Tag Archives: proteinuria

The Relationship Between Chronic Inflammation and Glucidic-Lipidic Profile Disorders in Kidney Transplant Recipients

DOI: 10.1515/amma-2015-0121

Introduction: Chronic inflammation has a proven role in atherogenesis, lipid profile parameters being related to cytokine production. In kidney transplant recipients, interleukin 6 (IL-6) is significantly associated with graft-related outcomes and also alterations of cholesterol and triglyceride metabolism. The aim of this study was to investigate the relationship between chronic inflammation and glucidic-lipidic metabolism disorders in a group of patients with kidney transplantation as renal replacement therapy.
Methods: A prospective observational study which enrolled thirtysix non-diabetic kidney transplant recipients was conducted in the Nephrology and Peritoneal Dialysis Department, County Clinic Hospital of Tirgu Mures. The study group was divided as following: recipients with serum IL-6 concentration higher than 3.8 pg/ml (group A) and IL-6 within the normal range (group B).
Results: Allograft recipients with higher serum IL-6 had significant higher erytrocyte sedimentation rate(ESR, p=0.0067). Patients with over-the-range levels of IL-6 had significant higher levels of serum cholesterol and LDL-cholesterol respectively (p=0.0242 and p=0.0081). Serum Apo-B was also significant higher in Group A than Group B. Protein excretion was significant higher in patients from group A (p=0.0013). No statistical significant relationship could be proven between elevated levels of IL-6 and hbA1c, insulin and glycosuria disturbances in the two groups. Also, we found no statistical significant association between resistivity and pulsatility indices (both hilum and intragraft) or carotid intima media thickness.
Conclusion: Serum interleukin 6 is related to lipid profile disorders and less to glucidic metabolism anomalies in non-diabetic kidney transplant recipients.

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Modification of Renal Permeability for Proteins after General Anesthesia with Sevoflurane and Desfluran

Introduction: Sevoflurane degradation by carbon dioxide absorbents during low-flow anesthesia lead to the formation of a haloalkene called compound A, which causes nephrotoxicity.
Material and methods: We determined proteinuria by spectophotometry at 600 nm, preoperatively and postoperatively at 24 and 72 hours in 52 patients undergoing general anesthesia with sevoflurane and 25 patients undergoing general anesthesia with Desfluran. We selected patients without previous renal disease, with anesthetic risk ASA I–III who underwent major abdominal and thoracic surgery lasting more than 150 minutes and we used a 2 l/minute FGF-fresh gas flow, with a MAC-minimal alveolar concentration of 1.5 to 1.8 for Sevoflurane, and of 6–8 MAC for Desfluran.
Results: Renal permeability is impaired by general anesthesia with Sevoflurane (p ˂ 0.0001) and Desfluran (p > 0,001). The amount of filtered protein has a maximum at 24 hours after surgery with gradual decrease within 72 hours, but without reaching the normal preoperative values.
Conclusions: There is proteinuria after exposure to volatile agents like Sevoflurane and Desfluran recording a maximum in the first 24 hours and there is also a tendency to normalization within 72 hours. We noticed a marked impairment of renal permeability in association with specific groups of pathology as septic patients, diabetics, hypertensives, especially after Sevoflurane anesthesia. There was no-one case of acute renal failure in which to criminalize Sevoflurane or Desfluran.

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Study on Changes of the Urea, Serum Creatinine and Glomerular Protein Permeability, after General Anesthesia with Sevoflurane

DOI: 10.1515/amma-2015-0053

Introduction: The widespread use of sevoflurane as an induction and maintenance volatile agent of general anesthesia demostrates an increased safety profile. Sevoflurane contact with CO2 absorbents lead to the occurrence of toxic compounds such as Compund A and Compound B . Among the side efffects of Sevoflurane remember the renal toxic effect much discussed in the literature but still unresolved. In previous research we have demonstrated the glomerular protein changes as a result of exposure to Sevoflurane. In the current study we intend to monitor the changes in blood urea nitrogen and serum creatinine after exposure to Sevoflurane.
Material and method: We included in our study 90 patients who were anesthetized in the Department of Anesthesiology of the County Mure Hospital during 01.10.2009-01.10.2014. They had normal values for blood urea nitrogen and serum creatinine and had no preoperative proteinuria. Serum and urine samples were taken preoperatively and at 24 and 72 hours postanesthetic and were analyzed in the laboratory. Proteinuria was determined by spectrophotometry.
Results: After protein quantitative determination by spectrophotometry and statistical anaysis we obtained significant differences by comparing the average preoperative/24 hours total protein (p<0.0001) and 24/72 hours (p<0.0001). There are no significant statistical differences by comparing the blood urea nitrogen at the three intervals (p<0.53) and no statistical changes for mean serum creatinine (p<0.18).
Conclusions: Changes in glomerular filtered proteins following exposure to Sevoflurane demonstrate its toxic effect on glomerular tubules. Lack of perioperative significant wich is why we recommend determining perioperative urinary protein as a marker of glomerular damage.

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