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Background and Aims Hyperphosphatemia is common in end-stage renal disease (ESRD) because of impaired renal phosphate excretion and is treated by dietary measures, dialysis techniques and the use of phosphate binder medication. It is one of the most important cardiovascular risk factors for dialysis patients. Our goal was to involve dialysis patients in the achievement of phosphate targets by self-adjusting the dose of Phosphate Binders (PB) on a meal-to-meal basis, according to the individual dietary P intake Method We conducted an interventional prospective single-arm study with a pre-post design. The inclusion criteria were patients with ESRD who had been receiving dialysis for more than three months, with dialysis schedule for four hours per session, three times per week, and who were older than 18 years of age. The primary endpoints of the study were the number of patients who reached the goal of serum phosphate before and after the training program and the weekly mean serum phosphate levels evaluated after the intervention period and compare them with the pre-intervention baseline levels. The secondary end-point was the burden of PB daily. All patients were trained in a self-administer PB program. A self-adjusted PB dose card was developed based on the phosphate food content list published by the National Technical University of Athens. The aim was to allow patients to immediately calculate the iP content of any food they consume easily. Phosphate Equivalent (PEQ) was defined as the weight of phosphorus having the same phosphate impact as a given weight of food. One PEQ corresponded in 100 mg of inorganic phosphorous and to one tablet of PB (one tablet of 800 mg of sevelamer). After 4 weeks (weeks 1-4) of washout from previous phosphate binders, eligible patients with serum phosphorus concentrations ≥ 6 mg/dl were included in the study. All patients received standard dietary phosphate counseling and a fixed dosing regimen of sevelamer PB was prescribed according to KDIGO and dialysis unit protocols for eight weeks (weeks 5-12 – pre-intervention period) In the 13th week, patients were asked to practice the self-administer PB program for eight more weeks. Results A total of 97 patients were screened for the study. 21 patients were excluded. 74 patients completed the study. The percentage of patients with uncontrolled phosphate levels reduced from 56.76% (42 out of 74) to 36.48 % (27 out of 74) in the post-intervention period. Of 9 patients who initially had a serum phosphorus level ≥9 mg/dl, 8 were reverted to phosphorus levels < 6 mg/dl at the end of the PEQ intervention period. There was a significant reduction of phosphate levels (prePEQ 7.42 ± 1.43 mg/dl vs. postPEQ 5.59 ± 1.82 mg/dL, p=0.036) and Ca × P levels (prePEQ: 67.1 ± 11.5 mg2/dL2; postPEQ: 51.9 ± 13.4 mg2/dL2, p=0.021) after patient education. There was a non-significant increase on serum calcium (pre PEQ: 8.13 ± 1.18 mg/dL; post PEQ: 8.56 ± 0.83mg/dL, p=0.515) and iPTH (prePEQ: 411 ± 376 pg/mL; postPEQ: 381 ± 321 pg/mL,p=0.13) Conclusion Our work shows that providing the patients with a relatively simple tool about the use of phosphate binders as PEQ is, we had a positive effect on the dialysis patients’ knowledge about the use of PB, phosphate content of their meals, and increase their sense of the necessity of the treatment and it was proved more effective than the standard fixed dose method. Using the PEQ education system was rewarding in an additional 20% of the patients with previous uncontrolled hyperphosphatemia. The PEQ education system is an efficient self-adjustment phosphate binder dosage tool in dialysis patients in reducing the serum phosphate level in our hemodialysis patients.

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.

Acute kidney injury (AKI) is a well-known complication in patients with chronic lymphocytic leukemia (CLL). It could occur via diverse mechanisms such as leukemic infiltration, extrarenal obstruction, tumor lysis syndrome, glomerular diseases, and medication side effects. The incidence of kidney disease at the diagnosis of CLL is about 10%. We report a case of AKI, in a patient with a known history of CLL, due to abdominal compartment syndrome, caused by extremely enlarged intra-abdominal lymph masses. To the best of our knowledge, no case of AKI due to such cause has been reported so far.

Residual Renal function (RRF) has an important role in the overall morbidity and mortality in hemodialysis patients. The role of angiotensin-converting enzyme inhibitor (ACEi) in preserving renal function in chronic proteinuric nephropathies is well documented. We test the hypothesis that enalapril (an ACEi) slows the rate of decline of RRF in patients starting hemodialysis. A prospective, randomized open-label study was carried out. 42 patients were randomized in two groups either in treatment with enalapril or no treatment at all. Our study has proven that enalapril has a significant effect on preserving residual renal function in patients starting dialysis at least during the first 12 months from the initiation of the hemodialysis. Further studies are necessary in order to investigate the potential long-term effect of ACEi on residual renal function and on morbidity and mortality in patients starting hemodialysis.

Hyperkalemia is a common clinical problem in dialysis patients. We wish to present an unusual case of severe hyperkalemia caused by fragmentation haemolysis in a dialysis patient with a prosthetic aortic valve. A 45-year-old man with a 5-year history of end-stage renal disease under dialysis, a known history of paroxysmal atrioventricular nodal re-entrant tachycardia and aortic valve replacement, presented to our department with a recent history of palpitation and profound generalized muscle weakness. The laboratory evaluation revealed severe hyperkalemia (potassium 8.5 mEq/l), anaemia, high levels of lactate dehydrogenase, indirect bilirubin and low levels of haptoglobin, and the peripheral blood smear showed a high percentage of schistocytes (3.8%). A diagnosis of hyperkalemia caused by fragmentation haemolysis attributed to the haemodynamic turbulence on an artificial surface caused by the supraventricular tachycardia was established. After normal sinus rhythm was restored the patient presented with complete remission to the pre-event values of all haemolysis indices.

Disturbances of carbohydrate metabolism are common in patients with chronic kidney disease (CKD). Possible pathogenetic mechanisms involve unresponsiveness of insulin receptor and/or a bland response of the beta cell at the stimulus of hyperglycaemia. It is known that vitamin D has an important role in the endocrine function of the pancreas, particularly in the insulin release process, and is one of the determinants of insulin resistance [1]. This metabolic complication may be implicated in the accelerated atherosclerotic process and is common in CKD. The aim of our study was to investigate the effect of vitamin D treatment on insulin resistance in patients with CKD stage 3. We included in our study 37 (25 men/12 women, age 51 ± 13 years old) non-diabetic patients with CKD stage 3 (eGFR 30–59 mL/min/1.73 m2 calculated with the Modification of Diet in Renal Disease formula). Patients with history of diabetes mellitus and previous therapy with vitamin D were excluded. The underlying kidney disease was obstructive nephropathy, secondary focal segmental glomerulosclerosis, membranous glomerulonephritis and unknown cause of CKD. In all patients, CKD–mineral and bone disorder (CKD–MBD) was established. All patients were treated at the beginning with dietary phosphorous restriction, phosphate-binding agents and calcium supplements. If intact parathyroid hormone (iPTH) values were persistently >70 pg/mL, administration of 1-alpha-hydroxyvitamin D3 in a single daily dose of 0.25 μg was initiated. Fasting glucose concentration, insulin levels, HbA1c, iPTH, Ca, P and insulin resistance evaluated by homeostasis model assessment index [HOMA index, calculated as: fasting glucose (mmol/L) × insulin (mU/mL) / 22.5] were measured before (T0) and 12 weeks after (T1) initiation of treatment. In all patients, an oral glucose tolerance test (OGTT) with an oral dose of 75 g of glucose was performed. No patient was under treatment with corticosteroids or erythropoietin for anaemia. Plasma levels of fasting glucose and insulin levels were comparable before (T0) and after (T1) treatment with vitamin D (Table 1). The HOMA index was statistically higher in time T0 than T1 indicating that insulin resistance was improved. Mean glucose OGTT levels were higher in T0. There was no statistical difference in calcium, phosphorous, HbA1c, pre- and post-treatment concentration, although the T1 calcium concentration was higher than T0. Table 1 Plasma levels of fasting glucose and insulin levels before and after treatment with vitamin D Vitamin D insufficiency is correlated with increased risk of all-cause and cardiovascular (CV) mortality in patients with stage 3 and 4 CKD [2]. Studies demonstrate a link between abnormalities in vitamin D metabolism and insulin resistance, a very common condition in patients with CKD. It is proven that insulin resistance is an independent predictor of morbidity and mortality for CV causes in non-diabetic patients with end-stage renal disease [3]. A few works have investigated the effect vitamin D has on insulin resistance in early stages of CKD. Our study has shown a beneficial effect of vitamin D supplementation in patients with CKD stage 3 on insulin resistance. The HOMA index and OGTT mean glucose plasma levels have significantly decreased after 1-alpha-hydroxyvitamin D3 treatment. Changes in PTH, a factor implicated in insulin resistance, were not significant during the study period and were not correlated with the amelioration of the HOMA index. Our conclusion was that vitamin D affected insulin metabolism directly and not through reduction of PTH in patients with stage 3 CKD. Insulin resistance is present in early stages of CKD and is associated with vitamin D metabolism. According to our data, treatment with vitamin D in patients with CKD stage 3 has a beneficial effect on insulin resistance assessed with the HOMA index. Of course, further randomized controlled large-scale studies are needed in order to assess long-term benefits in morbidity and mortality of those patients. Conflict of interest statement. None declared.

Sir, Various studies have linked inflammation and endothelial dysfunction in patients with chronic renal disease [1]. Plasma levels of adhesion molecules [soluble intracellular adhesion molecule-1 (sICAM) and soluble vascular adhesion molecule-1 (sVCAM)] are markers of endothelial dysfunction and also risk factors for cardiovascular disease in patients with IgA nephropathy (IgAN) [2]. It is known that vascular lesion begins long before its clinical manifestation and its pathogenesis involves endothelial dysfunction and low-grade inflammation. Numerous studies provide evidence that ACE inhibitors or angiotensin II receptor antagonists (ARBs) are more effective than other antihypertensive drugs in slowing the progressive decline in glomerular filtration rate in IgAN [3]. Our aim was to test whether blocking the renin–angiotensin system (RAS) with irbesartan decreases levels of adhesion molecules in patients with biopsy-proven IgAN. We included in our study 36 patients (M/F 26/10, 51 ± 12.5 years). The inclusion criteria were biopsy-proven IgAN (defined by standard morphologic and immunohistochemical criteria), serum creatinine ≤1.5 mg/dl and urinary protein excretion ≥500 mg/day in at least three consecutive determinations during the previous 6-month period. Exclusion criteria were diabetes mellitus, coronary artery disease, peripheral vascular disease, stroke, acute infection or the inflammatory process on course and marked hypercholesterolaemia. Blood samples were collected from all patients before (T0) and after 16 weeks (T1) of treatment with 300 mg of irbesartan given once daily in the morning. A thorough blood chemistry control was performed in all patients. Creatinine clearance was determined by using venous blood for serum levels of creatinine and a 24-h urine collection. Serum and urinary creatinine concentration was measured using the Jaffe method. Serum intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 were measured by immunosorbent assay (ELISA). Statistical analyses were performed using SPSS version 13.0 (SPSS, Chicago, IL, USA). Systolic (SBP) and diastolic blood pressure (DBP) was significantly lower after irbesartan was given (from SBP T0: 144 ± 19 mmHg DBP T0: 93 ± 9 mmHg to SBP T1: 129 ± 9 mmHg DBP T1: 88 ± 8 mmHg, P < 0.01). Proteinuria levels were also significantly lower after treatment: from 1.6 ± 0.7 g/24 h − T0 to 1.1 ± 0.9 g/24 h − T1 (P < 0.001). We observed a significant decrease of sICAM and sVCAM plasma levels in patients after treatment with irbesartan (sICAM T0: 628 ± 163 ng/ml to sICAM T1: 369 ± 112 ng/ml, P < 0.001; sVCAM T0: 1028 ± 649 ng/ml to sVCAM T1: 688 ± 248 ng/ml, P < 0.001) (Table ​(Table11). Table 1 Summary of before (T0) and (T1) the treatment in each parameter (BP, sICAM and sVCAM) Studies [2,4] have proven the important role of inflammation in the outcome of IgAN. Angiotensin type 1 (AT1) receptor antagonist significantly decreases proteinuria and slows renal deterioration in patients with IgAN. Our data suggest that treatment with irbesartan in patients with IgAN has a beneficial effect on inflammatory markers. The interfering with the inflammatory markers of AT1 antagonist could, at least partially, explain the effect of AT1 receptor blockade on renal survival in patients with IgAN. It is obvious that additional studies are needed to verify this hypothesis, especially in order to rule out the direct effect of lowering blood pressure on the inflammatory markers taken into consideration. Conflict of interest statement. None declared.