We evaluated the effect of pregabalin in the treatment of uraemic pruritus not due to secondary hyperparathyroidism. Sixteen haemodialysis patients suffering from uraemic pruritus resistant to conventional treatment started on pregabalin 25 mg/day orally. The parameters recorded were age, time on haemodialysis, haematocrit, Ca, PO₄ , Ca × PO₄ product, PTH, spKt/V, eosinophil counts and IgE. The effectiveness of pregabalin on uraemic pruritus was evaluated by using visual analogue scale before and after one month of treatment. Visual analogue scale consisted of a 10-cm horizontal line scored from 0 (no itch) to 10 (worst imaginable itch). Four patients discontinued treatment due to side effects and therefore were excluded from the study. The mean age of the remaining 12 patients was 61.2 ± 12.8 years, and the time on haemodialysis was 38 ± 39.1 months. The haematological and biochemical profile of the patients remained without significant change at the end of the observation period. There was a statistically significant difference between visual analogue scale values before and after the one month treatment period (7.44 ± 2.01 and 1.7 ± 1.31, respectively), p < 0.0003. Uraemic pruritus is a common and distressing symptom in patients undergoing haemodialysis. Pregabalin appears to be an effective alternative treatment.

Familial microscopic hematuria (FMH) is associated with a genetically heterogeneous group of conditions including the collagen-IV nephropathies, the heritable C3/CFHR5 nephropathy and the glomerulopathy with fibronectin deposits. The clinical course varies widely, ranging from isolated benign familial hematuria to end-stage renal disease (ESRD) later in life. We investigated 24 families using next generation sequencing (NGS) for 5 genes: COL4A3, COL4A4, COL4A5, CFHR5 and FN1. In 17 families (71%), we found 15 pathogenic mutations in COL4A3/A4/A5, 9 of them novel. In 5 families patients inherited classical AS with hemizygous X-linked COL4A5 mutations. Even more patients developed later-onset Alport-related nephropathy having inherited heterozygous COL4A3/A4 mutations that cause thin basement membranes. Amongst 62 heterozygous or hemizygous patients, 8 (13%) reached ESRD, while 25% of patients with heterozygous COL4A3/A4 mutations, aged >50-years, reached ESRD. In conclusion, COL4A mutations comprise a frequent cause of FMH. Heterozygous COL4A3/A4 mutations predispose to renal function impairment, supporting that thin basement membrane nephropathy is not always benign. The molecular diagnosis is essential for differentiating the X-linked from the autosomal recessive and dominant inheritance. Finally, NGS technology is established as the gold standard for the diagnosis of FMH and associated collagen-IV glomerulopathies, frequently averting the need for invasive renal biopsies.

Background. The evidence base regarding the safety of intravenous (IV) iron therapy in patients with chronic kidney disease (CKD) is incomplete and largely based on small studies of relatively short duration. Methods. FIND-CKD (ClinicalTrials.gov number NCT00994318) was a 1-year, open-label, multicenter, prospective study of patients with nondialysis-dependent CKD, anemia and iron deficiency randomized (1:1:2) to IV ferric carboxymaltose (FCM), targeting higher (400–600 µg/L) or lower (100–200 µg/L) ferritin, or oral iron. A post hoc analysis of adverse event rates per 100 patient-years was performed to assess the safety of FCM versus oral iron over an extended period. Results. The safety population included 616 patients. The incidence of one or more adverse events was 91.0, 100.0 and 105.0 per 100 patient-years in the high ferritin FCM, low ferritin FCM and oral iron groups, respectively. The incidence of adverse events with a suspected relation to study drug was 15.9, 17.8 and 36.7 per 100 patient-years in the three groups; for serious adverse events, the incidence was 28.2, 27.9 and 24.3 per 100 patient-years. The incidence of cardiac disorders and infections was similar between groups. At least one ferritin level ≥800 µg/L occurred in 26.6% of high ferritin FCM patients, with no associated increase in adverse events. No patient with ferritin ≥800 µg/L discontinued the study drug due to adverse events. Estimated glomerular filtration rate remained the stable in all groups. Conclusions. These results further support the conclusion that correction of iron deficiency anemia with IV FCM is safe in patients with nondialysis-dependent CKD.

In this paper, we investigated the incidence of depression and its relation to clinical, laboratory parameters and sleep disorders in 45 haemodialysis (HD) patients. They were divided into two groups. Group A (n = 29) had no depression, whereas Group B (n = 16) had clinically assessed depression. Subjects were compared in terms of socioeconomic, clinical, laboratory parameters and presence of sleep disorders. Groups were matched for age, sex, family status, education, self-esteem, coffee and alcohol consumption, psychiatric history, time on HD and laboratory (serum urea, creatinine, electrolytes, iron, albumin and lipids) parameters. Group B demonstrated significantly lower haemoglobin levels (11.13 ± 1.69 and 12.23 ± 1.31 g/dl, respectively; p < 0.01) and higher C-Reactive Protein (CRP) levels (1.82 ± 1.73 and 0.83 ± 0.6 mg/dl, respectively; p < 0.005) compared to Group A. Additionally, strong correlation was observed when Hamilton Depression Scale scores were related to haemoglobin (r =-0.30, p < 0.05), CRP (r = 0.38, p < 0.001) and AIS scores (r = 0.54, p < 0.0001). In conclusion, depression seems to be related to high CRP, low haemoglobin levels and sleep disorders.

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