46503631
ACP Journal Club. Urine dipstick readings ≥ 1+ had limited sensitivity but high specificity for detecting albuminuria in adults.
11453581
Proinflammatory effects of oxidative stress in chronic kidney disease: role of additional angiotensin II blockade.
Oxidative stress plays an important role in causing progressive chronic kidney disease (CKD). We examined the influence of add-on ANG II receptor blockade administered as losartan (50 mg/day for 1 mo) on oxidative stress and proinflammatory state of the kidney in patients with CKD. All subjects were taking an angiotensin-converting enzyme inhibitor plus other antihypertensive agents. Oxidative stress to lipids and proteins was measured by an HPLC assay for malondialdehyde (MDA) and carbonyl concentration, respectively. Urinary inflammation was measured by monocyte chemotactic protein-1 (MCP-1) excretion rate. The etiology of CKD was type 2 diabetes mellitus in 12 and glomerulonephritis in 4 patients. There was no change in proteinuria or 24-h ambulatory blood pressure (BP) with add-on ANG II receptor blockade with losartan therapy. Before losartan therapy, urinary protein and albumin oxidation were 99 and 71% higher, respectively, compared with in plasma (P < 0.05). There was a 35% reduction in urinary oxidized albumin with add-on losartan therapy (P = 0.036). Urinary and plasma MDA were elevated compared with age-matched controls. Urinary MDA was significantly reduced from 4.75 +/- 3.23 to 3.39 +/- 2.17 micromol/g creatinine with add-on losartan therapy. However, plasma MDA or oxidized proteins did not change in response to additional ANG II blockade. A good correlation was seen between the change in urinary oxidized albumin and MCP-1 levels (r = 0.61, P = 0.012). These data demonstrate that oxidative damage to urinary protein and lipids can be reduced with additional ANG II receptor blockade, independently of reductions in proteinuria or BP. Urinary measurements of markers of oxidative damage to lipids and proteins appear to be more sensitive than plasma measurements in patients with CKD. The significant association of the change in urinary MCP-1 with a reduction in oxidative stress supports the role of the redox state in the kidney with renal fibrosis and progressive kidney damage.
22176722
Alar web in cleft lip nose deformity: study in adult unilateral clefts.
BACKGROUND
The correction of alar webbing in unilateral cleft lip nose deformity is challenging because of progressive distortions in the alar web region during the period of growth. Alar webbing is a persistent universal deformity in both the primary and secondary cleft lip noses. The purpose of this article is to study the alar web deformity in adult patients with unilateral cleft lip noses.


METHODS
Twenty-five patients aged 13 years and older presenting with unilateral cleft nasal deformity were included. Preoperative and postoperative measurements of the nose, along with detailed intraoperative recording of the deformed anatomy, were done. Preoperative magnetic resonance imaging was also done in selected cases. Transcolumellar open rhinoplasty was performed in all the cases, and nasal septal straightening with centralization was done. Cleft alar base augmentation was done using bone graft to restore symmetry of the nasal tripod. Both the cleft and noncleft alar cartilages were extensively mobilized from the skin and mucosal sides. The overgrown and caudally slumped cleft-side alar cartilage was resected caudally and was then resuspended in a symmetrical position with the noncleft alar cartilage. A midline-strut septal cartilage extension graft was used to restore the tip aesthetics. The skin overlying the alar web was in-rolled after semilunar cartilage resection, and skin excision was also done to restore symmetry with the opposite vestibule. The remaining secondary cleft nasal and lip deformities were corrected depending upon the specific presenting pathologic abnormality.


RESULTS
The cleft alar cartilage was found to be caudally displaced in all the cases. The caudal border of the lateral crus was prolapsing in the cavity of the vestibule on the superomedial aspect and was tenting the skin in the area of the weak triangle, producing the characteristic alar web deformity. In the study group, the maximum width of the cleft alar cartilage at the level of the lateral crus was increased by approximately 4 mm when compared with the noncleft alar cartilage. The before- and after-rhinoplasty surgery results were objectively assessed using a patient, surgeon, and independent observer survey. The cosmetic result of the nasal tip complex was found to be very good and good (90%), satisfactory (5%), and poor (5%) in patients.


CONCLUSIONS
The alar web in unilateral cleft lip nose deformity is the result of caudal overgrowth and migration of the alar cartilage. The caudal edge of the prolapsed lateral crus overhangs the cleft-side nasal aperture on its superomedial aspect, producing this deformity. Satisfactory correction of this deformity should envisage caudal resection and repositioning of the dislocated alar cartilage along with caudal resection of the lateral crus with in-rolling of the skin after resection to achieve symmetric results in unilateral cleft lip rhinoplasty.
36005104
Volume Overload in Dialysis: The Elephant in the Room, No One Can See
interests of the authors. However, considering the totality of the evidence, I am less convinced that this marker is superior to other volume markers. First, there are few head-to-head studies comparing BIA to other established markers of volume. Second, there is no range that defines ‘normal’. Unlike blood pressure (BP) or cholesterol, there is no target that has been established. The normal values are obtained from healthy subjects whose body composition differs substantially from those on dialysis. Extrapolating from healthy subjects to those with ESRD on hemodialysis does not appear scientifically valid. Third, there is no study to my knowledge that demonstrates convincingly that compared to probing dry weight without BIA, BIA-guided dry weight reduction results in improved outcomes. Most data provided to support the use of BIA are associative and observational. A large amount of observational data does not prove causation. We therefore have to be cautious in interpreting these data as ‘strongly indicative of fluid overload’. Nearly all markers of volemia suffer from the same shortcomings. These shortcomings include lack of normative data, and data being largely observational and associative in nature. As an example, several observational studies suggest that B-type natriuretic peptide (BNP), NT-proBNP or other natriuretic peptides are associated with volume state among people with ESRD on dialysis [2–10] . However, only one study has been reported to date that relates the change in BNP to an intervention of probing dry weight [11] . In this study, a direct relationship existed at baseline between BNP and interdialytic ambulatory BP. Since interdialytic ambulatory BP is reVolume overload is the invisible threat to the health of dialysis patients. Currently, Medicare incentivizes the measurement of the dose of dialysis (urea reduction ratio) but has no measure of volume. Perhaps this is because the few who can recognize the epidemic nature of volume excess cannot agree on how to define it. Whereas, some have proposed interdialytic weight gain (IDWG) as a marker of volume, the in-depth review of Hecking et al. [1] quite clearly and importantly makes the distinction that IDWG should not be confused with hypervolemia. One has to wonder how IDWG got confused with dry weight in the first place. It appears that epidemiologists decided to use IDWG as a proxy of dry weight because of its ready availability in large databases. IDWG is a marker that is convenient; it can be measured easily and it can be related to outcomes such as all-cause mortality. This analysis was performed and a relationship emerged between IDWG and all-cause mortality. But establishing a relationship between IDWG and mortality does not establish causality. It could be numerous other factors, measured and unmeasured, associated with IDWG which may be causally related to mortality. Factors such as missing or cutting short dialysis, not taking medications as prescribed, and consuming a diet rich in phosphorus and potassium are some confounding factors that may also be associated with IDWG but may be more plausibly related to mortality. The authors discuss several markers of volume excess. Although several exist, one marker, bioimpedance analysis (BIA), is discussed in great detail. This is understandable given both the academic and intellectual property Published online: July 6, 2013 Nephrology American Journal of
207670106
Competing Risk Factor Analysis of End-Stage Renal Disease and Mortality in Chronic Kidney Disease
Background: Death and dialysis are competing outcomes in patients with chronic kidney disease (CKD). The factors associated with end-stage renal disease (ESRD) versus death in this population are unknown. The purpose of our study was to evaluate the competing risk of ESRD versus mortality and to evaluate the risk factors associated with these two outcomes. Methods: We prospectively recruited 220 consecutive patients at a Veterans Administration Medical Center attending a renal clinic who met the definition of CKD (estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m2 or urine protein/creatinine ratio of >0.22 g/g). Using age, race, proteinuria, eGFR, systolic blood pressure, and coronary artery disease as predictors, we calculated the competing end-points of ESRD or death using a competing Cox regression model. Results: The cumulative incidence for ESRD was 17.6% and death 18.5% during follow-up that lasted up to 7 years. ESRD was predicted by younger age (hazard ratio (HR) 0.91/year), black race (HR 2.75), higher systolic blood pressure (HR 1.02/mm Hg), proteinuria (HR 1.37/log urine protein/creatinine ratio) and low eGFR (0.014/log eGFR ml/min/1.73 m2). Death was predicted by older age (HR 1.07/year), lower eGFR (HR 0.43/log eGFR ml/min/1.73 m2), proteinuria (HR 1.26/log urine protein/creatinine ratio) and coronary artery disease (HR 2.52). The coefficients were statistically different for age (p < 0.001), log eGFR (p < 0.001) and systolic blood pressure (p = 0.04) for ESRD and death outcomes. Conclusions: The risk for mortality is similar to the risk of ESRD in the CKD population of veterans seen by nephrologists. Risk factors for ESRD and death appear to differ in this population. Certain clinical and demographic factors may discriminate between the end-points of death or dialysis and may influence decisions about planning for ESRD.
40070884
Relative plasma volume monitoring for identifying volume-sensitive and -resistant hypertension.
The measurement and management of volume state among long-term dialysis patients has not received much attention. Recent reports suggest that relative plasma volume monitoring may be useful in identifying patients who have volume excess. Among patients who have evidence of excess volume by relative plasma volume monitoring, excess volume removal leads to improvement in interdialytic ambulatory blood pressure. Implementation of this technique can result in improved classification of patients into volume-sensitive and -resistant categories and therefore improve the management of hypertension.
26068481
Efficacy and safety of iodopovidone pleurodesis through tube thoracostomy.
OBJECTIVE
To evaluate the efficacy and safety of iodopovidone as an agent for pleurodesis through tube thoracostomy in patients with recurrent pleural effusions and pneumothorax.


METHODS
This was a prospective study in which pleurodesis was performed with a solution of 20 mL 10% iodopovidone and 80 mL normal saline solution infused through a tube thoracostomy and left in the pleural cavity for 4 h.


RESULTS
A total of 64 patients (34 men) with a mean (+/-SD) age of 47.1 +/- 15.4 years were included. There were 37 cases of pleural effusion and 27 of pneumothorax. A complete response (neither reaccumulation of fluid nor recurrence of pneumothorax) was obtained in 32 (86.5%) patients with pleural effusion and 25 (92.6%) patients with pneumothorax. A second procedure (i.e. repeated pleurodesis) was attempted successfully in four patients in the pleural effusion group. All patients experienced chest pain to a varying degree as recorded on a Visual Analogue Scale (median 50.5, range 10-95). Seven patients developed fever and one immunocompromised patient developed empyema following the procedure. There were no recurrences at a median follow up of 5 months (range 3-15 months) in the pleural effusion group, and 13 months (range 6-24 months) in the pneumothorax group.


CONCLUSIONS
Iodopovidone can be used as an effective and safe agent for (chemical) pleurodesis (through tube thoracostomy), which is inexpensive and readily available.
30313777
It's Pneumocystis jiroveci not Pneumocystis carinii.
2006;129;498 Chest Saxena Ritesh Agarwal, Chandana Reddy, Ashutosh N. Aggarwal and Akshay K. carinii Pneumocystis Not Pneumocystis jiroveci It's http://chestjournal.chestpubs.org/content/129/2/498.full.html services can be found online on the World Wide Web at: The online version of this article, along with updated information and ISSN:0012-3692 ) http://chestjournal.chestpubs.org/site/misc/reprints.xhtml ( written permission of the copyright holder. this article or PDF may be reproduced or distributed without the prior Dundee Road, Northbrook, IL 60062. All rights reserved. No part of Copyright2006by the American College of Chest Physicians, 3300 Physicians. It has been published monthly since 1935. is the official journal of the American College of Chest Chest
9190892
Pulmonary oedema complicating snake bite due to Bungarus caeruleus.
Cardiotoxicity is an unusual manifestation of severe neurotoxic snake envenoming and is previously unreported with snake bites due to kraits. We describe a 26-year-old male Indian farmer who developed cardiogenic pulmonary oedema after neurotoxic snake envenoming by Bungarus caeruleus (Indian krait). We also review the literature on cardiac manifestations, the possible mechanisms and treatment of patients with cardiotoxicity accompanying neurotoxic snake envenoming. Cardiac involvement can complicate the course of snakebites. Recognition of cardiac involvement can warn the emergency physician and intensivist to be cautious, and anticipate the complications, such as pulmonary oedema, so that they can be rapidly and appropriately managed.
10252201
Pulmonary masses in allergic bronchopulmonary aspergillosis: mechanistic explanations.
Allergic bronchopulmonary aspergillosis (ABPA) is a disorder caused by hypersensitivity to Aspergillus antigens, and is currently the best recognized manifestation of Aspergillus-associated hypersensitivity disorders. ABPA occurs in 1–2% of patients with bronchial asthma and 2–15% of patients with cystic fibrosis.1 Patients with ABPA may present with recurrent asthma exacerbations, expectoration of dark brown mucus plugs, hemoptysis, or systemic symptoms such as fever, anorexia, malaise, or weight loss. The Rosenberg criteria2 are most widely used for diagnosis and include 8 major and 3 minor criteria. The major criteria (easily remembered by the mnemonic ARTEPICS) are: A Asthma R Radiographic fleeting pulmonary opacities T Skin test positive (type 1 reaction) for Aspergillus fumigatus E Eosinophilia P Precipitating antibodies (Immunoglobulin G [IgG]) in serum I Immunoglobulin E (IgE) in serum elevated ( 1,000 IU/mL) C Central bronchiectasis S Serum-specific IgG and IgE against A. fumigatus If 6 of the 8 primary criteria are met, the diagnosis is certain. The minor criteria are Aspergillus in sputum, expectoration of brownish-black mucus plugs, and delayed skin reaction to Aspergillus antigen (type 3 reaction). Patients with ABPA present with diverse radiographic manifestations, including finger-in-glove and toothpaste opacities, air-fluid levels from dilated bronchi, and tramline shadows from edematous bronchial walls.3 Highresolution CT characteristically shows central bronchiectasis, mucus-filled bronchi (bronchoceles), consolidation, and tree-in-bud appearance of centri-lobular nodules.4 Pulmonary masses in ABPA are uncommon but have been described in the literature.5-8 Proximal bronchoceles (often inseparable from the hilum) may simulate hilar mass.9 We report 3 patients with pulmonary masses and ABPA. We also discuss mechanisms by which ABPA might lead to such parenchymal lesions.
45728668
Pulmonary mucormycosis: two of a kind.
Mucormycosis is an uncommon infection caused by fungi of the class Zygomycetes, suborder Mucorales. It occurs predominantly in the immunodeficient host, the most common risk factor being diabetes mellitus. Pulmonary mucormycosis is a disease that is localized in the lungs or mediastinum. It usually presents in a fulminant manner, although a chronic presentation can also occur. We describe two cases of pulmonary mucormycosis in patients with diabetes mellitus, one with an acute and the other with a chronic presentation. A high level of clinical suspicion, combined surgical and medical therapy, and control of patient's underlying immunosuppression are the key to a successful outcome.