefore, the quantitative and qualitative evaluation of proteinuria is important for the diagnosis of renal disease.

Risk factors for encephalitis and death from West Nile virus infection: An analysis of hospitalized cases in Houston, Texas from 2002--2008

We conducted a nested case-control study to determine the significant risk factors for developing encephalitis from West Nile virus (WNV) infection. The purpose of this research project was to expand the previously published Houston study of 2002–2004 patients to include data on Houston patients from four additional years (2005–2008) to determine if there were any differences in risk factors shown to be associated with developing the more severe outcomes of WNV infection, encephalitis and death, by having this larger sample size. A re-analysis of the risk factors for encephalitis and death was conducted on all of the patients from 2002–2008 and was the focus of this proposed research. This analysis allowed for the determination to be made that there are differences in the outcome in the risk factors for encephalitis and death with an increased sample size. Retrospective medical chart reviews were completed for the 265 confirmed WNV hospitalized patients; 153 patients had encephalitis (WNE), 112 had either viral syndrome with fever (WNF) or meningitis (WNM); a total of 22 patients died. Univariate logistic regression analyses on demographic, comorbidities, and social risk factors was conducted in a similar manner as in the previously conducted study to determine the risk factors for developing encephalitis from WNV. A multivariate model was developed by using model building strategies for the multivariate logistic regression analysis. The hypothesis of this study was that there would be additional risk factors shown to be significant with the increase in sample size of the dataset. This analysis with a greater sample size and increased power supports the hypothesis in that there were additional risk factors shown to be statistically associated with the more severe outcomes of WNV infection (WNE or death). Based on univariate logistic regression results, these data showed that even though age of 20–44 years was statistically significant as a protecting effect for developing WNE in the original study, the expanded sample lacked significance. This study showed a significant WNE risk factor to be chronic alcohol abuse, when it was not significant in the original analysis. Other WNE risk factors identified in this analysis that showed to be significant but were not significant in the original analysis were cancer not in remission > 5 years, history of stroke, and chronic renal disease. When comparing the two analyses with death as an outcome, two risk factors that were shown to be significant in the original analysis but not in the expanded dataset analysis were diabetes mellitus and immunosuppression. Three risk factors shown to be significant in this expanded analysis but were not significant in the original study were illicit drug use, heroin or opiate use, and injection drug use. However, with the multiple logistic regression models, the same independent risk factors for developing encephalitis of age and history of hypertension including drug induced hypertension were consistent in both studies.^

Impacto de la implementación de un modelo de gestión integral de atención de la enfermedad y cuidado coordinado en la población en diálisis en Colombia

La atención hospitalaria en el costo global de la atención de los pacientes en diálisis es muy importante. Este estudio se realizó con el fin de evaluar resultados posteriores a la implementación de un modelo de gestión de la enfermedad y cuidado coordinado en una red de diálisis en Colombia, evaluando los cambios específicos en las tasas de hospitalización de una cohorte de pacientes renales con dos años de seguimiento. El modelo se enfoca básicamente en mejorar la atención de los pacientes en diálisis protocolizando en el manejo de comorbilidades (diabetes, riesgo cardiovascular, patologías infecciosas) y en el cuidado coordinado entre el tratamiento ambulatorio y hospitalario de los pacientes en diálisis asegurando la continuidad en el proceso de atención de los pacientes. El Estudio observacional analítico de cohortes compuesto por 2 fases una primera cohorte histórica retrospectiva y una segunda con dos cohortes prospectivas, incluyó pacientes mayores de 18 años, con más de 90 días en diálisis, con al menos tres meses de intervención con el modelo de gestión de enfermedad en la red Renal Therapy Services (RTS®). En conclusión, la realización de este estudio, se pudo asociar a la reducción en la atención hospitalaria de pacientes en diálisis y a una menor mortalidad, modelos como este y otras soluciones para mejorar los desenlaces en salud en los pacientes en diálisis deben seguir siendo implementados para aliviar la carga de la enfermedad y reducir los costos de la atención en salud de esta población.

Frequency of coronary artery disease in patients with renal artery stenosis without clinical manifestations of coronary insufficiency

Atherosclerotic renal artery stenosis (RAS) and coronary artery disease (CAD) arise from the same multiple risk factors. The purpose of this study was to assess the frequency of previously undiagnosed CAD in patients with angiographically confirmed RAS, by conducting coronary arteriography in the same setting. of 57 consecutive patients referred for renal arteriography on clinical grounds during a 14-month period, 28 had no RAS and 6 had RAS, but previously documented CAD. of the remainder 23 patients. 17 (74%; CI 56%-92%) had both RAS and CAD (7 single vessel, 4 two-vessel, and 7 multivessel disease). The clinical characteristics, such as age, blood pressure (BP) levels, signs of heart failure, were no different between those with and without CAD, although the 4 diabetic patients, the 4 patients with fundoscopic findings of grade III retinopathy, 11 of 14 with peripheral arterial disease, and 7 of 8 patients with prior stroke belonged in the CAD group. None developed complications as a result of the two consecutive procedures. The data suggest that in patients with RAS the frequency of silent CAD is high and cannot be predicted on clinical grounds alone, therefore coronary angiography should be routinely recommended in the same setting.

Phosphorus Is Associated with Coronary Artery Disease in Patients with Preserved Renal Function

High serum phosphorus levels have been associated with mortality and cardiovascular events in patients with chronic kidney disease and in the general population. In addition, high phosphorus levels have been shown to induce vascular calcification and endothelial dysfunction in vitro. The aim of this study was to evaluate the relation of phosphorus and coronary calcification and atherosclerosis in the setting of normal renal function. This was a cross-sectional study involving 290 patients with suspected coronary artery disease and undergoing elective coronary angiography, with a creatinine clearance >60 ml/min/1.73 m(2). Coronary artery obstruction was assessed by the Friesinger score and coronary artery calcification by multislice computed tomography. Serum phosphorus was higher in patients with an Agatston score >10 than in those with an Agatston score <= 10 (3.63 +/- 0.55 versus 3.49 +/- 0.52 mg/dl; p = 0.02). In the patients with Friesinger scores >4, serum phosphorus was higher (3.6 +/- 0.5 versus 3.5 +/- 0.6 mg/dl, p = 0.04) and median intact fibroblast growth factor 23 was lower (40.3 pg/ml versus 45.7 pg/ml, p = 0.01). Each 0.1-mg/dl higher serum phosphate was associated with a 7.4% higher odds of having a Friesinger score >4 (p = 0.03) and a 6.1% greater risk of having an Agatston score >10 (p = 0.01). Fibroblast growth factor 23 was a negative predictor of Friesinger score ( p = 0.002). In conclusion, phosphorus is positively associated with coronary artery calcification and obstruction in patients with suspected coronary artery disease and preserved renal function.

Chronic NSAID use and long-term decline of renal function in a prospective rheumatoid arthritis cohort study

OBJECTIVES Non-steroidal anti-inflammatory drugs (NSAIDs) may cause kidney damage. This study assessed the impact of prolonged NSAID exposure on renal function in a large rheumatoid arthritis (RA) patient cohort. METHODS Renal function was prospectively followed between 1996 and 2007 in 4101 RA patients with multilevel mixed models for longitudinal data over a mean period of 3.2 years. Among the 2739 'NSAID users' were 1290 patients treated with cyclooxygenase type 2 selective NSAIDs, while 1362 subjects were 'NSAID naive'. Primary outcome was the estimated glomerular filtration rate according to the Cockroft-Gault formula (eGFRCG), and secondary the Modification of Diet in Renal Disease and Chronic Kidney Disease Epidemiology Collaboration formula equations and serum creatinine concentrations. In sensitivity analyses, NSAID dosing effects were compared for patients with NSAID registration in ≤/>50%, ≤/>80% or ≤/>90% of assessments. FINDINGS In patients with baseline eGFRCG >30 mL/min, eGFRCG evolved without significant differences over time between 'NSAID users' (mean change in eGFRCG -0.87 mL/min/year, 95% CI -1.15 to -0.59) and 'NSAID naive' (-0.67 mL/min/year, 95% CI -1.26 to -0.09, p=0.63). In a multivariate Cox regression analysis adjusted for significant confounders age, sex, body mass index, arterial hypertension, heart disease and for other insignificant factors, NSAIDs were an independent predictor for accelerated renal function decline only in patients with advanced baseline renal impairment (eGFRCG <30 mL/min). Analyses with secondary outcomes and sensitivity analyses confirmed these results. CONCLUSIONS NSAIDs had no negative impact on renal function estimates but in patients with advanced renal impairment.