Renal allograft nephropathy in patient with type 1 diabetes mellitus

Ivannikova, E. V.; Vikulova, Olga K.

doi:10.14341/2072-0351-5984

Cited by 2 publications

(2 citation statements)

References 8 publications

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“…У 2 пациентов ввиду наличия дуоденоцистоанастомоза развился геморрагический цистит с частыми обострени-ями. Инфекция мочевых путей -один из возможных фак-торов снижения выживаемости почечного трансплантата, развивающаяся вследствие хронической иммуносупрес-сивной терапии, достаточно частого латентного бессим-птомного течения, что в конечном итоге может привести к сепсису [9]. Поэтому необходимо осуществлять строгий контроль клинико-лабораторных анализов мочи и свое-временно назначать антибактериальную терапию, ори-ентируясь на чувствительность инфекционного агента, отсутствие нефротоксического воздействия (фторхино-лоны, цефалоспорины).…”

Section: состояние функции почекunclassified

Late Diabetic Complications in Patients with Type 1 Diabetes who Received Simultaneous Pancreas-Kidney Transplantation

et al. 2015

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Aim. The aim of this study was to investigate late diabetic complications in patients with Type 1 diabetes mellitus (T1DM) who received simultaneous pancreas-kidney transplantation (SPK). Materials and Methods. The study included 16 patients with T1DM who received SPK. All patients underwent clinical examination and diagnostic investigation. Results. After SPK, 93.75% of the patients had a functioning pancreas transplant, and 100% had a functioning kidney transplant within 4?48 months [mean 21 months (10 is revealed; 36)). All patients had euglycaemia according to daily monitoring. The mean level of glycated haemoglobin (HbA1c) before surgery was 9.1% (range 8.7%?11%) and was 5.7% after surgery (5.55%?5.9%; p < 0.0001). The baseline level of insulin was 12.5 ?IU/ml (11.4?15.3 ?IU/ml) and the baseline level of C-peptide was 2.02 ng/ml (1.07?2.77 ng/ml). Normal renal function was observed (glomerular filtration rate 76 ml/min/1.73 m2 (68?90 ml/min/1.73 m2). Other laboratory findings included haemoglobin 127 g/l (120?130 g/l), serum parathyroid hormone 77.5 pg/ml (61?85 pg/ml), serum phosphate 1.2 mmol/l (1.07?1.3 mmol/l) and blood pressure 110(100?120)/70(64?80) mmHg. In 37.5% of the patients, vitrectomy and additional laser panretinal photocoagulation were performed for proliferative diabetic retinopathy. Other ophthalmological disorders included newly diagnosed cataract (81.25%), secondary cataract (25%) that required YAG discission in three patients, glaucoma (25%) and macular oedema (12.5%). Ulcers of the lower extremities were observed in 31.25% of the patients, and chronic osteoarthropathy was observed in four. One patient underwent amputation of index and ring fingers and resection of the first and third metatarsal heads to treat osteomyelitis. One patient underwent balloon angioplasty and stenting for advanced atherosclerotic stenosis of blood vessels of the lower extremities. Conclusions. Euglycaemia and recovery of renal function 6?48 months after SPK resulted in a significant decrease in diabetic complications without clinical signs of regression in some patients. However, some patients suffered progression of complications, reflecting their multifactorial causes. These findings highlight the need for timely diagnosis, treatment and long-term follow up to improve the quality of life and prognosis in patients with T1DM receiving SPK.

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Section: состояние функции почекunclassified

Late Diabetic Complications in Patients with Type 1 Diabetes who Received Simultaneous Pancreas-Kidney Transplantation

et al. 2015

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“…Проблема выживаемости трансплантата обу словлена развитием так называемой хронической трансплантационной нефропатии и рекуррентной ДН, проявляющейся снижением фильтрационной функции трансплантата. К факторам риска развития хрониче-ской трансплантационной нефропатии и, как следствие этого, отторжения трансплантата относят: пол, возраст реципиента и донора, продолжительность диализа, тип трансплантата (родственный или трупный), эф-фективность иммуносупрессивной терапии, контроль АД, профилактика инфекций и анемии [10]. Хрониче-ская декомпенсация углеводного обмена ответственна за формирование диабетического поражения почечного трансплантата.…”

Section: обсужденияunclassified