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Diabetes mellitus (DM) is the most important non-communicable disease after hypertension. Prevalence of type 2 DM has progressively increased over the last decades. In Italy, 11.8% of the general adult population can be identified as diabetic. The major complication of DM is diabetic nephropathy (DM-CKD), which develops in approximately one-third of diabetics. Achieving optimal glycemic control is the first therapeutic goal in the management of DM-CKD. In recent years, new antidiabetic drugs have been marketed (GLP1 analogues, DPP-4 inhibitors, SGLT-2 inhibitors) to ameliorate glycemia in patients nave or treated by means of traditional agents, such as sulfonylureas, metformin, glinides, insulin. However, use of these drugs in DM-CKD should be evaluated carefully, mainly because of the higher risk of hypoglycemia that requires dosing adjustments. Metformin still represents an adequate choice if proper dose adjustments are made on the basis of renal function. Sulfonylureas with limited renal clearance, i.e., gliquidone, glipizide and gliclazide are an alternative to metformin and more effective than repaglinide on glycemic control. Other antidiabetic agents with potential nephroprotective effects, namely DPP-4 inhibitors, incretin analogues and SGLT-2 inhibitors, may allow nephroprotective effects independent of glycemic control. Insulin remains the cornerstone of therapy when oral therapy is no longer effective.

Patients with non-dialysis-dependent chronic kidney disease (ND-CKD) often show anemia and iron deficiency despite oral iron supplementation caused by poor iron absorption, intolerance and non-compliance.

The appropriate vascular access for hemodialysis in patients with cardiac implantable electronic devices (CIED) is undefined. We describe two cases of end-stage renal disease patients with CIED and tunneled central venous catheter (CVC) who developed venous cava stenosis: (1) a 70-year-old man with sinus node disease and pacemaker in 2013, CVC, and a Brescia-Cimino forearm fistula in 2015; (2) a 75-year-old woman with previous ventricular arrhythmia with implanted defibrillator in 2014 and CVC in 2016. In either case, after about 1 year from CVC insertion, patients developed superior vena cava (SVC) syndrome due to stenosis diagnosed by axial computerized tomography. In case 1, the patient was not treated by angioplasty of SVC and removed CVC with partial resolving of symptoms. In case 2, a percutaneous transluminal angioplasty with placement of a new CVC was required. To analyze these reports in the context of available literature, we systematically reviewed studies that have analyzed the presence of central venous stenosis associated with the simultaneous presence of CIED and CVC. Five studies were found; two indicated an increased incidence of central venous stenosis, while three did not find any association. While more studies are definitely needed, we suggest that these patients may benefit from epicardial cardiac devices and the insertion of devices directly into the ventriculus. If the new devices are unavailable or contraindicated, peritoneal dialysis or intensive conservative treatment in older patients may be proposed as alternative options.

Hyperuricemia is defined as serum uric acid values greater than 6 mg/dl and could occur either due to hyperproduction or as a result of reduced renal excretion, which exceeds gut compensation. In Italy, prevalence is around 12% of the general population and increases in renal disease up to 60%. Recent experimental studies demonstrated a role of uric acid in the development of arterial hypertension and systemic arteriosclerosis, with an increase in cardiovascular risk. It also appears from observational studies that high uric acid is an independent risk factor associated with de novo onset of chronic kidney disease after adjustment of main confounding variables. Hyperuricemic subjects treated with febuxostat, a selective inhibitor of xantino-oxidase, showed in RCTs a better control of hyperuricaemia in comparison with those receiving allopurinol. Moreover, observational studies indicate that urate lowering treatment could be helpful in reducing cardiovascular events as well as in slowing the progression of chronic kidney disease; randomized controlled studies, designed to assess as primary outcome the nephroprotective effect of urate lowering treatment, are in progress.

Background: Although only high-flow arteriovenous fistulas (AVFs) are postulated to cause high-output cardiac failure (HOCF), there are currently no universally accepted criteria defining a high-flow fistula. Methods: To verify if vascular access blood flow (Qa) ≥ 2000 ml/min provides an accurate definition of high-flow fistula, we selected 29 consecutive patients with Qa ≥ 2000 ml/min at color-duplex ultrasound examination and assessed them for the presence of cardiac failure symptoms; transthoracic echocardiography was also performed. Results: Nineteen patients (65%) had heart failure symptoms and were classified with HOCF. At receiver operating characteristic (ROC) curve analysis, Qa ml/min values did not identify patients with heart failure symptoms but when AVF blood flow was indexed for height2.7, Qa ≥ 603 ml/min/m2.7detected the occurrence of HOCF with good accuracy (sensitivity 100%, specificity 60%, efficiency 86%, positive predictive value 83%, negative predictive value 100%, area under curve 0.75). At echocardiographic evaluation, patients with Qa ≥ 603 ml/min/m2.7had a more severe increase of left ventricular mass (63 ± 18 vs. 47 ± 7 g/m2.7, p < 0.003), left ventricular diastolic volume (140 ± 42 vs. 109 ± 14 ml, p < 0.007), left atrial volume (53 ± 23 vs. 39 ± 5 ml/m2, p < 0.015), a higher incidence of diastolic dysfunction (70 vs. 17%, p < 0.019) and higher CO reduction after AVF manual compression (2151 ± 875 vs. 1292 ± 527 ml/min, p < 0.009) than patients with Qa < 603 ml/min/m2.7. Conclusions: Indexation of AVF blood flow should be considered in defining high-flow fistula because the effect of Qa may differ in individuals of different sizes. A Qa value ≥ 603 ml/min/m2.7and its association with some echocardiographic alterations could identify patients at higher risk for HOCF.

Background Whether blood pressure (BP) plays an independent predictive role in the onset of decreased glomerular filtration rate (GFR) remains ill-defined because existing meta-analyses have incorporated data from studies that included individuals with low GFRs at baseline. This question is critical to optimize chronic kidney disease prevention in the general population. Study Design Systematic review and meta-analysis of longitudinal cohort studies. Setting & Population Adults from general population. Selection Criteria for Studies We identified in PubMed, EMBASE, and the Cochrane Library database all cohort studies evaluating the role of BP in the incidence of decreased estimated GFR (eGFR; defined as eGFR 2 ) in individuals without decreased kidney function at baseline. Predictors Hypertension (BP>140/90mmHg), prehypertension (systolic BP of 120-139 and/or diastolic BP of 80-89mmHg), and BP as a continuous variable. Outcomes Risk for decreased eGFR reported as relative risk (RR) and 95% CI. Heterogeneity ( I 2 ) was also evaluated. Results Data from 16 cohorts (315,321 participants) were analyzed. All studies had a Newcastle-Ottawa score in the range of 6 to 8, denoting high quality. During a mean follow-up of 6.5 years, decreased eGFR occurred in 6.6% of participants. The presence of prehypertension and hypertension increased renal risk (RRs of 1.19 [95% CI, 1.07-1.33; I 2 =23.8%] and 1.76 [95% CI, 1.58-1.97; I 2 =37.7%], respectively). Similarly, we found that every 10–mm Hg increase in systolic and diastolic BPs associated with higher risk for decreased eGFR (RRs of 1.08 [95% CI, 1.04-1.11; I 2 =60.0%] and 1.12 [95% CI, 1.04-1.20; I 2 =51.4%], respectively). Metaregression analysis showed greater risk with older age ( P =0.03), whereas other covariates were not significant. Limitations No individual patient-level data. Conclusions Prehypertension and hypertension, as BP levels, are independent predictors of decreased GFR in the general population, with the effect being more pronounced in the elderly. These findings are important for improving risk stratification in the general population.

Appropriate timing of starting chronic dialysis in patients with advanced chronic kidney disease (CKD) under nephrology care still is undefined. We systematically reviewed the most recent studies that have compared outcomes of stage 5-CKD under conservative versus substitutive treatment. Eleven studies, most in elderly patients, were identified. Results indicate no advantage of dialysis over conservative management in terms of survival, hospitalization or quality of life. This information is integrated with a case report on a middle-aged CKD patient followed in our clinic who has remained for 15 years in stage 5 despite severe disease. The patient is a diabetic woman who underwent right nephrectomy in 1994 because of renal tuberculosis. In 1999, she commenced regular nephrology care in our clinic and, since 2000, when she was 53 years old, her estimated glomerular filtration rate (eGFR) has been ≤15 ml/min/1.73 m(2). Over the last decade, despite, several episodes of acute kidney injury and placement of permanent percutaneous nephrostomy in 2001, renal function has remained remarkably stable, though severely impaired (eGFR 7.7-5.6 ml/min/1.73 m(2)). Our systematic analysis of the literature and this case report highlight the need for further studies, not limited exclusively to elderly patients, to verify the efficacy of non-dialysis treatment in stage 5-CKD patients. Meanwhile, nephrologists may consider that their intervention can safely prolong for several years the dialysis-free condition in ESRD independently of age.

The nephroprotective effect of the new anti-diabetic drugs acting on incretin system is suggested by preclinical studies. However, no study evaluating kidney effects of these drugs as primary outcome on the long term has been conducted in patients followed in diabetes centers. We designed a pilot observational study involving two diabetes clinics to evaluate the effect of prolonged treatment with saxagliptin on renal function in type 2 diabetics. Patients were enrolled if treated for at least 12 months with saxagliptin without concurrent changes to anti-hypertensive and lipid-lowering therapy. Primary outcome was to evaluate the effect of saxagliptin on albuminuria and estimated glomerular filtration rate (eGFR). Secondary outcomes were the effects of treatment on common clinical and laboratory parameters. Sixty-three patients were enrolled. After 12 months of treatment with saxagliptin, albuminuria declined from a mean (95%CI) of 39 (25-52) to 22 (14-30) mg/l (P20 mg/L) diminished by 27% versus baseline. The anti-albuminuric effect was independent of glycemic and blood pressure control. The eGFR remained unchanged after treatment in the presence of decreased glycated hemoglobin (from 7.1 to 6.7%). Therefore, this pilot study suggests that saxagliptin treatment in diabetic patients at high renal risk is associated with a reduction in albuminuria and GFR stability. Prospective trials are required to confirm the potential nephroprotective effects of saxagliptin.