Biomedical subjects
Publications and source records attributed to C Zoccali.
A 26-year-old patient with chronic renal failure presented a spinal cord infarction during haemodialysis. This is the first case of a patient with chronic renal failure maintained on chronic haemodialysis described in literature. In this case, the severity of vascular lesions documented by widespread vascular calcifications were particularly striking.
Before introducing a wrist device (NAIS-Matsushita) for blood pressure (BP) measurement in our Unit, we formally tested its validity. Since the wrist position is critical and BP in the clinical setting is often measured with patients lying in bed, we also estimated the error introduced by allowing the wrist to lay flat at the bed level. Ten normal subjects and 20 hypertensive patients took part in two consecutive studies. In the first study the subjects were sitting and the blood pressure was simultaneously taken with the auscultatory mercury sphygmomanometer on the left arm and with the NAIS on the right wrist. The wrist was kept at the heart level. In the second study two NAIS devices were used with the subjects lying in bed; the left wrist was allowed to stay at the bed level, while the right one was kept at the heart level. The diastolic BP was consistently underestimated (P< 0.001) by the wrist device (79 mmHg 95%CI: 75-83) as compared to the values obtained with the standard mercury sphygmomanometer (85 CI: 79-88). No significant difference was found in systolic BP (mercury: 135 CI: 127-143; wrist 134 CI: 126-141). In the second study the BP (systolic and diastolic) was markedly higher (P<0.001) when the wrist was kept at the bed level (systolic bed level: 144 CI: 135-152; systolic heart level: 135 CI:126-141; diastolic bed level: 83 CI:78-88; diastolic heart level: 76 CI:71-79).
Primary aldosteronism is a disorder characterized by hypertension and hypokalemia due to aldosterone secretion out of renin-angiotensin control. It is generally caused by aldosterone-producing adenoma or adrenocortical hyperplasia but, in some cases, it is due to genetic alterations. Familial type I hyperaldosteronism is the result of anomalous regulation of aldosterone secretion from ACTH (which normally regulates cortisol synthesis). Aldosterone hypersecretion can be suppressed by exogenous glucocortcoids such as dexamethasone. This autosomal dominant disorder is caused by unequal cross-over between two genes with wide sequence homology: CYP11B1 and CYP11B2. The hybrid gene is the product of fusion between the ACTH-responsive regulatory portion of the 11b-hydroxylase gene (CYP11B1) and the coding region of the aldosterone synthase gene (CYP11B2). Familial type I hyperaldosteronism is a disease with incomplete penetration and variable expressivity, especially in relation to hypertension. The marked variability in hypertension severity can mirror an interaction between the hybrid gene and other hereditary factors involved in the regulation of blood pressure. Familial type II hyperaldosteronism is another autosomal dominant form of hyperaldosteronism due to aldosterone hyper-secretion not suppressible by dexamethasone. This disorder is unrelated to mutation of the hybrid gene. The genetic cause of type II hyperaldosteronism is presently unknown, but a genome-wide search has revealed that the disorder is linked with a locus on chromosome 7 in a region that corresponds to cytogenetic band 7p22.
The dipstick test is the most sensitive test for microhematuria screening. In the general population asymptomatic microhematuria is not rare. In terms of clinical presentation hematuria can be classified in a double temporal dimension, i.e. according to the age of the patients and to its time course (resolution vs. persistence). In isolated microhematuria, red cells morphology is useful to establish the site of hematuria (glomerular vs. non glomerular). This is important mostly because in older patients this alteration may underlie a genito-urinary cancer. Microhematuria is probably one of the most sought for clinical signs of urinary diseases. It is fundamental that this clinical sign be always interpreted in a context considering other symptoms and clinical data.
Continuing medical education is an essential element of state-of-the-art medical practice. Continuing medical education as structured today in most countries, must be able to guarantee the quality of continuing medical education and its independence. There should, therefore, be an independent professional body at national level responsible for assessing and guaranteeing both quality and independence. This body will also have the power to oversee the participation of medical specialists in continuing medical education. A system of credits should was developed to express the professional value of continuing medical education activities. Each activity is credited with a certain score, which can be awarded to the participating specialist. Continuing medical education should remain an ethical obligation subject to the disciplinary authority of the profession itself. Continuing medical education should be both an individual and also a collective obligation of the profession; in order to promote and make it effective, each member state must provide the means of making continuing medical education available to all physicians. For the above reason the CME is a strategic way to improve the quality of the health system. In Italy new way to obtain CME credits are going to be issue in the near future.
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BACKGROUND: Guidelines have indicated the achievement of blood pressure target (BP <130/80 mmHg) as a priority in the conservative treatment of chronic kidney disease (CKD), but the current implementation of these recommendations in clinical practice is unknown. METHODS: We assessed control rates, treatment and clinical correlates of hypertension in 1201 adult non-dialyzed CKD patients followed up by a nephrologist for at least 6 months. RESULTS: Estimated glomerular filtration rate (GFR) was 32 (SD 15) mL/min/1.73 m2. BP target was not achieved in 88% of patients (95% confidence interval (95% CI): 86-90%). In 84% of patients, BP levels were also above the target at the first visit to the nephrology unit 4.5 yrs previously. The risk of not achieving BP target during the nephro-logy follow-up was associated with older age (odds ratio (OR): 1.24, 95% CI 1.06-1.45, p=0.008), diabetes (OR: 2.25, 95% CI 1.20-4.20, p=0.011), and the duration of hypertension (OR: 1.13, 95% CI 1.02-1.24, p=0.016). Among patients with uncontrolled BP, about 70% received multidrug antihypertensive therapy including renin-angiotensin system (RAS) inhibitors; conversely, diuretic treatment was prescribed in a minority of patients (37%), and at insufficient doses in half the cases, despite the insufficient implementation of a low salt diet (18%). CONCLUSIONS: BP target was not reached in most CKD patients routinely seen in the renal clinics. The main barrier to guideline implementation is possibly the inadequate treatment of extracellular volume expansion despite the large prevalence of factors, such as older age and diabetes, which further enhance the intrinsic BP salt sensitivity of CKD.
Adipose tissue is now considered an important system operating strictly in concert with other systems. The adipocyte is the main producer of two pleiotropic compounds, leptin and adiponectin, modulating inflammation and having multiple effects in disparate organs including the cardiovascular and the central nervous system. Leptin has disparate influences on various physiologic and organ systems including glucose homeostasis, hematopoiesis and the reproductive and cardiovascular systems and is a crucial hormone for the regulation of food intake and body weight. Peripherally, leptin modulates insulin sensitivity and high leptin triggers insulin resistance and vice versa. Obesity, a situation where circulating leptin attains very high levels is accompanied by increased bone mass, a phenomenon which may depend on direct stimulation of osteoblasts by leptin. However in animal models the stimulating effect of leptin on the osteoblast is counterbalanced by a strong inhibitor effect on bone formation in the central nervous system. Two recent studies reported an inverse link between leptin, bone mass and PTH in dialysis patients suggesting that leptin may be implicated in low bone turnover in these patients, likely by a mechanism involving the central nervous system. Leptin induces vascular calcifications in vitro. In uremic man leptin is unrelated to valvular calcifications but predicts incident cardiovascular events in overweight and obese dialysis patients. Leptin seems to be a relevant player in the emerging connection between bone and cardiovascular alterations in patients with end stage renal disease.
The relationship between hyperhomocysteinemia and cardiovascular damage is well known, whereas the role of this alteration in renal disease progression has been scarcely studied. Experimental studies demonstrated that exposure to high levels of homocysteinemia causes glomerular and interstitial damage which is remarcably proportional to the serum concentration of this aminoacid. Until now the renal effects of hyperhomocysteinemia in man has been investigated only in observational studies. The Hoorn study, a prospective study in a Dutch population, showed that the plasma homocysteine is a strong predictor of proteinuria in diabetic and non diabetic subjects. Findings in this study were recently confirmed in a cohort study in 7500 Japanese because plasma homocysteine predicted the onset of renal failure in this population. NO-dependent endothelial dysfunction triggered by homocysteine via reduction of the activity of the enzyme that metabolizes Asimmetric Dymethilarginine (dmethylarginine dymethilaminohydrolase) is a likely mechanism whereby hyperomocysteinemia causes cardiovascular and renal damage as well.
There are 44,000 dialysis patients in Italy and it is estimated that about 50% of them are hypertensive. In dialysis patients arterial blood pressure (BP) is highly variable, as it gradually increases in the interdialytic interval and decreases more or less rapidly during dialysis. Sodium retention and volume expansion play a major role in hypertension in these patients; and therefore, this alteration constitutes a main treatment target in this patient population. The great majority of patients also require antihypertensive drugs. The pharmacokinetics of these drugs are often modified by renal failure and peculiar dose adjustments must be adopted in this setting.
In the last few years the Italian Society of Nephrology has addressed many technical-scientific and management aspects to better patient satisfaction. Project No. 1 of the 2004-2006 programme on 'Quality and Accreditation of National Renal Units' focuses on four essential points. The first is the questionnaire mailed to all the Presidents and Regional Delegates on the relationship between Nephrology units, Local Government Health-System and the Regional Healthcare Agency. The results evidence that the 'political' decision-making power of nephrologists decreases in the absence of a national strategy. The second point, in collaboration with the National Census Group, includes the quality analysis and the standardization of resources (human and structural) and management of the Renal Units. The third point is based on 'Educational Courses for Quality and Accreditation' held in Rome (3-5 October 2005: L'Accreditamento all'Eccellenza dell'Unita' Operativa di Nefrologia, Dialisi e Trapianto; 17-19 October 2005: Il Manuale di Accreditamento della Specialità di Nefrologia). The courses aim at training members responsible for each region to hold courses in their specific region to create a network including each single Renal Unit to create an acceptable homogenous language on the models of analysis and on the correct use of 'The Guide for Excellence Accreditation'. The fourth point concerns both the on-line Guide for Excellence Accreditation and 'Peer Review Accreditation' and the NEQUASY (Nephrology Quality System) project. The manual must be 'user friendly' allowing each Centre to self-evaluate using national and regional standards.
The purpose of this study was to investigate the prevalence and aetiology of carpal tunnel syndrome (CTS) and the effect of open carpal tunnel decompression (CTD) in a group of patients on renal haemodialysis. In 91 patients attending a Renal Unit who were assessed only by clinical means, the prevalence of CTS was 7.1%. CTS development was not significantly correlated with known risk factors, in particular duration of dialysis and presence of an artero-venous fistula on the symptomatic limb. CTD led to a mean symptom-free period of 12 years. In summary, CTS is a frequent and serious disease affecting renal dialysis patients, but its aetiology remains uncertain. Nevertheless, CTD is an effective and lasting treatment for this condition.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.