Failure of transvenous ICD to terminate ventricular fibrillation in a patient with left ventricular noncompaction and polycystic kidneys.

Implantable cardioverter defibrillator (ICD) testing in patients with left ventricular noncompaction (LVNC) at the time of implantation and potential difficulties with ventricular fibrillation (VF) induction/termination in LVNC patients are often not stated in the literature. This report describes the failure of transvenous implantation of an ICD in a 40-year-old patient with LVNC and polycystic kidneys. A high defibrillation threshold (DFT) prevented termination of ICD-induced VF. This case suggests that DFT testing should be considered in any LVNC patient during ICD implantation. The association of LVNC and polycystic kidneys is also discussed.

High plasma retinol binding protein 4 (RBP4) is associated with systemic inflammation independently of low RBP4 adipose expression and is normalized by transplantation in nonobese, nondiabetic patients with chronic kidney disease.

OBJECTIVE: Adipose-secreted retinol binding protein 4 (RBP4) circulates in free (active) and transthyretin (TTR)-bound forms and may be associated with obesity-related inflammation. Potential involvement of plasma and adipose RBP4 in systemic inflammation in the absence of obesity and diabetes is unknown. Inflammation reduces survival in chronic kidney disease (CKD) [particularly in maintenance haemodialysis (MHD)], and plasma RBP4 may increase with renal dysfunction. We investigated (i) potential associations between RBP4 and inflammation in CKD and (ii) the role of adipose tissue in this putative interaction. DESIGN: Cross-sectional. PATIENTS: Nonobese, nondiabetic patients with CKD undergoing conservative (CT: n = 10) or MHD treatment (n = 25) and healthy control subjects (C: n = 11). Renal transplant recipients (n = 5) were studied to further assess the impact of restored near-normal renal function. MEASUREMENTS: Plasma RBP4, TTR and C-reactive protein (CRP), adipose RBP4 expression. RESULTS: Plasma RBP4, TTR and CRP were highest in MHD (P < 0·05). Adipose RBP4 mRNA was, however, comparably low in CT and MHD (P < 0·05 vs C), and all parameters were normalized in transplant recipients (P < 0·05 vs MHD). In all subjects (n = 51), creatinine and TTR (P < 0·05) but not adipose RBP4 mRNA were associated with plasma RBP4. Plasma RBP4 but not its adipose expression was in turn associated positively (P < 0·05) with CRP independently of creatinine-TTR. CONCLUSIONS: High plasma RBP4 and inflammation are clustered in CKD in the absence of obesity and diabetes and are normalized by transplantation. Adipose RBP4 expression is not involved in plasma RBP4 elevation, which appears to be mainly because of passive accumulation, or in CKD-associated inflammation.

Metabolic syndrome after kidney transplantation.

Metabolic syndrome (MS) can be linked to the progression of chronic renal transplant dysfunction (CRTD). Hyperfiltration in transplanted patients is a further risk factor for MS and for the progression of CRTD. Many studies show in kidney-transplanted subjects a prevalence of MS at 60% after 6 years posttransplantation. We studied 182 patients (126 men and 56 women) with functioning renal transplant in Messina and Rovigo Renal Units. In our patients we saw at 6 years postkidney transplant in men a prevalence of MS at 20% (NCEPATPIII criteria) or 30% (Rovigo-Messina more strict criteria), and women at 6 years posttransplantation a prevalence of MS at 25% (NCEPATPIII criteria) or 50% (Rovigo-Messina criteria). In our patients, the period of graft function was over 15 years. This result is due to continued follow-up of metabolic parameters and to moderate protein (0.8-0.9 g/kg/day), low lipid, and low caloric intake. These strategies permit the avoidance of hyperfiltration, the reduction of hyperlipidemia and obesity. Special attention is due to women 50-65 years old. In these patients the prevalence of metabolic syndrome 6 years posttransplant is very high (60%). Postmenopausal syndrome is an additional risk factor for MS, atherosclerosis, and the progression of CRTD.

Low fat adiponectin expression is associated with oxidative stress in nondiabetic humans with chronic kidney disease--impact on plasma adiponectin concentration.

In spite of association between high plasma adiponectin and high metabolic and cardiovascular (CV) risk, highest adiponectin increments retain CV and metabolic protective effects in advanced chronic kidney disease (CKD). Passive accumulation can favor CKD-associated hyperadiponectinemia but potential additional regulation by adipose tissue remains undefined. Oxidative stress (OS) is associated with metabolic and CV disease and with CKD [increasing from conservative treatment (CT) to maintenance hemodialysis (MHD)], and OS can reduce adiponectin expression in experimental models. OS (in the form of plasma thiobarbituric acid-reactive substances: TBARS), subcutaneous adipose adiponectin mRNA, and plasma adiponectin were studied in CKD patients (stages 4 and 5) on CT (n = 7) or MHD (n = 11). Compared with CT and controls (C: n = 6) MHD had highest TBARS and lowest adiponectin mRNA (P < 0.05) with lower adipose adiponectin protein (P < 0.05 vs. CT). MHD also had lower plasma adiponectin than CT, although both had higher adiponectin than C (P < 0.05). In renal transplant recipients (RT: CKD stage 3; n = 5) normal TBARS were, in turn, associated with normal adiponectin mRNA (P < 0.05 vs. MHD). In all CKD (n = 23), adiponectin mRNA was associated positively with adiponectin plasma concentration (P < 0.01). In all subjects (n = 29), adiponectin mRNA was related (P < 0.05) negatively with TBARS after adjusting for plasma C-reactive protein (CRP) or CRP and creatinine. Thus altered OS, adiponectin expression, and plasma concentration represent a novel cluster of metabolic and CV risk factors in MHD that are normalized in RT. The data suggest novel roles of 1) MHD-associated OS in modulating adiponectin expression and 2) adipose tissue in contributing to circulating adiponectin in advanced CKD.

Inflammation and adipose tissue in uremia.

Enhanced chronic systemic inflammation and reduced insulin sensitivity are often associated in patients with chronic renal failure, contributing to cardiovascular morbidity and mortality in these patients. Adipose tissue produces several hormones (adipocytokines including leptin, resistin, tumor necrosis factor-alpha, and adiponectin) that modulate both systemic inflammatory response and insulin action. High leptin, resistin, and tumor necrosis factor-alpha and low adiponectin are associated with proinflammatory conditions, whereas opposite patterns are commonly observed in the presence of increased insulin sensitivity, low inflammation, and reduced cardiovascular risk. Oxidative stress has also been shown recently to modulate adipocytokine production, resulting in a proinflammatory profile. Increments of plasma concentrations of both proinflammatory and anti-inflammatory adipocytokines have been reported in chronic renal failure, possibly caused by both passive accumulation from reduced renal excretion and metabolic abnormalities induced by uremia. The potential role of altered adipose tissue adipocytokine production in the onset of renal failure-associated inflammatory and metabolic derangements remains largely to be elucidated and is discussed in the current report.

Factors affecting nutritional status, response to exercise, and progression of chronic rejection in kidney transplant recipients.

The nutritional status and the function of a renal graft are satisfactory in kidney transplantation patients who observe their dietary prescription. A reduction in maximal exercise test capacity in kidney transplant recipients are thought to be a consequence of uremic muscle dysfunction and also of changes in muscle structure associated with immunosuppressive therapy. Daily regular physical activity is recommended. Patients with a functioning renal transplant, as well as hemodialyzed patients, have an increased risk for development of cardiovascular diseases such as hypertension, hyperlipidemia, hyperglycemia, and obesity. The reduction of obesity and of cardiovascular risk factors in these patients are goals to be obtained by adequate nutrition, exercise, and physical activity.

Long-term protein intake control in kidney transplant recipients: effect in kidney graft function and in nutritional status.

BACKGROUND: Reduction in renal mass is followed by progressive renal failure. The reduction in filtration surface area, caused by the absence of 50% of renal mass, in patients with customary salt intake is followed by expansion of extracellulary volume and systemic and glomerular hypertension. High protein intake may contribute to renal allograft injury arising from insufficient renal mass. METHODS: The authors studied outcome of 48 patients with kidney transplant to whom normocaloric diets and moderate intake of protein (0.8 g/kg), of sodium (3 g/d), and lipids (no more than 30% of total energy) were prescribed. Monthly 24-hour urea excretion and 24-hour sodium excretion were measured. Renal function was assessed by creatinine clearances and by renal scintigraphy. The 30 patients who followed prescriptions exactly were the compliant group (group 1). The other 18, who followed the diet prescribed only partially (their intakes were 1.4 g/kg of protein and 5 g/d of sodium) were the control group (group 2). RESULTS: Patients of the compliant group maintained unchanged renal function, whereas patients of the control group lost more than 40% of excretion efficiency as a mean. CONCLUSIONS: Dietary restrictions of protein and sodium can stabilize renal function in patients with kidney transplant. Wider use of this treatment is indicated.