Sun-064 Oxydative Stress, Inflammation And development of Chronic Kidney Diseases

Abstract

Introduction:We present a case of a 40-year-old woman with IVF gemellar pregnancy in the 28th week of gestation, with primary hyperparathyroidism which complicated the course of pregnancy causing acute pancreatitis and AKI, who was treated with CRRT and succesfully overcame a hypercalcemic crisis. Methods:Case report: On admission to the Obstetrics and gynecology clinic patient was somnolent, hypertensive, tachicardic, oliguric, respiratory stable with pretibial oedema. Laboratory data showed raised inflammatory markers, anemia, elevated serum amylases, urea, creatinine and hypokalemia. Abdominal ultrasound revealed an enlarged, voluminous pancreas, whereas chest radiograph showed a large left sided pleural effusion. An inital diagnosis of severe preeclampsia was determined, with suspected acute pancreatitis. Emergent cesarean delivery was performed. In the post partum period she was treated with isotonic saline infusions, antibiotic therapy (cephalosporins, carbapenems), antihypertensive drugs, anticonvulsants, antiedematous therapy with preventive doses of heparin. After two days she was transfered to the Intensive Care Unit. She was dyspnoic with compensated respiratory acidosis. Additional laboratory findings indicated high levels of serum lipases and severe hypercalcemia (total calcium: 3,99mmol/l, ionized calcium 2,47mmol/l, hyperphosphatemia 0,45mmol/l, high levels of parathyroid hormone 834pg/ml) and hypokalemia. CT of the chest and abdomen, revealed acute pancreatitis, bilateral pleural effusions and signs of AKI. Endocranial MR showed signs of brain edema. US of the thyroid and parathyroid gland identified a cystic formation with clear borders and intranodular vascularisation in the parenchyma of the lower left lobe, size 9x13x26mm, resembling an enlarged parathyreoid gland. Other causes of hypercalcemia were excluded. Results: Previous therapy was continued with the addition of hydration (rate of 200ml/h), proton -pump inhibitors, corticosteroids, bolus doses of furosemide and byphosphonates (calcitonin was unavailable). Two combined pre-dilution procedures were performed using heparin anticoagulation and normal calcium levels of 1,5mmol/l in the dialysate. Initially CVVHDF was started (Multifiltrate Kit 8 CVVHF 1000, surface 1,8m 2 ; flow dialysate 200-300ml/h; blood flow 180-100ml/h; dialytic fluid/substitute ratio was 1:1) and further changed to CVVH with continuous potassium substitution. After the first CRRT procedure, a decrease in calcium levels was noted, with tendency for further reduction, resulting in desired (total calcium 2,23mmol/l, ionized calcium levels 1.26mmol/l) and gradual normalisation of other laboratory findings. The patients state of consciousness improved, diuresis was established and complete hemodynamic stability was reached, after which, on the 12th day of treatment, she was transfered to the Clinic of endocrionology for further treatment. Conclusions: Combining CRRT modality with heparin anticoagulation and careful monitoring of electrolyte levels can contribute to adequate...

Zinc(Ⅱ)-induced Neuroimmunological Renal Chronic Kidney Disease Prevention and Suppressive Progression

“…NOX4 is the principal NOX isoform in the kidney [41]. NAD(P)H Oxidase is activated by ROS production in endothelial vascular smooth muscle and renal parenchymal cells that zinc induced NADPH oxidase activation can reduce chronic inflammation and oxidative stress in CKD [42]. The other, NADPH oxidases play a critical role in kidney damage and Nox2-containing NADPH oxidase plays a role in cyclosporine induced kidney damage, while Nox4-containing NADPH oxidase is involved in diabetes-induced kidney damage [43].…”