The Home Office Deduction

As a result of a recent Supreme Court decision, Commissioner v. Soliman, stricter guidelines have been imposed upon taxpayers regarding their eligibility to take a home office deduction under the "principle place of business" election. As a result of Soliman, determining a taxpayer's principal place of business went from a "facts and circumstances" test, tailored to each individual case, to tests that consider only two factors. Several pronouncements and publications have prescribed guidelines and examples that explain this decision. Soliman, however, has been subject to criticism by the tax profession. Some professionals believe these tests are too strict. The pronouncements have also been subject to scrutiny for being vague. The purpose of this thesis was to gather information from the practicing tax profession to determine what its views were regarding Soliman and the subsequent pronouncements. Surveys were given to fifteen tax professionals. The purpose of the surveys was to determine whether Soliman provided adequate guidelines for determining a taxpayer's principal place of business, as well as to analyze whether the recent IRS pronouncements are consistently interpreted and applied. Survey results support the finding that the effects of Soliman are not universally accepted, and that interpretation of its guidelines do not always produce consistent and dependable conclusions. Therefore, it is proposed that the courts revert to the "facts and circumstances" test that was used prior to Soliman.B.S. (Bachelor of Science

The Expression of Heat Shock Proteins 27 and 70 in Lupus Nephritis

Background: Heat shock protein (HSP ) up-regulation is a cytoprotective response following stress insults (toxic, ischemic, inflammatory and oxidative). Ob ject ive: To study the localization of HSP 27 and HSP 70 in the renal tissue of patients with lupus nephritis (LN) and correlate our findings with the severity of histological involvement (activity and chronicity indices) and the degree of renal function impairment. Pat ients and Methods: Seventy patients with LN (diffuse proliferative n=31, focal proliferative n=20, and membranous n=19) were included in the study. The distribution of HSP 27/HSP 70 was studied by immuno-histochemistry in renal biopsy sections. A double staining method for vimentin, a-smooth muscle actin, CD 34 and CD 68 (+) cells were performed to identify the type of glomerular cells expressing HSP s. The severity of immunostaining for HSP 27/70 was evaluated semiquantitively. Results : HSP 27 and HSP 70 were identified within the cytoplasm of tubular epithelial cells of all patients. Increased HSP 27 expression was noted within intrinsic glomerular cells in diffuse lupus nephritis whereas no glomerular expression was observed in focal proliferative and membranous LN. A significant positive correlation was found between HSP 27 expression in diffuse proliferative nephritis and the activity and total (activity + chronicity) indices. The severity of histological involvement was also related to the degree of renal function impairment. Conclusions: Up-regulation of heat shock protein expression was identified in patients with various types of LN, especially those with diffuse proliferative nephritis. The severity of HSP 27 expression was related to the activity and total indices. These results suggest a possible defensive role for HSP 27 in severe lupus nephritis

Littoral cell angioma of the spleen accompanied by haemophagocytic syndrome in a dialysis patient suffering from aa amyloidosis

Littoral cell angioma (LCA) is a rare form of vascular tumor unique to the spleen that arises from the specialized endothelial cells that line the splenic sinuses (littoral cells). Haemophagocytic syndrome (HS) is also a rare hematologic disorder that some times accompanies LCA. The authors describe a young dialysis patient with a history of familiar mediteranean fever and secondary amyloidosis who was found to have this rare association of AA amyloidosis with LCA and haemophagocytic syndrome

Impact of hydration status on haemodynamics, effects of acute blood pressure lowering treatment, and prognosis after stroke

BackgroundHigh blood pressure (BP) is common in acute stroke and associated with poor outcome, but the Efficacy of Nitric Oxide in Stroke (ENOS) trial showed no beneficial effect of antihypertensive treatment in this situation. Antihypertensive agents have accentuated effects in dehydrated patients. We assessed the impact of dehydration on haemodynamics, effects of antihypertensive treatment and prognosis in the ENOS trial.MethodsENOS randomised 4011 patients with acute stroke and raised systolic BP to glyceryl trinitrate (GTN) patch or no GTN, and to continue or to stop existing antihypertensive treatment within 48 hours of onset. The primary outcome was functional outcome (modified Rankin Scale, mRS) at day 90. Blood markers of dehydration at baseline were collected at two sites (n=310) and their relation to haemodynamics and outcome was assessed.ResultsThere were no significant associations between dehydration markers and fall in blood pressure from baseline to day 1, and no significant interaction with allocated treatment. Overall, increasing urea was associated with an unfavourable shift in mRS (OR 3.43, 95% CI 1.42 to 8.32, p=0.006) and increased risk of death at day 90 (HR 4.55, 95% CI 1.51 to 13.66, p=0.007).ConclusionsBlood pressure lowering treatment was safe in dehydrated patients, with no precipitous changes in BP, this supporting its use in acute stroke prior to blood markers of dehydration becoming available. Increased baseline urea was associated with poor prognosis after stroke

Estimated GFR reporting is not sufficient to allow detection of chronic kidney disease in an Italian regional hospital

<p>Abstract</p> <p>Background</p> <p>Chronic kidney disease (CKD) is an emerging worldwide problem. The lack of attention paid to kidney disease is well known and has been described in previous publications. However, little is known about the magnitude of the problem in highly specialized hospitals where serum creatinine values are used to estimate GFR values.</p> <p>Methods</p> <p>We performed a cross-sectional evaluation of hospitalized adult patients who were admitted to the medical or surgical department of Santa Maria della Misericordia Hospital in 2007. Information regarding admissions was derived from a database. Our goal was to assess the prevalence of CKD (defined as an estimated glomerular filtration rate [eGFR] < 60 mL/min/1.73 m²) and detection of CKD using diagnostic codes (Classification of Diseases, Ninth Revision, Clinical Modification [ICD-9-CM]). To reduce the impact of acute renal failure on the study, the last eGFR obtained during hospitalization was the value used for analysis, and intensive care and nephrology unit admissions were excluded. We also excluded patients who had ICD-9-CM codes for renal replacement therapy, acute renal failure, and contrast administration listed as discharge diagnoses.</p> <p>Results</p> <p>Of the 18,412 patients included in the study, 4,748 (25.8%) had reduced eGFRs, falling into the category of Kidney Disease Outcomes Quality Initiative (KDOQI) stage 3 (or higher) CKD. However, the diagnosis of CKD was only reported in 19% of these patients (904/4,748). It is therefore evident that there was a "gray area" corresponding to stage 3 CKD (eGFR 30-59 ml/min), in which most CKD diagnoses are missed. The ICD-9 code sensitivity for detecting CKD was significantly higher in patients with diabetes, hypertension, and cardiovascular disease (26.8%, 22.2%, and 23.7%, respectively) than in subjects without diabetes, hypertension, or cardiovascular disease (p < 0.001), but these values are low when the widely described relationship between such comorbidities and CKD is considered.</p> <p>Conclusion</p> <p>Although CKD was common in this patient population at a large inpatient regional hospital, the low rates of CKD detection emphasize the primary role nephrologists must play in continued medical education, and the need for ongoing efforts to train physicians (particularly primary care providers) regarding eGFR interpretation and systematic screening for CKD in high-risk patients (i.e., the elderly, diabetics, hypertensives, and patients with CV disease).</p

Genetic polymorphisms of the RAS-cytokine pathway and chronic kidney disease

Chronic kidney disease (CKD) in children is irreversible. It is associated with renal failure progression and atherosclerotic cardiovascular (CV) abnormalities. Nearly 60% of children with CKD are affected since birth with congenital or inherited kidney disorders. Preliminary evidence primarily from adult CKD studies indicates common genetic risk factors for CKD and atherosclerotic CV disease. Although multiple physiologic pathways share common genes for CKD and CV disease, substantial evidence supports our attention to the renin angiotensin system (RAS) and the interlinked inflammatory cascade because they modulate the progressions of renal and CV disease. Gene polymorphisms in the RAS-cytokine pathway, through altered gene expression of inflammatory cytokines, are potential factors that modulate the rate of CKD progression and CV abnormalities in patients with CKD. For studying such hypotheses, the cooperative efforts among scientific groups and the availability of robust and affordable technologies to genotype thousands of single nucleotide polymorphisms (SNPs) across the genome make genome-wide association studies an attractive paradigm for studying polygenic diseases such as CKD. Although attractive, such studies should be interpreted carefully, with a fundamental understanding of their potential weaknesses. Nevertheless, whole-genome association studies for diabetic nephropathy and future studies pertaining to other types of CKD will offer further insight for the development of targeted interventions to treat CKD and associated atherosclerotic CV abnormalities in the pediatric CKD population