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Background/Aims: The aim of this study is to investigate the utility of clinical [age, gender, mean arterial pressure (MAP)] and laboratory parameters [eGFR, hemoglobin (Hgb), serum levels of creatinine, uric acid, albumin, proteinuria, hematuria] and also histopathological lesions (Oxford classification parameters, crescents, intensity and pattern of staining for C3, C1Q, IgA, IgG, IgM) as progression markers in patients with IgA Nephropathy (IgAN). Methods: A total of 111 IgAN patients with a follow-up period >1 year or who reached kidney failure [GFR category G5 chronic kidney disease (CKD)] <1 year were investigated. Primary endpoint was the development of kidney failure or eGFR decline ≥50% from the baseline. Kaplan-Meier and Cox proportional hazards analyses were performed. Results: Mean follow-up period was 33±29 months. Thirty-seven (33.3%) patients progressed to kidney failure and 4 (3.6%) patients developed eGFR decline ≥50% from the baseline after a median of 23 and 65 months, respectively. In multivariate Cox regression analysis, baseline levels of Hgb (HR:0.782, 95% CI 0.559-0.973, p=0.037), serum uric acid (HR:1.293, 95% CI 1.023-1.621, p=0.046), eGFR (HR:0.966, 95% CI 0.947-0.984, p=0.004) and intensity of C3 staining (HR:1.550, 95% CI 1.198-1.976, p=0.049) predicted primary endpoint. Serum uric acid level was associated independently with T score (β=0.303, p=0.005) in patients with eGFR>30 ml/min/m2. Conclusions: Hyperuricemia and the deposition of C3 are independent risk factors for IgAN progression. [ABSTRACT FROM AUTHOR]

Background Data on use of interleukin (IL)-1 blockers in kidney transplant recipients (KTRs) with familial Mediterranean fever (FMF) are very limited. We aimed to evaluate the efficacy and safety of anakinra and canakinumab in the transplantation setting. Methods In this retrospective cohort study, we included KTRs who suffered from AA amyloidosis caused by FMF and treated with anakinra or canakinumab (study group, n  = 36). Using propensity score matching, we selected 36 patients without FMF or amyloidosis from our database of 696 KTRs as the control group. Primary outcomes were patient and graft survival. Biopsy-confirmed graft rejection, changes in estimated glomerular filtration rate (eGFR), high-sensitivity CRP (hsCRP), erythrocyte sedimentation rate (ESR), proteinuria and number of monthly attacks were secondary outcomes. Results All KTRs with FMF began IL-1 blocker therapy with anakinra and nine (25%) were switched to canakinumab. Overall death was more frequent in the study group (19.4% vs 0%) (P  = .005); however, overall graft loss was comparable between study (27.8%) and control groups (36.1%) (P  = .448). Five- and 10-year graft survival rates were significantly higher in the study group (94.4% and 83.3%, respectively) than in the control group (77.8% and 63.9%, respectively) (P  = .014 and P  < .001, respectively). Rejections were numerically lower in study group (8.3% vs 25%), but it did not reach to statistical significance (P  = .058). When compared with the pre-treatment period, with IL-1 blockers, the number of attacks per month (P  < .001), and eGFR (P  = .004), hsCRP (P  < .001) and ESR (P  = .026) levels were lower throughout the follow-up, whereas proteinuria levels were not. Conclusions Anakinra and canakinumab are effective in KTRs suffering from FMF; however, the mortality rate may be of concern. [ABSTRACT FROM AUTHOR]

We report a case that developed nephrotic syndrome during hospitalization for severe ovarian hyperstimulation syndrome without history of acute renal failure. During hospitalization, she developed persistent ascites and respiratory distress. The 24 hours urine protein analysis revealed significant proteinuria and renal biopsy showed global and segmental sclerosis in glomeruli, mesangial arteritis, proliferations in visceral epithelial cells (IgA nephropathy). To the best of our knowledge, such a complication will be presented for the first time in the literature. [ABSTRACT FROM AUTHOR]

Background. Membranous nephropathy (MN) is a common cause of nephrotic syndrome. In most cases it is idiopathic, while it may also be secondary to many diseases. In this study, prevalence of H. pylori infection and the effects of H. pylori eradication on proteinuria levels were investigated. Methods. Thirty five patients with MN (19 male), 12 patients with IgA nephropathy (4 male) and 12 patients with focal segmental glomerulosclerosis (FSGS) (8 male) were studied. The presence of H. pylori antigen was investigated in renal tissues obtained by biopsy, and the effects of H. pylori eradication on proteinuria levels were investigated. Results. Immunohistochemistry with H. pylori antigen revealed no positive staining in the glomeruli of all patients. 19 patients (54%) with MN, 10 (83%) with IgA nephropathy and 4 (33%) with FSGS were positive for H. pylori stool antigen test (P = 0.045). Patients with H. pylori infection were administered eradication therapy (lansoprazole, 30 mg twice daily, plus amoxicillin, 0.75 g twice daily, plus clarithromycin, 250 mg twice daily, for 14 days). Before the eradication therapy the mean proteinuria of patients with MN, IgA nephropathy and FSGS were 2.42 ± 3.24 g/day, 2.12 ± 1.63 g/day and 1.80 ± 1.32 g/day, respectively. Three months after eradication, baseline proteinuria levels of patients with MN significantly decreased to 1.26 ± 1.73 g/day (P = 0.031). In all three groups there were no significant differences with regard to serum creatinine, albumin and C-reactive protein levels before and after eradication therapy. Conclusions. The eradication of H. pylori infection may be effective to reduce proteinuria in patients with MN, while spontaneous remission of MN could not be excluded in this patient cohort. This trial is registered with NCT00983034. [ABSTRACT FROM AUTHOR]

Celiac disease (CD) may coexist with another autoimmune disorders. We presented a woman with coeliac disease coexistent with autoimmune hypothyroidism, nephrosclerosis and severe hyperparathyroidism. Forty years-old hypertensive woman, who had diarrhea without tenesmus, blood and mucus for 20 years, was admitted to hospital. Parathyroid hormone level was very high. Creatinine clearance was 44.5 ml/minute, and protein was 596mg/day. Renal biopsy revealed immunofluorescence negative chronic changes mimicking nephrosclerosis. The clinical and biochemical presentation of CD maybe complicated or differed from in renal failure patient. Especially management of serum phosphorus and PTH levels may have great importance. [ABSTRACT FROM AUTHOR]

Sarcoidosis is a multisystemic inflammatory disease characterized by noncaseating granulomatous inflammation of unknown origin. Although, renal involvement is rare, renal manifestations of sarcoidosis include abnormal calcium metabolism, nephrocalcinosis, nephrolithiasis, nephrotic syndrome and glomerulonephritis. We report a case of sarcoidosis presented with nephrotic syndrome and diagnosed as Ig A nephropathy [ABSTRACT FROM AUTHOR]

We report a case that developed nephrotic syndrome during hospitalization for severe ovarian hyperstimulation syndrome without history of acute renal failure. During hospi- talization, she developed persistent ascites and respiratory distress. The 24 hours urine protein analysis revealed significant proteinuria and renal biopsy showed global and seg- mental sclerosis in glomeruli, mesangial arteritis, proliferations in visceral epithelial cells (IgA nephropathy). To the best of our knowledge, such a complication will be presented for the first time in the literature.