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A Stepwise Diagnosis of Sarcoidosis Presenting with Renal Impairment and Hypercalcemia

: 269-273. 15. Vagal AS, Shipley R, Meyer CA. Radiological manifestations of sarcoidosis. Clinics in Dermatology 2007; 25: 312-325. Kishor S, Turner ML, Borg BB, et al. Cutaneous sarcoidosis and primary biliary cirrhosis: A chance association or related diseases? J Am Acad Dermatol 2008; 58: 326-335. Rajoriya N, Wotton CJ, Yeates DG, et al. Immune-mediated and chronic inflammatory disease in people with sarcoidosis: disease associations in a large UK database. Postgrad Med J 2009; 85: 233-237. 16. Bear RA, Handelsman S, Lang A, et al. Clinical and

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Membranoproliferative Glomerulonephritis Type 1 Secondary to an Infected Ventriculoperitoneal Shunt: a Case Report

Abstract

Ventricular shunting is the usual method for treatment of congenital or acquired hydrocephalus. Immune-mediated glomerulonephritis (shunt nephritis) is a rare but life-threatening complication of this neurosurgical technique. Intraglomerular deposition of circulating immune complexes and the subsequent activation of the classical pathway of serum complement’s cascade result in glomerular inflammation. Membranoproliferative gomerulonephritis is the most common histologic pattern observed in renal biopsy. The diagnosis needs high suspicion and is based on clinical and laboratory findings. Deterioration of renal function in association with signs of infection and low levels of serum complement’s proteins C3 and C4 make the diagnosis possible. The prognosis is variable and depends on the time of diagnosis after the onset of glomerular injury. The optimal treatment includes timely removal of the infected shunt in combination with aggressive antibiotic therapy. In this paper we present the case of a membranoproliferative glomerulonephritis type 1 in a patient with a ventriculoperitoneal shunt. Although this type of shunting is considered safer than the ventriculoatrial one, the risk of complications such as an immune-mediated glomerulonephritis still exists.

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MicroRNA in kidney disease

Abstract

Clinical and laboratory findings of kidney disease in an adult may find an explanation in kidney functional and/or structural abnormalities that already existed during infancy and childhood, but that may have been missed or underdiagnosed. All the cardiovascular abnormalities that occur in adults with chronic kidney disease are also present in children with chronic kidney disease. Complications in childhood chronic kidney disease will have consequences well beyond pediatric age and influence outcomes of affected young adults with disease. Kidney dysfunction appears early in the course of kidney disease and has been observed in children and adults with chronic kidney disease, condition characterised with kidney fibrosis. Transforming growth factor beta is recognized as a major mediator of kidney fibrosis. New evidence illustrates the relationship between transforming growth factor beta signaling and microRNAs expression during kidney diseases development. MicroRNAs play important roles in kidney development and kidney diseases; they are naturally occurring, 22-nucleotide, noncoding RNAs that mediate posttranscriptional gene regulation. Dysregulation of miRNA expression is an indicator of several diseases including chronic kidney disease. Targeting microRNAs should be a therapeutic potential to ameliorate the disease related to fibrosis. The discovery that circulating miRNAs are detectable in serum and plasma, and that their expression varies as a result of disease, presents great potential to be used as biomarkers in kidney disease prevention and diagnosis.

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Podocytes and Proteinuric Kidney Disease

Abstract

Glomerular disease is the most common cause of endstage renal disease (ESRD), accounting for almost two thirds of cases. In glomerular disease, alterations of po-docytes are of particular importance. Podocyte loss represents a central mediator of glomerular sclerosis. Toxic, genetic, immune, infectious, oxidant, metabolic, hemody-namic, and other mechanisms can all target the podo-cytes. These mechanisms provide new insight into the unique dynamic microenvironment that each individual podocyte inhabits and how it can turn hostile to survival. At the same time, they raise new therapeutic challenges to preserve glomerular function by containing podocyte injury and limiting its spread, both in podo-cytopathies and in other progressive glomerular diseases. Treatment strategies should aim at enhancing podocyte survival. The renin-angiotensin axis blockade, apart from its antifibrotic and intraglomerular hemodynamic effects, has an important role in preventing podocyte loss. However, only long-term observational studies can clarify if many patients will benefit from podocyte-targeted treatment such as abatacept or similar agents.

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Drusen Formation in Type II Membranoproliferative Glomerulonephritis after Renal Transplantation

Abstract

Type II membranoproliferative glomerulonephritis (MPGN) is a systemic disease that almost invariably recurs in renal allografts. This is a case of a 45-year-old woman with biopsy proven type II MPGN that led to renal failure 10 years after diagnosis. During the fifth month after cadaveric transplantation she was treated with pulse doses of methylprednisolone owing to acute T-cell mediated rejection without pathohistological signs of type II MPGN recurrence. One month later the patient was hospitalized due to acute bilateral vision deterioration. Ophthalmoscopy showed bilateral, multifocal drusen, concentrating in the posterior pole, and exudative ablation of the retinal pigment epithelium. Ocular coherence tomography (OCT) revealed focal retinal pigment epithelial elevation and detachments. The patient was treated with methylprednisolone (1 mg/kg) for 3 days. Therapy led to regression of exudation and flattening of the pigment epithelial detachments with discrete subjective visual improvement. Type II MPGN almost invariably recurs and leads to graft failure in 50% of cases. Our patient had evident chronic eye changes due to type II MPGN leaving allograft function intact during the first year of follow-up. Considering these potentially devastating effects of the disease, type II MPGN patients should be observed carefully from both the renal and eye point of view, because the severity of ocular changes, like in our case, is not always in line with allograft function.

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Alexithymia Construct in Dialysis Patients

Abstract

Introduction. The concept of alexithymia means dysfunction in emotional awareness, social attachment, and interpersonal relating. The study was performed to evaluate the alexithymia construct in patients treated with chronic maintenance haemodialysis.

Methods. TAS-20 was applied as a measure of alexithymia to a group of 230 patients, mean age 55.5±13.5 years, recruited from three dialysis centers.

Results. The results obtained showed that 50% of patients were alexithymic, and 18% had possible alexithy-mia. A small positive correlation was shown between age and obtained scores for alexithymia (r=0.025). Duration of dialysis also positively influenced the alexithymia scores (r=0.013). In addition, the duration of dialysis was significantly influenced by age (ANOVA 0.004, p<0.05). Factors analysis showed that F1 and F2 were not influenced by age or duration of dialysis. Only factor F3 (externally oriented thinking) was very perceptible and influenced by the age and the duration of dialysis (ANOVA p=0.016; <0.05).

No significant differences in scores between males and females were obtained. Only F1 was higher in males (p<0.05). The scores obtained for alexithymia were compared between healthy population and cancer and dialysis patients. Patients with chronic diseases were more alexithymic than healthy people (p< 0.05).

Conclusions. The alexithymia construct is a permanent personality trait related to neurobiological brain specifics. An alexithymia construct can influence the prognosis and outcome of dialysis patients as well as of other diseases. The psychological support for mediating alexithy-mia should be included in the therapeutic protocols, especially for end-stage renal diseases.

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Preeclampsia: from Pathophysiology to Treatment

preeclampsia. Am J Obstet Gynecol 2012; 207(4): 337. 19. Chaiworapongsa T, Chaemsaithong P, Yeo L, et al. Preeclampsia part 1: current understanding of its Pathophysiology. Nature Reviews Nephrology 2014; 10: 466-480. 20. Kublickiene KR, Cockell AP, Nisell H, et al. Role of nitric oxide in the regulation of vascular tone in pressurized and perfused resistance myometrial arteries from term pregnant women. Am J Obstet Gynecol 1997; 177: 1263-1269. 21. Cockell AP, Poston L. Flow-mediated vasodilatation is enhanced in normal

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Vitamin D Status has no Influence on the Incidence of Recurrent Urinary Tract Infections after Kidney Transplantation

-192. 13. Kubak MB, Holt CD. Infectious Complications in Kidney Transplantation and their Management. In: Handbook of Kidney Transplantation, ed. G. M. Danovitch, 2 ed., Boston, A Little, Brown 1996; 187-213. 14. Courbebaisse M, Souberbielle, Thervet E. Vitamin D and transplantation. In: R.R. Watson (ed.), Handbook of vitamin D in human health: Prevention, treatment and toxicity. Human Health Handbooks Wageningen Academic Publishers 2013, 4: 566-587. 15. Liu PT, Stenger S, Li H, et al . Toll-like receptor triggering of a vitamin D-mediated human

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Immune Renal Injury: Similarities and Differences Between Glomerular Diseases and Transplantation

-1659. 4. Land W. Innate autoimmunity: history and current knowledge. Clin Transplant 2007; 5: 575-584. 5. Debiec H, Guigonis V, Mougenot B, et al . Antenatal membranous glomerulonephritis due to neutral endopeptidase antibodies. N Engl J Med 2002; 346: 2053-2060. 6. Beck LH Jr, Bonegio RG, Lambeau G, et al . M-type phospholipase A2 receptor as target antigen in idiopathic membranous nephropathy. N Engl J Med 2009; 361: 11-21. 7. Puttarajappa C, Shapiro R, Henkie P. Antibody-Mediated Rejection in Kidney Transplantation: A Review. J Transplant

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