Cardiovascular events are the major cause of death in renal transplant recipients. The detection of left ventricular hypertrophy (LVH) raises probability of adverse prognosis. On the other hand, partial regressions of LVH that is known to occur after renal transplantations (RT) may considerably decrease the risk. The aim of this study was revealing of major risk factors associated with progression/regression of LVH during the first and the second years after renal transplantations. We examined 102 renal transplant patients (64.7% males, 35.3% females, age 39 ± 11 years). The median of glomerular filtration rate was 49 (38; 67) ml/min; the ischemic heart disease (IHD) was diagnosed in 30.4% of recipients. Echocardiographic LV dimensions were recorded using standard technique. The LVH was detected if left ventricular mass index (LVMI) exceeded 134 g/m² for men and 110 g/m² for women. In first 8 months after RT the LVH criteria were met in more than 50% of patients; after 9 months after RT LVH was found only in 30% patients. Renal transplant dysfunction, hypertension, proteinuria, hypoalbuminemia, functioning of arteriovenous fistula, infections, and hemodialysis treatment were defined as factors associated with the LVH. Prevalence of LVH was significantly higher in patients with IHD. The risk for LVH was also increased in cases of acute rejection. 62 patients were repetitively examined by echocardiography. The LVH criteria appeared in 55% cases after 4.5 months and only in 33.5% after 17.5 months after RT (p = 0.008). The LVMI decreased from 129 (105; 158) to 113 (92; 146) g/m², (p = 0.009). According to the progression or regression of LVH we subdivide all patients into three groups: (i) those without LVH during the follow-up period (35%), (ii) patient with a significant decrease in LVMI by the end of follow-up (34%), and (iii) group with a significant increase in LVMI at 17.5 months (31%). Regression of LVH was usually accompanied by normal renal transplant function, normalization of blood pressure, hemoglobin level, and arteriovenous fistula closure. Progression of LVH was associated with proteinuria, hypoalbuminemia, and IHD. The median of LVMI in patients treated with ACE inhibitors (ACEi) was significantly lower than in recipients without ACEi (119 (100; 135) vs . 140 (108; 165) g/m², р = 0.006).

The papers shows the morphological findings of and clinical and demographic data on 61 patients with non-amyloid form of renal monoclonal immunoglobulin deposition disease (MIDD) unassociated with AL-amyloidosis and/or Bence Jones cast nephropathy: 40 cases of light-chain deposition disease, 18 cases of light-and-heavy chain deposition disease and 3 cases of heavy-chain deposition disease. According to the composition of the paraprotein deposits, the cases were distributed as follows: k (30), l (10), IgG/k (6), IgA/k (6), IgG/l (4), IgA/l (2) and g (3). Light microscopy revealed three variants of the glomerular pattern: diffuse nodular glomerulopathy (42.6%), diffuse mesangial dilation (27.9%) and intact glomeruli (29.5%). Varying severity of tubular atrophy was noted in 95% of cases. Tubular, glomerular, and smooth muscle basement membrane deposits substantially differed in immunofluorescent (100, 91.8 и 54.1%, respectively) and ultrastructural studies (55.7, 45.9 и 4.9%, respectively). Azotemia (68.9%) and proteinuria (55.8%) were most commonly revealed. Nephrotic syndrome and heavy proteinuria together made 27.9%.

Parathyroid function, calcium-phosphorus metabolism, bone structure and mineral density were studied in 104 patients (63 women and 41 men aged 18-71) with chronic renal failure (CRF) treated with continuous ambulatory peritoneal dialysis (CAPD) for 6-46 months. Patients were divided into 3 groups depending on plasma parathyroid hormone (PTH) concentration and activity of general alkaline phosphatase (AP): 1 - patients with supposed normal bone metabolism (PTH 150-450 pg/ml, AP 205 ± 49 un/l), 2 - those with secondary hyperparathyroidism (HPT, PTH > 450 pg/ml, AP 354 ± 171 un/l), and 3 - those with adynamic (low metabolic) bone disease (ABD, PTH < 150 pg/ml, AP 82 ± 25 un/l). Group 2 patients suffered from congenital and hereditary nephropathy significantly more often than other patients and had a higher rate of extremity bone fractures. Plasma phosphorus was equally increased in all patients; ionized calcium (Ca²⁺) concentration was decreased in patients of groups 1 and 2 and increased in patients of group 3. In all patients, the rate of osteopenic syndrome in distal forearm was 63.5%, in proximal femur - 59.3%, and in lumbar spine - 49.2%, and appeared to be equivalent in all skeletal areas. The rate of osteopenia in distal forearm and in proximal femur in patients of group 2 was significantly higher than in group 1 (p = 0.034). Group 2 patients were the most deficient of bone mass, especially in bones with cortical structure. In CRF patients receiving CAPD substitution therapy, the secondary hyperparathyroidism prevails (51.9%). These patients have the highest bone mineral deficiency and the highest rate of the latter (mainly in bones with cortical structure) which is a risk factor for bone fractures.

This article presents the results of identification of mutations in the podocin gene ( NPHS2 ) in 50 Russian children with sporadic steroid-resistant nephrotic syndrome (SRNS) and in the control group of 50 healthy children. One novel heterozygous nonsense mutation of c.259 G>T ( p.87Glu>X ) was identified in the exon 1 of the NPHS2 gene in a SRNS child with FSGS. We also found one kind of single nucleotide polymorphism c.872+7A>G in the intron 7 of the NPHS2 gene in 3/50 SRNS patients and in 5/50 children in control (6% and 10%, respectively, р > 0.05). Our results indicate that mutation-detected rate in the NPHS2 gene in Russian children with sporadic SRNS was low. Preliminary data suggest that there is a genetic heterogeneity of SRNS in Russian children.

Combination of lupus nephritis and antiphospholipid syndrome nephropathy may occure in patients with SLE, complicated with antiphospholipid syndrome, in 32-68% of cases. Clinical manifestations of antiphospholipid syndrome nephropathy and proliferative lupus nephritis, such as arterial hypertension and progressive renal failure may be similar, and often only renal biopsy can help to make a proper diagnosis and choose adequate treatment strategy. Serial renal biopsies may help not only in assessing degree of activity and the progression of chronicity of lupus nephritis, but may also show possible class transformation. Transitions in lupus nephritis are not unusual and almost any class has been documented to go to any other class. Successful treatment of diffuse proliferative lupus nephritis may result in the transformation to membranous LN. The pediatric patient with biopsy proven LN class IV developed flare with dialysis-dependent renal failure due to superimposition of thrombotic microangiopathy. The case illustrates the difficulties of diagnostics, only the second biopsy, performed 7 months later and after 4 month of aggressive immunosupression with steroids and cyclophosphamide, indicated the presence of thrombotic microangiopathy with glomerular ischemia and transformation of the LN to class V. Interestingly, there were no other clinical symptoms of APS, anticardiolipin antybodies were in normal range, and only presence of lupus anticoagulant, found after second biopsy, supported diagnosis of APS. Addition of long-term anticoagulant therapy lead to partial restoration of renal function, so that patient became dialysis-free after 22 months of treatment. Supportive treatment with low-dose steroids, mycophenolates and warfarin allows to maintain remission over 18 months.

Hemodialysis patients require parenteral iron to replenish/maintain sufficient iron stores and optimize erythropoietin (EPO) use. Two parenteral iron preparations are available in the UK, iron dextran (CosmoFer) and iron sucrose (Venofer). Debate about their safety profiles continues. We performed an observational study of chronic kidney disease patients and a prospective crossover study in hemodialysis patients to examine the comparative safety and tolerability of CosmoFer and Venofer. Side effects, hemoglobin, ferritin and EPO dose were recorded. One hundred and forty-four patients received CosmoFer (2294 doses) and 110 received Venofer (2111 doses). Fifteen reactions occurred with no anaphylactic episodes in either group. Thirty-nine patients (28 men), mean age 60.5 years, on intravenous Venofer were converted to CosmoFer for 6 months. They were then converted back to Venofer. No differences in hemoglobin, EPO dose or ferritin levels throughout the study were observed. Side effects were minor after 546 and 507 doses of CosmoFer and Venofer (13 reactions (eight CosmoFer, five Venofer) occurred in eight patients). Conversion from Venofer to CosmoFer led to a cost saving of £77 per patient over the 6-month study period. In this study, the two forms of therapy were equally safe and effective. Examination of a larger cohort of patients is necessary to verify these findings and potentially reassess European Best Practice Guidelines.