An Inflammatory Pseudotumor in the Costo-Vertebral Gutter: Case Report with Literature Review

Background and Importance: Inflammatory pseudotumors are benign tumors-like lesions of unknown cause. The most familiar sites for inflammatory pseudotumors are the orbit and respiratory tract. An inflammatory pseudo tumor of costo-vertebral junction is rare. Case Presentation: We presented here a 50-year-old male with two month history of progressive left cervico-brachial pain. The MRI showed an expansive process at the left costo-vertebral gutter with epidural extension through the lateral foramen, causing spinal cord compression from C7 to D3. The thoraco-abdominal CT scan did not identify other lesions. Conclusion: The inflammatory pseudotumor is a chronic inflammatory process of unknown origin. The location of the costo-vertebral gutter is rare and the treatment involves surgery, steroids and radiotherapy

The inflammatory profile of chronic kidney disease patients

Background: Chronic kidney disease is a worldwide public health issue which is associated with an increased risk of end-stage renal failure and cardiovascular disease. Systemic inflammation exists during chronic renal failure. Recent researches have highlighted the pivotal role of inflammation between renal and cardiovascular disease. The aim of our study is to determine the inflammatory profile of the patient suffering from chronic kidney disease and the influence of hemodialysis on this profile.Methods: We carried out a cross sectional study on 93 patients in the Nephrology Department at Hedi Chaker University Hospital, Sfax, South of Tunisia. Among those patients, 72 patients underwent hemodialysis and 21 patients had chronic kidney disease at stage 3. Clinical data and antecedents were collected. Biological samples were taken after informing the patients and taking their consent. Biological data consisted in lipid profile, albumin rate, hemoglobin rate, uric acid concentration and the usual markers of inflammation noting sedimentation rate, C - reactive protein and orosomucoid.Results: Hemodialysis group of the 72 patients had mean hemodialysis vintage of 54.6 ± 43 months. The inflammatory profile was worse in hemodialysis patients compared to chronic kidney disease patients. Both sedimentation rate, C - reactive protein and orosomucoid were higher in hemodialysis group than in chronic kidney disease group with 71 ± 35.3 mm vs. 42.1 ± 15.5 mm (p < 0.05); 14.6 ± 28.7 mg/l vs. 6.7 ± 8 mg/l (p = 0.02); 1.3 ± 0.7g/l vs. 0.9 ± 0.4 g/l (p = 0.01), respectively.Conclusion: Inflammation increases in dialysis patient. It deserves the nephrologist’s consideration in order to minimize its harmful effects. The monitoring of inflammation markers must be integrated into the nephrologist’s medical practice

Identification of compound heterozygous patients with primary hyperoxaluria type 1: clinical evaluations and in silico investigations

Abstract Background Primary hyperoxaluria type 1 (PH1) is an autosomal recessive inherited disorder of glyoxylate metabolism in which excessive oxalates are formed by the liver and excreted by the kidneys. Calcium oxalate crystallizes in the urine, leading to urolithiasis, nephrocalcinosis, and consequent renal failure if treatment is not initiated promptly. Mutations in the AGXT gene which encodes the hepatic peroxisomal enzyme alanine:glyoxylate aminotransferase are responsible of PH1. In the present work, we aimed to analyze AGXT gene and in silico investigations performed in four patients with PH1 among two non consanguineous families. Methods Exhaustive gene sequencing was performed after PCR amplification of coding exons and introns boundaries. Bioinformatic tools were used to predict the impact of AGXT variants on gene expression as well as on the protein structure and function. Results Direct sequencing of all exons of AGXT gene revealed the emergence of multiple mutations in compound heterozygous state in the two studied families. Two patients were compound heterozygous for the c.731 T > C, c.32C > T, c.1020A > G and c.33_34insC and presented clinically with recurrent urinary tract infection, multiple urolithiasis and nephrocalcinosis under the age of 1 year and a persistent hyperoxaluria at the age of diagnosis. The two other patients presenting a less severe phenotypes were heterozygous for c.731 T > C and homozygous for the c.32C > T and c.1020A > G or compound heterozygous for c.26C > A and c.65A > G variants. Conclusion In Summary, we provided relevance regarding the compound heterozygous mutations in non consanguineous PH1 families with variable severity