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Background: Ascitic fluid polymorphonuclear leucocyte count (PMN) is known to be the gold standard for spontaneous bacterial peritonitis (SBP) diagnosis. The aim of this work was to assess ascitic calprotectin for SBP diagnosis. Serum C-reactive protein (CRP), high sensitivity C-reactive protein (hsCRP), nitrous oxide, ascitic PMN, ascitic leucocyte esterase and ascitic calprotectin were measured. Results: The average age of our patients was 55.25 ± 7.89 years, mostly males (n = 51, 63.8%), anti-HCV antibodies were positive in (n = 61, 76.3%). Sixty-four patients (80%) were Child-Pugh C and their average MELD was 24.29 ± 8.06. Patients with SBP had statistically significant higher median MELD score (26.5 vs. 19) and higher average Child-Pugh score (12.18 ± 1.74 vs. 10.5 ± 1.97). Forty patients had SBP and 40 patients were without SBP. Both the serum and ascitic nitrous oxide did not differ statistically between patients with and without SBP. In contrast, patients with SBP had higher median serum CRP (49 vs. 12 mg/dL), hsCRP (58,000 vs. 23,750 ng/dL) and ascitic calprotectin (7.57 vs. 1.1 ng/mL). The ascitic leucocyte esterase test was positive in 95% of SBP patients in contrast to 2.5% patients without SBP. Ascitic calprotectin >2 ng/mL had 90% sensitivity, 92.5% specificity, 92.3% positive predictive value and 90.2% negative predictive value. MELD, CRP, hsCRP and ascitic calprotectin are independent predictors of SBP. Conclusion: Ascitic calprotectin is a useful marker for SBP diagnosis.

Background and aim of work Endothelial dysfunction, atherosclerosis, and cardiovascular disease are strongly linked to chronic kidney disease. It has been hypothesized that visfatin may play an important role in uremia-related atherosclerosis and the relation between visfatin and endothelial dysfunction has been proved. We aimed to study and characterize the relation of visfatin to some clinical and biochemical parameters among chronic renal failure (CRF) patients on regular hemodialysis. Patients and methods This study was carried out on a total of 90 individuals, divided into two groups: group A included 68 patients with CRF on regular hemodialysis (44 men and 24 women) and group B included 22 healthy individuals as controls (four men and 18 women). All participants were subjected to the following: full clinical assessment, BMI assessment, FBS (Fasting blood sugar), PPBS (postprandial blood sugar), Hb level, lipid profile, serum urea, creatinine, potassium, phosphorus, and serum visfatin. Results Serum visfatin concentration was significantly high in group A (uremic on hemodialysis) compared with group B (control) (48.95 ng/ml ±11.62 compared with 22.65 ng/ml ± 5.24; P < 0.001); a highly significant positive correlation was found between serum visfatin and serum low-density lipoprotein (r = 0.39; P < 0.001) and a significant positive correlation between serum visfatin and serum triglycerides and serum uric acid (r = 0.28; P < 0.05 and r = −0.24; P < 0.05), respectively, whereas a highly significant negative correlation between serum visfatin and Hb (r = −0.43; P < 0.001) and a significant negative correlation between serum visfatin and serum urea (r = −0.25; P < 0.05), blood sugar, both fasting and postprandial (r = −0.34; P < 0.001 and r = −0.39; P < 0.001), respectively, were found in the patients in group A, without a significant correlation either to high-density lipoprotein, serum creatinine, the etiology of CRF, or to the duration of dialysis in the patients in group A. Conclusion This study proves the association of serum visfatin with CRF, unrelated to the biochemical parameter of kidney functions; however, further studies to examine visfatin expression within renal tissue may clarify its definitive role in CRF.

This prospective study's objective was to determine the impact of lung Boost exerciser on pulmonary functions in iron deficiency anaemia. Forty patients (18 males and 22 females) with iron deficiency anaemia were recruited from haematology department in AL-Kasr Al Ainy hospital where the study was conducted. Participants were aged between 20 to 35 years old. They were assigned randomly into two groups; study group(A) which were twenty patients received lung boost exerciser program for thirty minutes, three times/week in addition to medical treatment and twenty patients in control group(B) received medical treatment only. The exercise lasted from 5­20 minutes including 15 deep breaths, and 15-second rest in between. The total treatment period for both groups was twelve weeks. Pulmonary Functions which included Peak Expiratory Flow (PEF), Forced Vital Capacity (FVC), Forced Expiratory Volume in the First Second (FEV1), and the ratio of FEV1 to FVC (FEV1/FVC) were evaluated for all patients in both groups at the beginning of the study and after 12 weeks by using spirometer.

Introduction Cardiovascular disease has increased as a complication of chronic kidney disease even in the absence of diabetes or hypertension. Angiopoietin-1 and 2 are 55 kDa antagonistic nonredundant gatekeepers of endothelial activation and thus are potential important factors in accelerated atherosclerosis. Aim of the study The aim of the study was to determine angiopoietin-2 level in patients on hemodialysis (stage 5) and in the predialytic stages (stages 3 and 4) and to find the relationship between angiopoietin-2 levels and glomerular filtration rate in the predialytic stages. Patient and methods We prospectively studied 75 patients divided into three groups and 12 healthy controls. Group 1 included 33 patients on maintenance hemodialysis three times a week; group 2 included 21 patients with stage 3 chronic kidney disease; and group 3 included 21 patients with stage 4 chronic kidney disease. Results We found highly significant (P < 0.01) increase in mean serum angiopoietin-2 levels in all three groups compared with the control. The mean angiopoietin-2 in group 1 was 1669.09 ± 472.64 pg/ml, in group 2 was 1206.91 ± 154.26 pg/ml, in group 3 was 1642.24 ± 113.01 pg/ml, and in control was 476.29 ± 150.37 pg/ml. Furthermore, we found highly significant (P < 0.01) increase in group 1 compared with group 2 and group 3, and in group 3 compared with group 2. Our result revealed significant negative correlation of angiopoietin-2 level with estimated glomerular filtration rate in group 2 (r – 0.858, P < 0.01) and group 3 (r – 0.825, P < 0.01), with hemoglobin in group 1 (r – 0.438, P < 0.01), and with BMI (r − 0.468, P < 0.05) and cholesterol (r − 0.503, P<0.05) in group 3; significant positive correlation was observed with uric acid (r 0.456, P < 0.05) in group 3. Conclusion Circulating angiopoietin-2 is a putative marker and potential mediator of atherosclerosis, is inversely related to glomerular filtration rate, and is increased with advanced chronic kidney disease. Normolipidemia in chronic kidney disease patients does not prevent atherosclerotic burden; this is because of the presence of other markers such as angiopoietin-2.