Severe ADAMTS13 deficiency (activity < 10%) is pathognomonic of thrombotic thrombocytopenic purpura. ADAMTS13 testing is time-consuming and unavailable in many hospitals. Recently, a seven-variables score named PLASMIC score, has been developed to stratify acute patients, based on their risk of having a severe ADAMTS13 deficiency. We present the application of this score in a cohort of patients referred to our Center. From 2012 to 2017, 42 patients with suspected thrombotic microangiopathies from 6 Centers were referred to Hemostasis and Thrombosis Center of "Casa Sollievo della Sofferenza" Hospital/Research Institute for ADAMTS13 testing. For all patients, relevant medical and laboratory information were collected. To obtain the statistical measure of the discriminatory power of PLASMIC scoring system, the Area Under the Curve Receiver Operating Characteristic (AUC ROC) was calculated. We were able to calculate the PLASMIC score in 27 out of 42 patients; we found a good discrimination performance of the score with a resulting AUC value of 0.86 (95% CI 0.71-1.0; p = 0.015). All patients but one with a high risk PLASMIC score (6-7) showed a severe deficiency. Among patients belonging to the intermediate risk (PLASMIC score 5) group, 2 showed normal ADAMTS13 activity and 2 levels below 10%. In none of the patients in the low risk group (PLASMIC score 0-4), a severe ADAMTS13 deficiency was found. Present results confirm and extend previous data regarding the predictive value of the PLASMIC score. Indeed, it shows a good diagnostic performance and can be useful for decision makers to properly and promptly define the better therapeutic approach.

Abstract:The PLASMIC score for the prediction of a likelihood of a severe ADAMTS13 deficiency represents a valid pre-test diagnostic tool to identify patients with thrombotic thrombocytopenic purpura.

INTRODUCTION AND AIMS:Osmotic changes during hemodialysis have been reported to cause development of cerebral edema and intracranial hypertension in some patients. Patients with pre-existing acute brain injury are likely at increased risk. Such patients are few and only case reports have been published. Furthermore continuous hemodialysis (CRRT) has been suggested to be less likely to cause increases in intracranial pressure compared to intermittent hemodialysis (IHD) Aim : To study changes in intracranial pressure (ICP) during hemodialysis in patients with acute brain injury in the intensive care unit. METHODS: All patients with acute brain injury admitted to our intensive care units who were treated with IHD or CRRT while undergoing ICP monitoring from 2012-2016 were identified retrospectively. Patients were excluded if ICP values were not documented during hemodialysis. Data from each patient's first dialysis session in the intensive care unit were collected. For CRRT data from the first 8 hours of dialysis were collected. Area under the curve divided by time (AUC/t) for ICP was calculated separately before and during dialysis. Total plasma osmolarity was estimated before and after the dialysis session. RESULTS: Thirteen patients were included. During hemodialysis, ICP increased from a baseline of 11.9 mmHg (median; interquartile range 6.3-14.7) to a maximum of 21 mmHg (18-27) (p ¼ 0.0024), and AUC/t for ICP was greater during dialysis (15.2 (13.4-18.8) vs. 11.7 mmHg (6.4-15.1), p ¼ 0.042).The magnitude of the increase was independent of dialysis modality, but occurred earlier in patients treated with IHD (N¼4) compared to CRRT (N¼9) (75 (30-90) vs. 375 min (180-420) after start of treatment, p ¼ 0.0095). The maximum increase in ICP during dialysis correlated positively to the baseline plasma urea concentration (Spearman's r ¼ 0.69, p ¼ 0.017). Biochemical data before and after the initial hemodialysis session are shown in the table below (as median (interquartile range)). CONCLUSIONS: Despite its limitations the present study is, to our knowledge currently the largest cohort of its kind published. We found that hemodialysis is followed by a clinically significant increase in ICP in patients with acute brain injury regardless the choice of hemodialysis modality (CRRT vs IHD). The increase in ICP during CRRT seems equal to the increase during IHD, but occurs somewhat later which must be considered when observing these patients. Changes in estimated osmolarity were rather modest, but maximum ICP during hemodialysis correlated positively to the plasma urea concentration before start of treatment. measures were used as developmental cohort. Primary outcome was development of CIN, defined as 25% increase of serum creatinine within 2-6 days after contrast exposure. A predictive model was developed using logistic regression analyses. The model was evaluated for prognostic utility in independent cohort from other tertiary hospital (N¼555 SP231 RISK PREDICTION OF CONTRAST INDUCED NEPHROPATHY IN CANCER PATIENTS UNDERG...

Background and Aims Chronic kidney disease (CKD) is a systemic condition because it modifies all organs' function due to an imbalance in plasma volume, electrolytes, hormones, and proteins. Indeed, at the nervous system level, mild cognitive impairment (MCI), sleep disorders and depression often accompany CKD. MCI partially explains the low quality of life of CKD patients, comparable to that of metastatic cancer patients. Mild Cognitive Impairment (MCI) has a high prevalence in this cohort (27-62%). Nevertheless, scattered literature data suggest that CKD patients can also have poor motor control, evidenced by a higher risk of falls, postural instability, reduced gait speed. In this cohort, few data are available regarding the motor circuits called central pattern generators, which control physiological tremor. Specifically, uraemic encephalopathy accentuates physiological tremor, which is regulated by central and peripheral oscillators. Overall, subtle changes in motor control often accompany other forms of MCI. Therefore, this study aimed at evaluating the effects of chronic kidney disease on cognitive and motor functions using up-to-date technologies to record physiological tremor and innovative data analysis. Method This retrospective case-control study enrolled 313 patients (139 controls, 79 CKD patients stage III-IV, 35 kidney transplant (Tx), 60 dialysis (HD) patients). These groups were comparable for age and weight. Creatininemia, azotemia, LDL, HDL, hemoglobin, and proteinuria were used for correlative analyses. We evaluated the chronotype using the Morningness-Eveningness Questionnaire (MEQ) and the degree of sleepiness using the Epworth Sleepiness Scale (ESS). Cognitive impairment was assessed by the Montreal Cognitive Assessment test (MoCA). Cognitive domains of the MoCA score were projected onto brain regions using CerebroViz library in R and a new transformation matrix derived from fMRI literature data. UMAP algorithm was used to identify patients' subgroups. The physiological tremor was recorded on patients maintaining the dominant arm extended using the smartphone App Phyphox. The tremor frequency spectrum was extracted by Fourier analysis. Results The sleepiness score (ESS) was significantly increased in HD (ESS = 5±0.4) compared to the healthy controls (ESS= 4±0.41) whereas was not significantly modified in CKD patients (3.24± 0.32). The chronotype was also not significantly different among the various groups. The mean score of the MoCA test was significantly lower in CKD, Tx, and HD groups (CKD MoCA =24.5±0.3; Tx MoCA =25.4±0.6; HD MoCA =24.6±0.7) than controls (MoCA score=28±0.1). A different pattern of impairment in the cognitive domains of MoCA was evidenced in the various groups using the CerebroViz projection and UMAP tools. MoCA score was inversely correlated with proteinuria (Pearson coefficient=-0.47; p&lt;0.05). The higher frequencies of the physiological tremor (11-13 Hz) were significantly more represented in Tx patients compared to controls (p&lt;0.05). Conversely, the lower frequencies (1-4 Hz) were significantly less represented in the HD group compared to controls (p&lt;0.05). The peak frequency was inversely correlated with age in all patients (Pearson coefficient= -0.45; p&lt;0.05) and inversely associated with azotemia levels, particularly in HD patients (Pearson coefficient=0.43; p&lt;0.05). Conclusion Our results suggest that CKD patients present altered cognitive and motor control patterns, linked in part to the proteinuria level, suggesting a pathogenetic role of endothelial dysfunction. The characteristic motor, sleepiness and cognitive patterns of HD patients might be due to the arteriovenous fistula or the other peculiarities of these patients. These results might help identify new early markers of brain dysfunction in these patients, with the possibility of delaying or reversing cognitive decay.

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