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001-es BibID:BIBFORM061605
Első szerző:Agarwal, Mohit
Cím:Severe Symptomatic Hypocalcemia after Denosumab Administration in an End-Stage Renal Disease Patient on Peritoneal Dialysis with Controlled Secondary Hyperparathyroidism / Mohit Agarwal, Éva Csongrádi, Christian A. Koch, Luis A. Juncos, Vonda Echols, Mihály Tapolyai, Tibor Fülöp
Dátum:2013
Megjegyzések:We report the 1st case of severe, symptomatic hypocalcemia after denosumab (RANKLinhibitor) treatment in a peritoneal dialysis patient with secondary hyperparathyroidismand osteoporosis. A 58-year-old Caucasian female has been receiving chronicambulatory peritoneal dialysis for four years secondary to polycystic kidney disease.Laboratory studies revealed: albumin-corrected calcium 9.0 mg/dL, phosphorus 5 mg/dL,alkaline phosphatase (ALP) 58 U/L [normal, 40-105], albumin 3.4 gm/dL [normal, 3.6-5.4]and intact parathyroid hormone (PTH) 315 pg/mL [normal, 40-72]. Marked osteoporosiswas noted on the DXA scan, preventing her from renal transplantation considerations.She had failed conventional medical treatment, including per os calcium, monthlyergocalciferol (50,000 units/month), activated vitamin-D analog (doxercalciferol) andrenal-failure adjusted alendronate (70 mg twice a month). She was started onsubcutaneous denosumab 60 mg every 6 months. After her first dose, she developed aprogressive drop of calcium, phosphorus, bicarbonate and magnesium, in spite ofmassive escalation of doxercalciferol and calcium supplementation. Hypocalcemianadired at 6.3 mg/dL with symptomatic tetany, requiring a brief hospitalizationapproximately 7 weeks after denosumab treatment. Her elevated PTH rose furthertransiently (647 pg/mL), along with ALP (123 U/L). Bone-mineral parameters normalizedapproximately 3 months after denosumab administration. The observed phenomenonresembled the phenotype of "hungry bone syndrome" observed after surgicalparathyroidectomy.Conclusion: Treatment decisions based on bone densitometry results alone are nottransposable between patients with or without end-stage renal disease. Denosumab maylead to critical hypocalcemia in dialysis patients and further aggravate existing secondaryhyperparathyroidism.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:British Journal of Medicine & Medical Research. - 3 : 4 (2013), p. 1398-1406. -
További szerzők:Csongrádi Éva (1969-) (szakorvos) Koch, Christian A. Juncos, Luis A. Echols, Vonda Tapolyai Mihály (1968-) (nefrológus) Fülöp Tibor (1957-) (kardiológus)
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2.

001-es BibID:BIBFORM061583
Első szerző:Csongrádi Éva (szakorvos)
Cím:Role of carbon monoxide in kidney function : is a little carbon monoxide good for the kidney? / Csongradi, E., Juncos, L. A., Drummond, H. A., Vera, T., Stec, D. E.
Dátum:2012
Megjegyzések:Carbon monoxide (CO) is an endogenously produced gas resulting from the degradation of hemeby heme oxygense or from fatty acid oxidation. Heme oxygenase (HO) enzymes are constitutivelyexpressed in the kidney (HO-2) and HO-1 is induced in the kidney in response to severalphysiological and pathological stimuli. While the beneficial actions of HO in the kidney have beenrecognized for some time, the important role of CO in mediating these effects has not been fullyexamined. Recent studies using CO inhalation therapy and carbon monoxide releasing molecules(CORMs) are demonstrating that increases in CO alone can be beneficial to the kidney in severalforms of acute renal injury by limiting oxidative injury, decreasing cell apoptosis, and promotingcell survival pathways. Renal CO is also emerging as a major regulator of renal vascular andtubular function acting to protect the renal vasculature against excessive vasoconstriction and topromote natriuresis by limiting sodium reabsorption in tubule cells. Within this review, recentstudies on the physiological actions of CO in the kidney will be explored as well as the potentialtherapeutic avenues that are being developed targeting CO in the kidney which may be beneficialin diseases such as acute renal failure and hypertension.
Tárgyszavak:Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban
Heme oxygenase
renal failure
blood pressure
bilirubin
acute renal injury
Megjelenés:Current pharmaceutical biotechnology 13 : 6 (2012), p.819-826. -
További szerzők:Juncos, Luis A. Drummond, Heather A. Vera, Trinity Stec, David E.
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001-es BibID:BIBFORM061609
Első szerző:Ferguson, Lee M.
Cím:Recurring Extracorporeal Circuit Clotting During Continuous Renal Replacement Therapy in Fungal Sepsis / Ferguson, Lee M., Dreisbach, Albert W., Csongrádi, Éva, Juncos, Luis A., Fulop, Tibor
Dátum:2013
ISSN:0002-9629
Megjegyzések:The relative effectiveness of anticoagulation strategies during continuous renal replacement therapy (CRRT) may vary according to the clinical circumstances. In this study, the case of a 46-year-old man who developed fungal mediastinitis with the pathogen Scedosporium prolificans after coronary bypass surgery is reported. Numerous debridements and multiple antifungal agents were not effective in this patient. Miltefosine, a non-Food and Drug Administration-approved agent, was started after institutional review board request and approval. CRRT was initiated with regional citrate anticoagulation (RCA) for clinical sepsis with acute kidney injury. Subsequently, crescendo clotting of the extracorporeal circuit (ECC) occurred. Multiple interventions, including escalating RCA, adding increasing heparin to RCA and exchanging the dialysis catheter, were not effective. Argatroban anticoagulation was started without further ECC clotting, and the patient recovered from both acute kidney injury and septic shock, despite continued miltefosine administration. Sepsis may contribute to recurrent ECC clotting. Argatroban, a direct thrombin inhibitor, had a disproportionate effectiveness to maintain ECC patency in this patient.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal Of The Medical Sciences. - 345 : 3 (2013), p. 256-258. -
További szerzők:Dreisbach, Albert W. Csongrádi Éva (1969-) (szakorvos) Juncos, Luis A. Fülöp Tibor (1957-) (kardiológus)
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