Cardiovascular diseases represent the main causes of morbidity and mortality in patients with chronic kidney disease (CKD). According to a well-established classification, cardiovascular involvement in CKD can be set in the context of cardiorenal syndrome type 4. Left ventricular hypertrophy (LVH) represents a key feature to provide an accurate picture of systolic-diastolic left heart involvement in CKD patients. Cardiovascular involvement is present in about 80% of prevalent hemodialysis patients, and it is evident in CKD patients since stage IIIb-IV renal disease (according to the K/DOQI CKD classification). According to the definition of cardiorenal syndrome type 4, kidney disease is detected before the development of heart failure, although timing of the diagnosis is not always possible. The evaluation of LVH is a bit heterogeneous, and few standard imaging methods can provide the accuracy of either CT- or MRI-derived left ventricular mass. Key principles in the treatment of LVH in CKD patients are mainly based on anemia and blood pressure control, together with the management of secondary hyperparathyroidism and sudden cardiac death prevention. This review is mainly focused on the clinical aspects of CKD-related LVH to provide practical guidelines both for cardiologists and nephrologists in the daily clinical approach to CKD patients.

Cardiovascular diseases such as coronary artery disease, congestive heart failure, arrhythmias and sudden cardiac death represent main causes of morbidity and mortality in patients with chronic kidney disease (CKD). Pathogenesis includes close linkage between heart and kidneys and involves traditional and non-traditional cardiovascular risk factors. According to a well-established classification of cardiorenal syndrome, cardiovascular involvement in CKD is known as "type-4 cardiorenal syndrome" (chronic renocardiac). The following review makes an overview about epidemiology, pathophysiology, diagnosis and treatment of cardiovascular complications in CKD patients.

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Maturity-onset diabetes of the young (MODY), a monogenic subset of Type II (non-insulin-dependent) diabetes mellitus, is caused by mutations in at least five different genes: HNF-4a-MODY1 [1], GCK-MODY2 [2], HNF-1a-MODY3 [3], IPF-1-MODY4 [4], and HNF-1b-MODY5 [5]. MODYis an autosomal dominant disorder with an onset typically under 25 years of age, and usually accounts for 2 % to 5 % of all patients with Type II diabetes but a true estimate is challenging because patients with MODY are often wrongly diagnosed as having Type I or Type II diabetes. Late-onset Type II diabetes is a polygenic heterogeneous disorder whose pathogenesis is not clear. We regard Type II diabetes as a genetically continuous spectrum of early-onset to late-onset diabetes, partially due to mutations in the MODY genes. The prevalence of HNF-1a, GCK and HNF-4a mutations in MODY patients varies among different populations. Up to now four missense mutations in the MODY2 [6,7] and none in the MODY3 gene have been identified in Italian MODY patients. The aim of our study Diabetologia (2001) AbstractAims/hypothesis. Maturity-onset-diabetes of the young (MODY) is caused by mutations in at least five different genes. Our aim was to determine the prevalence of the most common MODY genes in Italian families with early-onset Type II (non-insulin-dependent) diabetes mellitus. Methods. We screened 28 Italian early-onset Type II diabetic families (diagnosis < 35 years) for mutations in the hepatic nuclear factor-4a, (MODY1), glucokinase (MODY2) and hepatic nuclear factor-1a (MODY3). Both strands of exons, flanking introns and minimal promoter regions of the above-mentioned genes were amplified using polymerase chain reaction and were sequenced directly. Results. We identified four different mutations, three of which are not described, (W113X, G42P43fsCC ® A, H514R) and four new polymorphisms (G184G, T513T, IVS3-nt47delG, IVS1-nt53C ® G) in the hepatic nuclear factor-1a gene, two new potential mutations (G44S, IVS4nt + 7C ® T) and three new polymorphisms (promoter-nt84C ® G, IVS9 + nt8C ® T, IVS9 + nt49G ® A) in the glucokinase gene, and a new polymorphism (IVS1c-nt11T ® G) in the hepatic nuclear factor-4a gene. Conclusion/interpretation. Mutations in the hepatic nuclear factor-1a and glucokinase are associated with Type II diabetes in 14 % and 7 % of Italian families, respectively. Our findings provide an impetus for screening Italian MODY and early-non Type II diabetic families for mutations in the above mentioned genes to identify relatives at risk who could benefit from primary prevention care. [Diabetologia (2001) 44: 1326±1329]Keywords Type II diabetes mellitus, genetics, hepatocyte nuclear factor-1a, hepatocyte nuclear factor-4a, glucokinase, MODY, Italian, mutation, polymorphism. Corresponding author: C. Gragnoli, Molecular Endocrinology, WEL 320, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114, USA E-mail: cgragnoli@partners.org Abbreviations: HNF, hepatocyte nuclear factor; GCK, glucokinase; IPF-1, insulin promoter factor-1...

BackgroundCardiac valve calcifications are present in dialysis patients and regarded as dependent on a deranged mineral metabolism. Few data are available for patients with chronic kidney disease (CKD) not on dialysis. This study evaluates the potential association between the extent of cardiac valve calcification and levels of intact parathyroid hormone (i-PTH), phosphorus, calcium, 25-OH vitamin D, fibroblast growth factor 23 (FGF-23), Klotho and C-reactive protein (CRP) simultaneously measured in patients with mild to moderate CKD.MethodsConsecutive non-hospitalized patients referring to five nephrology units were evaluated. Inclusion criteria were age >18 years, CKD Stages 3–4, and the presence of aortic and/or mitral valve calcification assessed by echocardiography as routinely clinical evaluation. Patients underwent clinical examination and routine biochemistry. Baseline i-PTH, phosphorus, calcium, 25-OH vitamin D, FGF-23, Klotho and CRP were simultaneously ascertained.ResultsExtent of aortic valve calcification (n = 100 patients) was moderate in 68 patients and mild in the remaining patients. Mitral valve calcification (n = 96 patients) score was 1, 2 and 3 in 61, 34 and 1 patients, respectively. In univariate analysis, no association was found between extent of mitral valve calcification and markers of mineral metabolism and CRP; aortic valve extent of calcification was positively associated with i-PTH (r2 = 0.212; P = 0.03) and FGF-23 (r2 = 0.272; P = 0.01), and negatively with Klotho (r2 = −0.208; P = 0.04). In multivariable analysis, extent of aortic valve calcification was associated with FGF-23 (P = 0.01) and PTH (P = 0.01) levels.ConclusionsExtent of aortic valve calcification is associated to FGF-23 and PTH in naïve CKD patients with mild to moderate CKD. Further studies should examine whether FGF-23 assay should be included in routine clinical evaluation of CKD as part of cardiovascular risk stratification.