[Thrombotic microangiopathy after kidney transplantation]. / Tromboticka mikroangiopatija nakon transplantacije bubrega.

The term thrombotic microangiopathy (TMA) encompasses different disturbances that are usually classified as thrombotic thrombocytopenic purpura (TTP) or haemolytic-uraemic syndrome (HUS). These syndromes are characterized by thrombocytopenia, microangipathic haemolytic anaemia, neurological deficits and renal failure. Etiology of TMA include exotoxins, drug toxicity (cyclosporin, tacrolimus, ticlopidine, clopidogrel, mitomycin), but also familiar forms associated with deficiency of factor H (HUS) or vWF protease activity (TTP). TMA in renal transplant recipients may evolve de novo or may recur in patients who were diagnosed with TMA as the primary renal disease. We present a case of renal transplant recipient with ESRD of unknown etiology, who was diagnosed with TMA 3 years after transplantation. After discontinuation of cyclosporine, she was treated with therapeutic plasma exchange (TPE). Cytomegalovirus reactivation demanded discontinuation of the chronic program of TPE, what was followed by worsening of graft function and demand for dialysis one year after the diagnosis of TMA. Patients with TMA should be carefully followed-up after renal transplantation for the signs of disease recurrence. Withdrawal of precipitating factors is of outstanding importance. TPE is used to limit the endothelial damage and to limit the microangiopathic process. However, its efficacy is unclear. Our case demonstrates that TPE may improve graft survival, with the possibility of inducing opportunistic infections. International registries are needed to establish the guidelines for follow-up and treatment of renal transplant recipients with TMA.

Complications of therapeutic plasma exchange: experience with 4857 treatments.

Plasma exchange (PE) is a technique of extracorporeal blood purification which removes large molecular weight substances from plasma. The Department of Dialysis, Zagreb University Hospital Center's database, which includes data on 509 patients, or 4857 PE treatments, was retrospectively analyzed to test the safety of PE. A total of 231 adverse reactions were recorded (4.75% of treatments). The most common complications were paresthesias (2.7%), hematoma at the puncture site (2.4%), clotting (1.7%), mild to moderate allergic reactions (urticaria; 1.6%) and bleeding (0.06%). True anaphylactoid reactions were recorded in five procedures. The incidence of severe, potentially life-threatening adverse reactions was 0.12%. The prophylactic use of calcium and potassium was responsible for a low incidence of electrolyte disturbances. There was no lethal outcome associated with PE. When carried out by experienced staff, PE is a relatively safe procedure. The use of fresh frozen plasma is associated with a higher rate of adverse reactions.

[Primary cytomegalovirus infection after combined cadaveric transplantation of the liver and kidney]. / Primoinfekcija citomegalovirusom nakon kombinirane kadavericne transplantacije jetre i bubrega.

Seronegative transplant recipients are at a high risk of developing primary cytomegalovirus (CMV) infection. The D+/R--constellation produces a 60%-80% probability of CMV disease. In such cases CMV prophylaxis is justified. Presentation of a 12-year old boy who developed a primary CMV infection following A combined liver-kidney transplantation; evaluation of prophylactic options and review of some difficulties in the diagnosis of CMV infection. A cadaveric liver-kidney transplantation (Tx) was done in a 12-year old boy with ESRD due to type I primary hyperoxaluria. CMV status: D+, R-; number of mismatches: 5. PRA 0; kidney cold ischemia time (CIT): 13.54 h; liver CIT: 10.10 h; immediate diuresis; Immunosuppression protocol: anti IL-2 receptor antibodies, steroids, mycophenolate mofetil (MMF); cyclosporine introduced on day 6. Over the first week, daily hemodialyses were done in order to remove oxalate deposits. Kidney and liver biopsies: no ACR, no oxalate deposits. CMV prophylaxis with ganciclovir started on day 0. Routine serology and PCR for CMV follow-up showed: pp 65, IgM and IgG, CMV. DNA (Murex CMV. DNA Hybrid Capture test 2.0): negative over the first 3 months. Day 98: CMV pp 65 positive, IgM neg, DNA neg. Day 108: pp 65 neg, IgM positive, IgG neg. CMV. DNA positive (15 x 105 copies/ml). Clinical status: except for mild Cushing, liver tests and kidney function were normal. Ganciclovir was administered intravenously (i.v.) and after 14 days continued perorally. A few days later, leukopenia with severe neutropenia (neutrophil count: 400) and right otitis media developed. MMF and ganciclovir were withdrawn for a few days and reintroduced after WBC count reconstitution. We had no possibility to monitor MMF. Day 150 pp 65 neg, IgM still positive, IgG neg. No clinical signs of infection. Liver and kidney functions normal. After liver-kidney transplantation in a CMV high-risk pediatric patient (D+/R-), asymptomatic CMV primary infection developed. Although ganciclovir prophylaxis could not prevent the infection, it was mild and delayed. Due to bone marrow suppression, discontinuation of MMF and ganciclovir was necessary. Antigenemia assay pp 65 did not correlate very well with CMV viremia so it could not be recommended as a routine test. It should be used in combination with other CMV tests.