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Introduction Parkinson’s disease has long been considered as a neurodegenerative disorder of pure motor expression. Motor dysfunction in Parkinson’s disease and other parkinsonian disorders is frequently accompanied by nonmotor signs and symptoms, including cognitive impairment, apathy, anxiety, and depression. Among psychiatric disorders comorbid with Parkinson’s disease, depression is probably the most important in terms of frequency and impact.ObjectivesThe aim of this presentation was to illustrate the importance of considering depressive symptoms in patients with Parkinson’s disease.MethodsA case report describing a patient with depressive symptoms in a patient with Parkinson’s disease and literature review.ResultsWe report a case of a 57-year-old woman who presented symptoms of Parkinson’s disease for two years. She was treated with Benserazide (Madopar). She was referred to our department for depressive symptomatology. The patient suffered from fatigue, insomnia, loss of sexual desire, sadness, anhedonia, and social withdrawal during the last three months. The diagnosis of depression was not immediately retained. Finally, a major depressive episode was diagnosed. Fluoxetine (20mg per day) was prescribed with clinical improvement.Conclusions The diagnosis of a depressive episode is most often complex, due to an overlap symptomatic of both disorders. The depression comorbid to Parkinson’s disease because of its frequency and impact, requires specific identification and management early.

IntroductionObsessive-compulsive symptoms (OCS) are common in schizophrenia, with a prevalence ranging from 12 to 25%. They affect negatively disease outcome. Patients with comorbid OCS present more frequently resistant psychotic symptoms. Besides, the appearance and aggravation of OSC are more commonly reported with atypical antipsychotics.ObjectivesTo present through a clinical case and a brief literature review the treatment challenge of obsessive-compulsive symptoms in schizophrenia.MethodsWe reported the case of Mr. M.S., treated in our department since 2008 for comorbid schizophrenia and OCS, and discussed therapeutic alternatives through a literature review.ResultsMr. M.S. a 34-year-old male diagnosed with comorbid schizophrenia and OCS at age 20. To control psychotic symptoms, the patient received several trials of anti-psychotics with little improvement. We concluded that it was resistant schizophrenia. The introduction of clozapine reaching 300 mg daily led to significant improvement of psychotic symptoms but worsened OCS. The adjunction of fluoxetine and cognitive-behavioral therapy (CBT) was unsuccessful to manage obsessive symptoms. We opted for the association of aripiprazole 20 mg daily and clozapine, the doses of which were gradually tapered down to 150 mg daily. This association has guaranteed the improvement of both psychotic and obsessive symptoms.ConclusionsConclusion This clinical vignette highlights the need for clinical awareness about the possible exacerbation of OCS with atypical antipsychotics in schizophrenia.DisclosureNo significant relationships.

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with proteinuria and 56 % diabetic subjects were taking ACE/ARB. 92 % of CKD subjects with hypertension were taking antihypertensive drug with more than half (54%) receiving calcium channel blocker. 25 % of diabetic subject were on metformin and 57 % were receiving statins. Use of calcium-based phosphate binder was 41% in subject with serum phosphate level>4.5 mg/dl. Sodium bicarbonate therapy was seen in less than 55% of the patients, Statin in less than 42% and Vitamin D analogues in less than 13 % of subjects at all stages of CKD.Conclusions: Pills burden in patients with CKD was high. ACE inhibitors are relatively less prescribed than other anti-hypertensives.No conflict of interest

Objective: This study aimed to verify the impact of predialysis systolic pressure (PDSP) on patients’ mortality. Design and method: We reviewed files of incident patients, in one reference center of hemodialysis, between January 2009 and June 2010. Arterial pressure was measured by sphygmomanometer before initiating the patient's first dialysis session. We considered: as “high PDSP” a SP equals or over 180 mmHg; as “low PDSP” a PS equals or less than 100 mmHg. Univariate and multivariate analysis were performed to study PDSP association with absolute mortality at five years. Odds ratio (OR) was subject to a 95% confidence interval. We used Kaplan Meier method for survival curves. Results: One hundred eleven patients were included. Sex ratio was 1.7 M/W. At dialysis initiation: mean age was 55 ± 14.9 years. Sixty nine patients (62%) were hypertensive; all of them were under antihypertensive agents. MAP, SP and DP were respectively 98.8 ± 16.3 mmHg, 139.4 ± 25.4 mmHg and 79.1 ± 14 mmHg. Mean urinary output was 1156 ± 542 ml/day and initial serum creatinine 887 ± 271 μmol/l. In univariate analysis, absolute mortality at five years was associated with low PDSP (p = 0.001, OR = 4.8). This association was pronounced among orderlies (p = 0.001) and diabetic patients (p = 0.001). High PDSP was also associated with absolute mortality at five years (p = 0.03; OR = 1.67). In multivariate study, neither low nor high PDSP were associated to mortality. Survival was decreased for patients with low PDSP (log-rank p = 0.001) (Figure 1) and high PDSP (log-rank p = 0.03) (Figure 2). Conclusions: These results suggest the presence of a “U” curve relationship between PDSP and mortality. Further studies, with larger populations, are needed to determine the potential use of low PDSP as a mortality risk factor.

Among the 5 patients with acute tubulointerstitial nephritis, 4 were biopsy-proven, and 1 was presumed based on the clinical history of recent NSAID use.Renal biopsies were performed in six patients, and histopathological diagnoses were pigment cast nephropathy (n=1), acute tubulointerstitial nephritis (n=4), and infection-related GN (n=1). Among the four patients with acute tubulointerstitial nephritis, two had exposures to NSAIDs and native medications, while a clear aetiology could not be identified in the other two. One patient, in addition, had the incidental finding of extramedullary haematopoiesis in the kidney, which was secondary to HIV-related bone marrow fibrosis.The overall mortality rate was 41.4% (5 patients died during hospitalisation, 7 patients died during follow-up). Seven patients remained dialysis-dependent at the time of discharge/death. Conclusions: While we identified a very vast spectrum of AKI, overwhelmingly the most common cause in our hospital population remains sepsis. A significant proportion required renal replacement therapy, and the patients in our cohort suffered a high mortality rate. Limitations include observational study design, referral bias, and small sample size.