Dusan Bozic

Influence of infiltrate densityin interstitium on the prognosis of primary glomerulonephritis

Background/Aim. Development of inflammatory changes, fibrosis and loss of morphological structures of the interstitium have an important role in pathogenesis of primary glomerulonephritis, affecting the development, course and prognosis of the disease. The aim of this study was to determine the influence of changes in the interstitium on the prognosis of primary glomerulonephritis. Methods. The research included 216 patients suffering from different types of primary glumeronephritis treated at the Clinic for Nephrology and Clinical Immunology of the Clinical Center of Vojvodina, Serbia who were being monitored on average for 77.5 months. After determining on pathohistological diagnosis of the type of glomerulonephritis, renal changes in the interstitium were quantified. Numerical density in the tissue volume unit and structure of infiltrates of the interstitium were established by using the Weibel system (M42) incorporated into light microscope. Routine analyses were performed by using standard laboratory procedure. Results. During the research period the highest numerical density of infiltrates was verified in extracapillary glomerulonephritis (147,869 × mm-3), slightly less in membranoproliferative glomerulonephritis (116,800 × mm-3) and focal segmental glomerulosclerosis (96,147 × mm-3), and the least being in glomerulonephritis with minimal changes (11,416 × mm-3). In all types of glomerulonephritis, apart from glomerulonephritis with minimal changes, there was a significantly (p < 0.0005) higher numerical density and incidence of infiltrate cells in relation to the control group. By comparing the numerical density of infiltrates of all cells to the parameters of renal function, a significant (p < 0.01) correlation of these phenomena was established. In order to get a better insight into the speed of progression of renal failure by setting a numerical limit of the density of infiltrates < 100,000 / > 100,000 cells/mm3, regardless of the type of glomerulonephritis, a prognostic predictor was established on the basis of which the patients with lower infiltration of the interstitium had significantly (p < 0.005) lower progression of renal failure. Conclusion. Density of infiltrates in the interstitium in primary glomerulonephritis is an important early prognostic predictor of progression of renal failure.

Post-transplant lymphoproliferative disorder after kidney transplantation

Online first: March 31, 2017 SUMMARY Introduction Post-transplant lymphoproliferative disorder (PTLD) is one of the most severe and often fatal complications observed after solid organ and bone marrow transplantations. Case outline We present a case of a patient born in 1989 who underwent a living related donor renal transplantation at the age of 16. Induction therapy implied the administration of anti-thymocyte globulin and corticosteroids, and maintenance therapy encompassed a combination of three immunosuppressive agents – tacrolimus, mycophenolate mofetil, and corticosteroid. The patient experienced first complications six months after transplantation, manifested as aggravation of tonsillitis symptoms and subsequent dysphagia. Histopathological and immunohistochemical finding of tonsillectomy specimens suggested polymorphic PTLD (with high expression of Epstein–Barr virus latent membrane protein antigen). Definitive diagnosis of diffuse large B-cell lymphoma (CD20+) was established upon analysis of oesophageal bioptate. Antiviral therapy was applied, along with rituximab and a combination of cyclophosphamide, doxorubicin (hydroxydaunomycin), vincristine, and prednisolone (CHOP therapy), whilst the dosage of basic immunosuppressive drugs was reduced. Complex diagnostic procedures confirmed the absence of disease recurrence and stable graft function five years after completing the PTLD therapy. Conclusion The presented case of our patient, who developed PTLD after renal transplantation, demonstrated that appropriate early diagnosis, reduction of immunosuppressive regimens, and vigilant application of immunomodulatory and chemotherapy could result in complete disease remission, yet preserving and maintaining the stable function of the transplant.

Platelet turnover and function in end-stage renal disease

Background/Aim. End-stage renal disease (ESRD) is characterized by significant impairment of platelet functions which may cause bleeding or thrombotic complications. The iam of this study was the aim of this study was the assessement of platelet turnover and function and their correlation with inflammatory and procoagulant markers in ESRD patients as well as platelet indicies comparison between ESRD diabetic and ESRD non-diabetic patients. Methods. The prospective, observational clinical study included 63 ESRD patients and 30 age and sex matched healthy volunteers. Following laboratory parameters of platelet turnover and function (platelet count, reticulated platelets, platelet indices, whole blood impedance platelet aggregation), inflammatory and procoagulant markers (number of neutrophils, neutrophil to lymphocyte ratio, C-reactive protein, plasma fibrinogen, D dimer, von Willebrand factor) were obtained. Results. Platelet turnover (% of reticulated platelets) was significantly higher (3.8 ± 2.3 vs. 2.3 ± 1.3; p < 0.01) and platelet aggregation tests induced by thrombin receptor activiting peptide (TRAP) (p < 0.01), adenosine diphospate (ADP) (p < 0.05), arachidonic acid (ASPI) (p < 0.05) and collagen (p < 0.05) were markedly increased in the ESRD patients compared to the control group. The comparison of chronic inflammation and procoagulant markers revealed higher values in all patients comparing to the group of healthy subjects (p < 0.01 regarding all parameters). There was no difference between the ESRD diabetic and ESRD non-diabetic patients. Conclusion. Results point out increased platelet turnover in ESRD as a consequence of platelet activation and consumption induced by clotting system hyperactivity and chronic inflammation. None of the examined parameters do not predict bleeding occurrence.

Radiocontrast - induced nephropathy

Introduction Hospital-acquired acute renal failure increased in the last years from about 5 to 6.4%, while mortality remained high and according to newest investigations it is about 60% on average. Radiocontrast-induced nephropathy is the third cause of death in hospital-acquired acute renal failure. Risk factors for radiocontrast-induced nephropathy Risk factors for radiocontrast-induced nephropathy include: the existing kidney disease diabetes, dehydratation, multiple myeloma, older age and earlier kidney damage by contrast substances. Course of radiocontrast-induced nephropathy The clinical course of radiocontrast-induced nephropathy may manifest from asymptomatic picture to development of oliguric form of acute renal failure. Prevention and treatment modalities of radiocontrast-induced nephropathy Modalities of prevention and treatment of radiocontrast-induced nephropathy are as follows: adequate hydration of patients, appropriate application of diuretics, calcium channel blockers nonionizing radiocontrast and preventive haemodialysis. Experimental studies in prevention and treatment of radiocontrast-induced nephropathy Experimental studies indicate application of atrial natriuretic peptide, endothelin, prostaglandin. Case review Two patients treated at the Clinic for Nephrology and Clinical Immunology in Novi Sad, presented with radiocontrast-induced nephropathy. In one patient it appeared after panaortography and in the second after computerized tomography of the abdomen. In both cases aggravation occurred due to already existing renal failure caused by radiocontrast substances. Conclusion The problem is particularly important because there is a large number of patients in whom there is a risk of radiocontrast-induced nephropathy and it is necessary to carry out adequate prophylaxis and accurate assessment of kidney function before application of radiocontrast substances.