In-depth review: is hepcidin a marker for the heart and the kidney?

Iron is an essential trace element involved in oxidation-reduction reactions, oxygen transport and storage, and energy metabolism. Iron in excess can be toxic for cells, since iron produces reactive oxygen species and is important for survival of pathogenic microbes. There is a fine-tuning in the regulation of serum iron levels, determined by intestinal absorption, macrophage iron recycling, and mobilization of hepatocyte stores versus iron utilization, primarily by erythroid cells in the bone marrow. Hepcidin is the major regulatory hormone of systemic iron homeostasis and is upregulated during inflammation. Hepcidin metabolism is altered in chronic kidney disease. Ferroportin is an iron export protein and mediates iron release into the circulation from duodenal enterocytes, splenic reticuloendothelial macrophages, and hepatocytes. Systemic iron homeostasis is controlled by the hepcidin-ferroportin axis at the sites of iron entry into the circulation. Hepcidin binds to ferroportin, induces its internalization and intracellular degradation, and thus inhibits iron absorption from enterocytes, and iron release from macrophages and hepatocytes. Recent data suggest that hepcidin, by slowing or preventing the mobilization of iron from macrophages, may promote atherosclerosis and may be associated with increased cardiovascular disease risk. This article reviews the current data regarding the molecular and cellular pathways of systemic and autocrine hepcidin production and seeks the answer to the question whether changes in hepcidin translate into clinical outcomes of all-cause and cardiovascular mortality, and cardiovascular and renal end-points.

Early assessment of renal resistance index and long-term renal function in renal transplant recipients.

BACKGROUND: The effect of the intrarenal arterial resistance index (RI) on long-term renal functions is not well known. We examined the predictive value of intrarenal RI on long-term allograft outcomes. METHODS: We retrospectively investigated 121 stable renal transplant recipients, followed for a mean of 63.21 +/- 19.9 months after renal transplant. Patients with complications during the first six months after transplant were not included. Color Doppler ultrasonography was done to calculate the intrarenal RI within the first four weeks after transplant. RESULTS: Older recipient age, high pulse pressure, active smoking, and proteinuria were associated with a higher intrarenal RI. Multivariate analyses revealed that renal RI and donor age were independent predictors of allograft outcome. Kaplan-Meier estimates of cumulative graft survival were significantly worse in patients who had an RI of 0.7 or more than they were in patients who had an RI of less than 0.7 (p = .005). Development of chronic allograft nephropathy (CAN) was significantly higher in patients who had an RI of 0.7 or more (p = .02). CONCLUSIONS: Renal RI determined within the first month after renal transplant predicts long-term allograft function and development of CAN in renal transplant recipients.

Is there a link between hyperuricemia, morning blood pressure surge, and non-dipping blood pressure pattern in metabolic syndrome patients?

BACKGROUND: Hypertensive patients usually have a blunted nocturnal decrease, or even increase, in blood pressure during sleep. There is also a tendency for increased occurrence of cardiovascular events between 6 and 12 am due to increased morning blood pressure surge (MBPS). Co-occurrence of metabolic syndrome (MetS) and hypertension is also a common problem. Hyperuricemia might trigger the development of hypertension, chronic renal failure, and insulin resistance. In this study, we aimed to determine whether there is a relationship between hyperuricemia, MetS, nocturnal blood pressure changes, and MBPS. METHOD: A total of 81 newly diagnosed hypertensive MetS patients were included in this study. Ambulatory blood pressure monitoring of patients was done and patients' height, weight, and waist and hip circumferences were recorded. Fasting blood glucose (FBG), lipid profile, creatinine, potassium, uric acid, hematocrit levels were studied. RESULTS: Non-dipper (ie, those whose blood pressure did not drop overnight) patients had higher waist-hip ratios (WHR) (P = 0.003), uric acid (P = 0.0001), FBG (P = 0.001), total and low-density lipoprotein cholesterol levels (P = 0.0001). Risk analysis revealed that hyperuricemia was a risk factor for non-dipping pattern (P < 0.0001, odds ratio = 8.1, 95% confidence interval = 1.9-33.7). Patients in the highest quadrant for uric acid levels had higher FBG (P = 0.001), low-density lipoprotein cholesterol (P = 0.017), WHR (P = 0.01), MBPS (P = 0.003), and night diastolic blood pressure compared with lowest quadrant patients (P = 0.013). Uric acid levels were also positively correlated with night ambulatory blood pressure (ABP) (r = 0.268, P =0.05), night diastolic blood pressure (r =0.3, P =0.05), and MBPS (r =0.3, P =0.05). CONCLUSION: Evaluation of hypertensive patients should also include an assessment of uric acid level and anthropometric measurements such as abdominal obesity. Hyperuricemia seems to be closely related to undesired blood pressure patterns and this may signal to the clinician that an appropriate therapeutic approach is required.