The WHO has defined type II Diabetes Mellitus (DMII) as an epidemic disease. Indeed worldwide, diabetic patients are estimated to be 400 millions and this number is bound to grow in the next decades 1.Diabetic nephropathy (DN) develops in 20-40% of patients with DM 2.It is a condition generally characterized by presence of proteinuria and leads to a progressive reduction in kidney function and ultimately to End Stage Renal Disease (ESRD). Although DN represents a frequent complication in patients with DM it is well known that diabetic patients may develop kidney disease due to any other cause. Several studies have shown that about 30% of diabetic patients undergoing a kidney biopsy will be diagnosed with a non diabetic renal disease ( NDRD) 3.This suggests the importance of kidney biopsy in patients with DM.. Aim of our study was to evaluate the frequency of NDRD in our population, to identify pre-existing clinical or humoral parameters in patients with histological diagnosis of DN vs NDRD also evaluating the different clinical outcomes in patients with diagnosis of DN vs NDRD and identifying histological patterns of DN which may be associated to worst clinical outcomes. In this single centre retrospective observational study we evaluated all type II diabetic patients having undergone kidney biopsy in ICS Maugeri Spa SB in Pavia from May 2002 to December 2018 Our population included 71 patients with diagnosis of DMII having undergone kidney biopsy. Among these 36 (51%) had a histological diagnosis of DN, 29 ( 40%) of NDRD and 6 ( 9%) had both DN+NDRD. Of the NDRD patients 21% were diagnosed with membranous nephropathy 17% with nephroangiosclerosis, 10% with focal segmental glomerulosclerosis and 10% acute tubular necrosis.We found DN patients compared to NDRD had a greater DM II vintage (12 years vs 9,5 years), higher HbA1C (7,4% vs 6,5%, p<0.001), were more frequently on insulin( 67% vs 14%, p<0.002) and were more frequently affected by diabetic retinopathy ( 89% vs 3,5% p<0.001)There was no difference between DN and NDRD in terms of hypertension diagnosis or degree and proteinuria or creatinine value at biopsy ( proteinuria median value in both groups 3 g/24 h and creatinine DN (1,48 mg/dL), vs NDRD (1,43 mg/dL)).Interestingly, 24 months post biopsy however proteinuria values in NDRD reduced significantly while remaining stable in DN, with a significant difference from DN at 24 months ( p<0.018). Consistently with this data also creatinine values were higher in DN vs NDRD. We postulated this could be a consequence of targeted therapeutic intervention in NDRD .We next evaluated in DN the exhistence of a correlation between degree of histological damage and clinical outcome.We analyzed biopsies from 10 DN patients having a follow up of at least 24 months and assigned to each a score based on degree of glomerulosclerosis (0-3), tubulointerstitial(0-5) and vascular damage (0-5). Our data shows a correlation between severity of glomerular damage ( score>2) and worsening of proteinuria and creatinine over a 24 month period although not statistically significant probably due to small sample size In a population of DMII patients undergoing kidney biopsy 40% of patients had NDRD. NDRD appeared to have better clinical outcome ( lower proteinuria and lower creatinine) over time probably as a result of targeted therapy, also degree of gloerular damage in DN correlated with worse prognosis. Although some pre-exhisting conditions such as diabetic retinopathy are highly predictable of DN diagnosis our data supports the essential role of kidney biopsy in diabetic patients.Alltogether our data demonstrates the value of performing kidney biopsy in DMII patients
Abstract Introduction Ventricular arrhythmias (VA) represent a common complication of myocardial infarction (MI). Typically, they occur in two scenarios: during acute MI, related to ongoing ischemia, as ventricular tachycardia (VT) or ventricular fibrillation (VF), or in the context of a late phase of MI, related to the presence of a scar, as monomorphic VT (mVT). Despite the above, their occurrence may be atypical. Clinical Case 55–year–old man affected by obesity, diabetes and hypertension, admitted to our department for subacute MI. Coronarography showed three–vessel disease with indication for surgical revascularization. Thirty hours after admission, in absence of symptoms, occurrence of cardiovascular arrest due to mVT, which degenerated into VF. After resuscitation, ECG and Echo findings did not change compared to those observed at admission, excluding the presence of current ischemia. A blood gas analysis excluded dysionias. Few minutes later, arrhythmic recurrence of mVT degenerated into VF. This was refractory to electrical and antiarrhythmic therapy and stopped only after percutaneous left stellate ganglion block (LSGB) and deep sedation. Then, emergency surgical revascularization was performed. In the early postoperative days, during weaning attempts from sedation and ECMO support, that had become necessary due to hemodynamic instability after surgery, numerous recurrences of mVT, regressed only after deepening of sedation, multiple external shocks, antiarrhythmic polytherapy, and LSGB. A new coronarography documented patency of coronary artery bypass grafts. On 6th postoperative day, discontinuation of deep sedation and weaning from circulatory support without recurrence of VA. The patient was discharged from the intensive care unit and started on a rehabilitation pathway. Conclusions mVTs are commonly related to the presence of a scar, formed late after MI, or to the context of ongoing ischemia in acute MI. However, it should be remembered that even during the subacute phase of MI, arrhythmic instability might still occur. The responsible mechanisms are not completely known but it can be assumed that, even in the absence of a new ischemic event, the process of scar maturation may have led to a transient proarrhythmic substrate, responsible for the arrhythmic storm. Further studies are needed to clarify the mechanisms of arrhythmogenesis in the subacute phase of MI.
Trace elements are involved in many metabolic processes. They circulate prevalently bound to protein. In literature few studies deal with metal metabolism in adult patients with proteinuria, so we decided to further investigate metal metabolism in proteinuric patients.We studied 27 patients (14 male, 13 female), mean age 61.6+/-17 years with different degrees of renal function, serum albumin and proteinuria. Metal concentrations of copper (Cu), zinc (Zn) and aluminum (Al) were measured in serum and urine. No patient had environmental exposure to these metals.The serum Zn level was below the normal range in 11 patients. The serum Cu level was reduced in 5 patients. The Al serum level was elevated in 4 patients. Six patients had reduced and 6 patients had elevated Zn excretion. The urinary Cu excretion was elevated in 6 patients. The urinary Al excretion was elevated in 1 patient. Trace metal concentrations were related neither to renal function nor to total serum protein or albumin levels. Serum zinc was directly correlated with proteinuria and urinary zinc and negatively correlated with testosterone levels in both sexes.Adult patients with proteinuria have several modification of trace metal concentration in serum and urine. Serum concentration of metals did not depend on renal function or serum protein levels. Urinary Zn excretion was directly related to proteinuria and serum Zn levels. A negative correlation between serum Zn levels and testosterone was found in both sexes. Renal failure reduced urinary excretion of Cu and Al.
Renal dysfunction is one of the most common and threatening complications in heart transplant recipients. Even if ciclosporin seems to play a central role in inducing renal damage, other factors may concur or predispose to renal injury. In order to identify factors responsible for renal dysfunction, we retrospectively studied a cohort of 114 cardiac transplant recipients during a follow-up period of at least 3 years. The patients had a normal renal function before and 0.5 months after heart transplantation. Doubling of baseline serum creatinine or attainment of serum creatinine steadily above 176.8 µmol/l (2.0 mg/dl) was used as criterion to define the end-point renal dysfunction. A series of clinical and laboratory variables were obtained from the patients’ charts at different time intervals, and their prognostic value for the occurrence of renal dysfunction was calculated by Cox proportional hazards models. 23 out of 114 patients reached the end point after a median time period of 21 months. High serum triglyceride, alanine aminotransferase, alkaline phosphatase, ciclosporin, urea, glucose, and hemoglobin levels were shown to be associated with the development of renal dysfunction. Four variables, i.e., triglyceride, ciclosporin, urea, and alkaline phosphatase, had an independent prognostic value. Our results confirm a role for ciclosporin in inducing renal dysfunction and identify hyperlipidemia and an increased plasma urea level as risk factors for renal dysfunction in heart transplant recipients.
