Degrees Of Chronic Renal Failure Research Articles

Assessment of lest ventricular hypertrophy and left ventricular diastolic dysfunction cardiovascular in patients of chronic renal failure by echocardiography

Introduction - Chronic renal failure, regardless of the cause, is the presence of kidney damage or a reduced level of kidney function for three months or longer. It is a group of signs and symptoms brought on by slow and long-term renal damage. The most frequent cardiovascular finding in people on dialysis is LVH. Objective - To estimate the prevalence of left ventricular hypertrophy and left ventricular diastolic dysfunction by echocardiography in patients with chronic renal failure. Method – this was an observational cross-sectional study at the Department of General Medicine among IPD patients, Tertiary Care Hospital, Surat. Result - Left ventricular hypertrophy out of 34 cases 22 (64.71%) cases were show left ventricular hypertrophy with an odd ratio of 3.208 (1.049, 9.81) and a p-value 0.0378 which was statically significant. prevalence of diastolic dysfunction was 79%. comparison of renal function test and echocardiographic change of chronic renal failure. In the renal function test serum, creatinine and EGFR were show a p-value < 0.001 which was statistically significant. Conclusion - Cardiac dysfunction and LVH are frequently noted in individuals with chronic renal failure at the time of commencement of dialysis. cardiovascular abnormalities in the form of LVH and diastolic dysfunction which antedate severe systolic dysfunction are frequently observed in milder degrees of chronic renal failure

Deletion of the P2Y2 receptor aggravates internal elastic lamina calcification in chronic kidney disease mice through upregulation of alkaline phosphatase and lipocalin-2.

Calcification of the medial layer, inducing arterial stiffness, contributes significantly to cardiovascular mortality in patients with chronic kidney disease (CKD). Extracellular nucleotides block the mineralization of arteries by binding to purinergic receptors including the P2Y2 receptor. This study investigates whether deletion of the P2Y2 receptor influences the development of arterial media calcification in CKD mice. Animals were divided into: (i) wild type mice with normal renal function (control diet) (n= 8), (ii) P2Y2 R-/- mice with normal renal function (n= 8), (iii) wild type mice with CKD (n= 27), and (iv) P2Y2 R-/- mice with CKD (n= 22). To induce CKD, animals received an alternating (0.2-0.3%) adenine diet for 7 weeks. All CKD groups developed a similar degree of chronic renal failure as reflected by high serum creatinine and phosphorus levels. Also, the presence of CKD induced calcification in the heart and medial layer of the aortic wall. However, deletion of the P2Y2 receptor makes CKD mice more susceptible to the development of calcification in the heart and aorta (aortic calcium scores (median ± IQR), CKD-wild type: 0.34 ± 4.3mg calcium/g wet tissue and CKD-P2Y2 R-/- : 4.0± 13.2mg calcium/g wet tissue). As indicated by serum and aortic mRNA markers, this P2Y2 R-/- mediated increase in CKD-related arterial media calcification was associated with an elevation of calcification stimulators, including alkaline phosphatase and inflammatory molecules interleukin-6 and lipocalin 2. The P2Y2 receptor should be considered as an interesting therapeutic target for tackling CKD-related arterial media calcification.

Time changes of renal dimensions and variations of glomerular filtration rate in chronic kidney disease patients.

The aim of this longitudinal prospective study was to search if even in the absence of total or partial nephrectomy the kidney size can increase as the kidney function improves. We randomly enrolled 80 adult patients with various degrees of chronic renal failure but non-dialysis dependent neither totally or partially nephrectomized nor affected by any of the pathological conditions that can increase kidney size. The patients underwent a first examination comprehensive of a blood sample and renal ultrasonography and then were submitted to a therapeutic intervention aimed at removing all nephrotoxic agents to finally be subjected to a last similar medical examination. The statistical analysis displayed a strong positive correlation between the percentage variation of the renal diameters' average and the time changes of the GFR (r 0.731; p < 0.01) as well as the percentage variation of the GFR and the time changes variations of the right (r 0.487; p < 0.01) and left cortical kidney thickness (r 0.519; p < 0.01) and finally a strong negative correlation between the removal of nephrotoxic agents and the percentage variation of the renal diameters' average (r - 0.293; p < 0.01) and the time changes of the GFR (r - 0.429; p < 0.01). In patients with chronic kidney disease, even in the absence of total or partial nephrectomy, under the stimulus of the removal of any nephrotoxic agents, there may be a limited increase in renal size according to a model that sees them vary according to the changes in GFR.

Hepatocyte growth factor exerts beneficial effects on mice with type II diabetes‑induced chronic renal failure via the NF‑κB pathway.

Type II diabetes is associated with a low quality of life and inflammation, and is often accompanied by varying degrees of chronic renal failure. Chronic renal failure is considered one of the most important factors that aggravates diabetes and contributes to renal insufficiency in patients with diabetes though cellular fibrosis. It has previously been reported that hepatocyte growth factor (HGF) serves extensive biological roles, and is a multifunctional antifibrotic factor that is involved in kidney development, acute injury and regeneration. The present study aimed to investigate whether HGF exerts beneficial effects on type II diabetes‑induced chronic renal failure in a mouse model. Plasma concentration levels of HGF, tumor necrosis factor (TNF)‑α, monocyte chemoattractant protein (MCP)‑1, interleukin (IL)‑1 and IL‑6 were analyzed prior to and following treatment with HGF. Blood urea nitrogen, plasma creatinine concentrations, and electrolyte, total serum protein, parathyroid hormone and C‑reactive protein levels were analyzed by ELISA. The mechanism underlying the effects of the HGF‑mediated signaling pathway was also investigated in mice with type II diabetes‑induced chronic renal failure. Histological analysis was used to determine the therapeutic effects of HGF on mice with type II diabetes‑induced chronic renal failure. The results indicated that HGF exhibited lower plasma concentrations in mice with type II diabetes‑induced chronic renal failure compared with in healthy mice. In addition, treatment with HGF relieved chronic renal failure via inhibition of inflammation. The results indicated that TNF‑α, MCP‑1 and IL‑1 serum concentration levels were downregulated following treatment with HGF. Conversely, IL‑6 and vascular endothelial growth factor concentration was increased in the HGF‑treated mice compared with in the control mice. The results also demonstrated that HGF treatment downregulated the expression of nuclear factor (NF)‑κB molecules, and target molecules C‑C motif chemokine ligand (Ccl)2, Ccl5, intercellular adhesion molecule 1 and TNF‑α. The present study demonstrated that HGF markedly improved renal failure induced by type II diabetes in a mouse model; histological analyses revealed that renal cell injury was improved following treatment with HGF. In conclusion, these results suggested that HGF may exert beneficial effects on type II diabetes‑induced chronic renal failure via regulation of the NF‑κB signaling pathway.

HUMORAL IMMUNITY TO THE DAMAGE OF LIPID METABOLISM IN PATIENTS WITH RENOCARDIAC SYNDROME

A total of 289 patients with chronic renocardiac syndrome, 204 of them with chronic glomerulonephritis and 85 diabetic nephropathy. The worsening of the lipid metabolism, depending on the degree of chronic renal failure (CRF), I noted in the degree of CKD, manifested increased low density lipoprotein (LDL) of 1.22 times (p=0.004), triglycerides (p=0.02), atherogenicity index (p&lt;0.0001) and decreased high-density lipoprotein (HDL) cholesterol (p&lt;0.001). The coefficient of LDL / HDL ratio was greatest in patients with CRF I, which indicates the most intense pro-atherogenic processes in these patients. The biological role of education lipoprotein immune complexes (LPIC) is confirmed by us revealed a statistically significant negative correlation between the ratio and the atherogenic LDL IgG (r=- 0,3; p=0.04), and LDL atherogenic factor IgM (r=-0,46, p=0.01) in patients with chronic renal failure group 1. A statistically significant negative correlation between daily proteinuria and LDL IgG, LDL IgM (r=-0,3; p=0,005; r=-0,4; p=0.004, respectively), which suggests the assumption of our damaging effect LPIC on the renal glomerulus.

Can we reliably predict the level of anticoagulation after enoxaparin injection in elderly patients with renal failure?

The aim of this study was to evaluate the activity of anti-activated factor X (anti-Xa) in patients with different degrees of chronic renal failure (CRF), treated with therapeutic doses of low molecular weight heparin. This prospective study evaluated the effect of age, renal function, BMI, gender, in determining the efficacy and safety of treatment with enoxaparin, evaluated by assessing the anti-Xa. The therapeutic anticoagulant range was set between 0.20 and 0.70U/mL. Two hospital geriatric units. 98 patients (64 men, 34 women, mean age 82years) with CRF, treated with enoxaparin at therapeutic dosage, for deep vein thrombosis or acute coronary syndrome. Anti-Xa was assessed 4h after the third administration of LMWH using Chromogenix test. Renal function was assessed by calculating creatinine clearance according to Cockcroft formula. The dose of enoxaparin ranged between 53 and 200U/kg; total 4000-16000U/day. The mean anti-Xa was 0.41U/mL (95% CI 0.36-0.45). Multiple regression analysis selected only the dose of enoxaparin, but not age, creatinine clearance, BMI, gender, as a predictor of anti-Xa serum levels. In seven patients anti-Xa was above the range but none of them received more than 150U/Kg enoxaparin (100U/kg if creatinine clearance <30mL/min). Ten patients (eight men, two women) showed suboptimal levels of anti-Xa, regardless enoxaparin dose or creatinine clearance. Enoxaparin dose reduction according to renal function decreases the risk of overdosing and potentially the risk of bleeding. The risk of under dosing seems less predictable; therefore, anti-Xa assay may be useful in severe clinical situations that require higher anticoagulant activity.

The alteration in peripheral neutrophils of patients with chronic kidney disease

Abstract Recent findings have demonstrated the impaired functions of neutrophils of patients with chronic renal failure. The purpose of our research was to study oxidative modified proteins, as well as the histone spectrum in neutrophils drawn from patients with chronic kidney disease, and to estimate the ability of neutrophils to form spontaneous neutrophil extracellular traps. In this work, we have assumed that metabolic alteration in neutrophils may develop at early stages of chronic kidney disease. Materials and methods: Neutrophils obtained from patients with various stages of chronic kidney disease and degrees of chronic renal failure were used. As control, blood samples obtained from 32 healthy individuals was employed. In the examined neutrophils, advanced oxidation protein products, protein reactive carbonyl derivatives, as well as nucleosomal histones were detected. The ability of neutrophils to form spontaneous neutrophil extracellular traps was estimated. Our results have demonstrated an increase of nucleosomal histones in neutrophils of all patients with chronic kidney disease. Moreover, our work fixes the rate of growth of intracellular advanced oxidation protein products and the decreasing of protein reactive carbonyl derivatives in neutrophils from patients with chronic kidney disease. Furthermore, we demonstrate the presence of the neutrophils with altered oxidative status and the decomposition of the histone spectrum in the circulation of patients with chronic kidney disease.

The Determination of Oxidized Proteins and Albumin in Plasma of Chronic Kidney Disease Patients

Background: The study of oxidized proteins in blood of chronic kidney disease patients has been made without taking an initial clinical form of disease into account. The purpose of the research is to study oxidized proteins and albumin in blood plasma of patients with chronic glomerulonephritis and chronic pyelonephritis as an initial clinical form of chronic kidney disease. Methods: Blood plasma taken from 132 patients with various stages of chronic kidney disease and degree of chronic renal failure has been used for investigation. Blood of 32 healthy donors has been used for control testing. In blood plasma, modified proteins (protein reactive carbonyl products, advanced oxidative protein products), and albumin have been estimated. Results: In blood plasma of patients with chronic glomerulonephritis, as an initial clinical form of the chronic kidney disease, the significant increase in all types of oxidized proteins and significant decrease in albumin have been observed, comparing to the control samples. In blood plasma of patients with chronic pyelonephritis, as an initial clinical form of the chronic kidney disease, the significant increase in protein reactive carbonyl products has been observed comparing to the control samples only. Conclusions: the obtained results may unravel new targets for pharmacological intervention at an early stage of chronic kidney disease based on the initial clinical form of the disease

0361: Impaired P2Y12 inhibition by clopidogrel in patients with kidney transplantation

Several studies have indicated that impaired GFR is an important predictor factor associated with impaired platelet inhibition by clopidogrel. In chronic kidney disease, the presence of low platelet inhibition by clopidogrel is associated with adverse outcome following PCI and stenting. In the present study, we sought to determine if renal transplantation per se alters clopidogrel pharmacodynamics. 36 patients with kidney transplantation were enrolled in one single center (Nephrology Department, Hôpitaux Universitaires de Strasbourg). Control patients were 126 patients with different degrees of chronic renal failure, tested in the same conditions. Inclusion criteria were patients under clopidogrel treatment of 75mg per day for at least 8 days. Unstable patients or those presenting with any conditions that could account for reduced platelet inhibition by clopidogrel (heart failure, shock) were excluded. Treatment and medical history were collected at inclusion. Clopidogrel pharmacodynamics was studied using the VASP assay. Patients with kidney transplantation were younger (58.3 vs 72.6 years, p<0.001), less likely diabetics (39% vs 57%, p=0.12), presented a lower BMI (25.2 sv 27.2 p=0,05), the estimated glomerular filtration rate with the MDRD formula is better (47.9 vs 39.5ml/mn/1.73m2, p=0.15), and there is less inflammation. 89% patients in the transplantation group were under anti-calcineurin and 50% under steroids at low dose. Platelet reactivity Index a marker of the extent of P2Y12 inhibition was significantly higher in the transplantation group vs controls (60.1% vs 51.2% p=0.014). By multivariate analysis, high BMI and kidney transplantation were important predictors of residual platelet reactivity under clopidogrel treatment. After adjustment on eGFR with the MDRD formula, kidney transplantation remains an important predictor of alter P2Y12 inhibition. In kidney transplantation patients treated by clopidogrel, impaired platelet inhibition exist, even after adjustment on estimated glomerular filtration rate. The mechanisms by which immunosuppressive treatments may alter clopidogrel pharmacodynamics requires further investigation

Characterization of a Rat Model of Moderate Chronic Renal Failure—Focus on Hematological, Biochemical, and Cardio-Renal Profiles

The pathophysiological modifications underlying chronic renal failure seems to be dependent on the insufficiency degree, which will determine the moment to start therapy. As there is yet limited information about animal models of moderate chronic renal failure, we intended to perform a complete characterization of the hematological and cardio-renal alterations induced by partial nephrectomy. Blood samples from control and chronic renal failure rats were collected at 0, 3, 9, and 15 weeks in order to evaluate renal function, hematological parameters, iron metabolism, blood lipids, peripheral sympathetic nervous system, and inflammatory and redox status markers. BP, tissues trophy indexes, and kidney histomorphology were also assessed. Our data are consistent with a sustained moderate degree of chronic renal failure with a quickly compensated modest anaemia, though presenting iron metabolism disturbances. Despite the reasonable degree of functionality of the remnant kidney, as suggested by the anaemia correction and by the kidney hypertrophy and moderate lesions, several important cardiovascular modifications were developed. Our model presented hypertension, dyslipidemia, erythropoietic disturbances, sympathetic activation, and oxidative stress. This model might be a good tool to study the cellular/molecular mechanisms underlying moderate stages of chronic renal failure and to evaluate the therapeutic efficacy for prevention and treatment/correction of cardio-renal anaemia syndromes and complications in early stages.

Salivary Phosphate Secretion in Chronic Kidney Disease

Hyperphosphatemia is an important contributor to cardiovascular calcification in chronic renal failure (CRF) patients. Cardiovascular calcifications are responsible for the high morbidity and mortality in patients undergoing hemodialysis (HD). Despite dietary phosphate reduction and treatment with phosphate binders, serum phosphorus level, as recommended by K/DOQI guidelines, is achieved only by 50% of dialysis patients. Thus it is necessary to identify other therapeutic approaches to reducing serum phosphate. Phosphate may be secreted in the saliva, which is then swallowed, and this provides a source of endogenous phosphate and thus contributes to the hyperphosphatemia in CRF. This study evaluated salivary phosphate in 68 HD patients and 110 subjects with various degrees of CRF, compared with 30 healthy subjects. Saxon's test confirmed normal salivary secretion volume in all subjects. Salivary and serum phosphate and calcium and serum parathyroid hormone were measured. Both HD and CRF patients had significantly higher salivary phosphate levels compared with healthy control subjects. In the latter group of patients, salivary phosphate correlated positively with serum creatinine (P < .0001) and the glomerular filtration rate (P < .0001). These results suggest that the level of salivary phosphate may provide a better marker than serum phosphate for the initiation of treatment of hyperphosphatemia in CRF and HD patients. The results may also offer a new horizon in the therapy of hyperphosphatemia by establishing measures to bind salivary phosphate in the mouth, and before saliva is swallowed.

Sleep quality in patients with chronic renal failure: A 3-year longitudinal study

Background Despite the high prevalence of sleep disorders in patients with kidney disease, no relationship has been demonstrated between sleep quality and the degree of renal function in cross-sectional studies. A prospective trial was, therefore, started in patients with chronic renal failure (CRF) to evaluate whether a link exists between the modifications of these parameters observed during a three-year follow-up period. Methods Sleep quality was determined by the Pittsburgh Sleep Quality Index (PSQI) at baseline and after two and three years (Time 0, 2 and 3, respectively) in 78 patients with various degrees of CRF in association with the main clinical and biochemical variables. Results The baseline PSQI averaged 6.2 ± 3.8 (range: 0–21, with higher values indicating worse sleep quality) and was significantly increased at both Time 2 and 3 (8.8 ± 3.7 and 10.2 ± 3.5, respectively, P < 0.0001 vs baseline), whereas creatinine clearance progressively decreased (45 ± 24 vs 41 ± 26 and 32 ± 20 ml/min, at time 0, 2 and 3, respectively, P < 0.0001), although an independent association with PSQI could not be demonstrated after adjustment for confounding factors ( P = 0.90, mixed linear model). Conclusions Our data suggest that the progression of renal disease is accompanied by a progressive worsening of sleep quality; age is strongly related to both phenomena. PSQI represents an easy tool to use to detect sleep disorders and to more effectively evaluate renal patients; the prevention of sleep disorders by early and appropriate treatments could beneficially influence the course of the disease.

Excellent response to the clinical treatment of tophaceous gout

Gout continues to be a health problem around the world, and the treatment may turn into a real challenge when the patient presents a certain degree of chronic renal failure (CRF). We discuss a case of tophaceous gout in a 68-year-old male patient without urolithiasis and with uric acid (UA) underexcretion and CRF (creatinine clearance of 42 ml/min). Uricosuric treatment with benzbromarone and urinary alkalinization was administered, and acute gouty attacks improved substantially. Subsequently, allopurinol was added to the treatment to accelerate tophi reduction in the hands, feet, elbows and knees. After 30 months of treatment, serum UA declined from 10 to 3.2 mg/dl. Urinary UA excretion of 0.44 g/24 h in the baseline rose to 0.85 g/24 h, returning to the baseline value after 30 months. UA clearance tripled, rising from 3.05 ml/min before treatment to 9.48 ml/min, and remained at this level. It is worth stressing that even in cases of severe tophaceous gout, the response to clinical treatment may be satisfactory with substantial reduction of tophi and full acute gouty attack remission even in patients presenting a certain degree of CRF.

High Plasma Adenine Concentration in Chronic Renal Failure and Its Relation to Erythrocyte ATP

Background: Concentration of plasma adenine has been found to increase in chronic renal failure (CRF). The aim of the present study was to evaluate whether high plasma adenine concentration contributes to the elevated ATP in erythrocytes of patients with CRF. Methods: Three groups of patients with CRF were studied: (A) 30 patients with different degree of CRF; (B) 11 patients on hemodialysis, and (C) 12 patients after successful renal transplantation. Concentrations of plasma adenine and erythrocyte adenine nucleotides were measured in groups A, B and C. Furthermore, adenine incorporation into erythrocyte adenine nucleotide pool was measured in group A. Results: A positive correlation between plasma adenine and creatinine concentrations was found in CRF as well as between plasma adenine and erythrocyte ATP. Furthermore, positive correlation was evident between the rate of adenine incorporation into erythrocyte adenine nucleotide pool and the severity of CRF. A significant reduction in both plasma adenine and erythrocyte ATP was observed immediately following hemodalysis, but 2 days later, high predialysis plasma adenine and erythrocyte ATP concentrations were restored. Following successful renal transplantation erythrocyte ATP and plasma adenine concentrations reached control values. Conclusion: Our results provide evidence that plasma adenine concentration increases in parallel to the progress of the disease and that it could be responsible for the increase in erythrocyte ATP of patients with CRF.

Serum soluble Fas (CD95) and Fas ligand profiles in chronic kidney failure

Apoptosis, or programmed cell death, is an active form of cell death that is initiated by a number of stimuli and is intricately regulated. Apoptosis in both excessive and reduced amounts has pathophysiologic implications. Accelerated programmed cell death has been observed in leukocytes among patients with chronic renal failure (CRF). This has been ascribed in part to the retention of uremic toxins. The Fas/Fas ligand (FasL) system is a key regulatory apoptotic pathway. Membrane-bound Fas is a cell-surface receptor that transduces apoptosis after interaction with membrane-bound or soluble FasL (sFasL). By contrast, soluble Fas (sFas) binds sFasL and inhibits its activity. In an attempt to examine the balance between these soluble factors in uremia, we measured soluble sFas and sFasL levels in the serum of healthy control subjects and patients with various degrees of CRF and examined the distribution of the various molecular mass fractions of these proteins in uremic serum. In brief, serum was obtained from 15 healthy volunteers, 17 patients with CRF, 11 patients undergoing maintenance hemodialysis (HD), and 7 patients undergoing peritoneal dialysis (PD). Serum sFas and sFasL were measured by enzyme-linked immunosorbent assay, and their molecular distribution was determined by sodium dodecyl sulfate–polyacrylamide gel electrophoresis followed by immunoblot. Compared with results in healthy control subjects, sFas levels were significantly higher in patients with CRF and in patients undergoing dialysis. There was a significant inverse correlation between sFas levels and creatinine clearance. Serum sFasL levels were not different among the four groups. However, the sFas-to-sFasL ratio was significantly lower in healthy control subjects as compared with patients with CRF and patients undergoing dialysis. Immunoblots and densitometric analyses of sFas and sFasL depicted a known 48-kd sFas, a known 27-kd sFasL, and a 60-kd sFas-sFasL protein aggregate signal. In conclusion, serum sFas levels are increased in patients with various degrees of CRF and may bind circulating sFasL, thereby minimizing mediation of cellular apoptosis. (J Lab Clin Med 2000;136:320-27)

Vitamin D receptor genotype influences parathyroid hormone and calcitriol levels in predialysis patients

BsmI vitamin D receptor (VDR) gene polymorphism has been associated with the severity of hyperparathyroidism in patients on hemodialysis. The aim of this study was to analyze the influence of this polymorphism on parathyroid function and serum calcitriol levels in patients with different degrees of chronic renal failure (CRF) before dialysis. A total of 248 CRF patients, divided into three groups according to creatinine clearance (CCr; mild CRF group> 60 to </=85 ml/min, N = 54; moderate CRF group> 35 to </=60 ml/min, N = 113; severe CRF group> 10 to </=35 ml/min, N = 81), had their serum intact parathyroid hormone (iPTH) and calcitriol levels measured and BsmI genotype frequencies estimated by polymerase chain reaction (PCR) analysis. Diabetics, those on treatment with steroids, vitamin D or derivatives, and phosphorus binding agents were excluded. All those with serum calcium levels of <2.25 mmol/liter or> 2.5 mmol/liter and serum phosphorus levels of> 1.6 mmol/liter or who needed phosphorus binding agents were excluded. The statistical analysis was done with the general factorial analysis of variance entering first PTH and then calcitriol as the dependent variable; the genotype (BB, Bb and bb), sex and CCr group were defined as factors; and covariables included serum calcium, serum phosphorus, 1/creatinine versus time slope, PTH when calcitriol was the dependent variable, and calcitriol when PTH was the dependent variable. When serum PTH levels were entered as the dependent variable, serum calcium, CCr group, and the interaction of genotype with the CCr group were found to be significant factors (P = 0.025, P <0.001 and P = 0.039, respectively). When serum calcitriol levels were entered as the dependent variable, genotype, the interaction of genotype with CCr, the CCr group, and the 1/creatine versus time slope were found to be significant (P = 0.027, P = 0.028, P <0.001 and P = 0.044, respectively). The marginal means of PTH, adjusted with the general factorial analysis of variance across the three groups were: (a) mild CRF group, BB 5.3 pmol/liter (CI 0 to 13.8), Bb 5.5 pmol/liter (CI 2 to 9), bb 5.4 pmol/liter (CI 0.6 to 10.2); (b) moderate CRF group, BB 6.2 pmol/liter (CI 1.5 to 10.9), Bb 7.8 pmol/liter (CI 5.3 to 10.3), bb 7.5 pmol/liter (CI 4.8 to 10.1); (c) severe CRF group, BB 9.3 pmol/liter (CI 4.2 to 14.3), Bb 17.1 pmol/liter (CI 13.9 to 20.2), bb 21.9 pmol/liter (CI 18.7 to 25.2). The marginal means of calcitriol adjusted with the general factorial analysis of variance across the three groups were: (a) mild CRF group, BB 47 pg/ml (CI 37 to 57), Bb 40.9 pg/ml (CI 37 to 44.8), bb 32.6 pg/ml (CI 26.8 to 38. 4); (b) moderate CRF group, BB 24.1 pg/ml (CI 18.3 to 29.8), Bb 26.6 pg/ml (CI 23.5 to 29.7), bb 25.3 pg/ml (CI 22 to 28.6); (c) severe CRF group, BB 27.4 pg/ml (CI 21.3 to 33.5), Bb 19.4 pg/ml (CI 15.5 to 23.2), bb 20.4 pg/ml (CI 16.1 to 24.7). The progression of hyperparathyroidism is slower in predialysis patients with BB genotypes than in the other genotypes. Also, calcitriol levels are less reduced in the BB genotype, which may act to lessen the severity of secondary hyperparathyroidism.

The 4 year outcome following the demonstration of bilateral renal pelvic dilatation on pre-natal renal ultrasound.

There is little in the literature regarding long-term prognosis in cases of fetal pyelectasis and calyceal dilatation. The aim of this study was to correlate antenatal ultrasound findings with outcome in a large group of children, most of whom had routine antenatal mid-trimester scans. 75 babies with bilateral pyelectasis and calyceal dilatation in the pre-natal period and complete radiological and clinical data were identified over a 3 year period. Pre-natal ultrasound was correlated with results of post-natal investigation and the frequency of post-natal surgery was established. Follow-up was documented to discharge or to at least 4 years of age. Prognosis was related to the degree of pelvic dilatation, but neonatal morbidity was much more likely to be associated with pre-natal calyceal dilatation and/or hydroureter. 68% (51 of 75) of babies had insignificant abnormalities on post-natal investigation, defined as either transient fetal pyelectasis and calyceal dilatation, extrarenal pelves, or transient neonatal pyelectasis and calyceal dilatation. Five babies died in the neonatal period, all classified as either moderate or severe disease. Of the surviving 70 cases (93.3%), 27% had renal anomalies that required treatment by prophylactic antibiotics or surgery. The remaining babies were conservatively managed and followed as outpatients. One child required transplantation and a further two had a severe degree of chronic renal failure by the age of 4 years. These data will be of value in prospective counselling.

Analysis of Factors Influencing Chronic Renal Failure Progression

One of the most important characteristics of chronic renal failure (CRF) is its progression to end stage renal disease. CRF progression depends of many factors indicated in numerous experimental and clinical studies. The present study was undertaken with the aim to examine the role of sex, etiology of CRF, renal function at the beginning of the study, hypertension and protein intake on CRF progression. Ninety-two patients (47 female and 45 male) aged between 17 and 70, with various underlying kidney diseases and various degrees of CRF were followed for 8 years. CRF progression was expressed as Creatinine clearance (CCr) and reciprocal values of serum Creatinine (SCr) against time. CRF progression was slower in women than in men, but not significantly. Patients with diabetic nephropathy (b = 0,00006) and glomerulonephritis (b = 0,00005) had faster progression of CRF than patients with nephrosclero-sis (b = 0,00002), tubulointerstitial nephritis (b - 0,00003) and polycys-tic kidney disease (b = 0,00003). The fastest progression of CRF was in patients with the lowest SCr values at the beginning of the study. Proper regulation of blood pressure was the most important factor in slowing down CRF progression, independently of kind of antihypertensive drugs. Neither angiotensin converting enzyme inhibitors (b = -0,00001) nor calcium channel Mockers (b = -0,00002) showed better effects on CRF progression slowing down in comparison with other antihypertensive drugs (b = -0,00001). Low protein die t slowed down CRF progression, but not significantly.In conclusion, our retrospective study confirms that CRF progression depends on sex, underlying renal diseases and serum Creatinine levels at the beginning of the study. Good regulation of blood pressure and low protein diet can slow down CRF progression.

Is there a lesser hyperparathyroidism in diabetic patients with chronic renal failure?

Diabetic patients on dialysis have lower levels of parathyroid hormone (PTH); however, there is no data regarding PTH levels with different degrees of chronic renal failure (CRF). We compared 58 diabetic patients with different degrees of CRF with 268 non-diabetic patients with CRF (serum creatinine >1.2 mg/dl). In both groups, we investigated the main biochemical parameters together with plasma calcium, phosphorus, magnesium, PTH and calcitriol. Diabetic patients showed lower levels of PTH than non-diabetics (P=0.003). The differences were observed in patients with creatinine clearance <70ml/min. We also observed differences in phosphorus, magnesium and tubular resorption of phosphate. In the group of diabetic patients, serum glucose correlated inversely with PTH. Our study suggests that poor control of diabetes (hyperglycaemia) may play a role in the pathogenesis of the hypoparathyroidism observed in patients with diabetes and CRF.

Plasma mevalonate concentrations in uremic patients

Mevalonic acid (mevalonate or MVA), is an obligate precursor in the biosynthetic pathway of cholesterol. It is partially metabolized by the kidneys and its plasma concentrations are an index of endogenous cholesterol synthesis. The aim of the present study was to evaluate plasma MVA concentrations in uremic patients with different degrees of chronic renal failure (CRF; group A), and the effects of a single hemodialysis treatment on plasma MVA in a group of patients with end-stage renal disease (ESRD; group B). CRF patients exhibited a higher mean basal mevalonate concentration (13.3 +/- 6.5 ng/ml) than control subjects (4.68 +/- 1.32 ng/ml; P < 0.001). A statistically significant direct correlation was evident in CRF patients between mevalonate and creatinine plasma levels (r = 0.86; P < 0.001). A single hemodialysis treatment was associated with a significant reduction of plasma mevalonate concentrations four hours after the hemodialysis session (-57%; P < 0.001) and an increase up to the basal values 24 hours after the end of the treatment. In conclusion, our results demonstrated: (i) higher plasma MVA concentrations in patients with decreased renal function; (ii) a direct relationship between plasma MVA levels and the degree of kidney failure as expressed by creatinine plasma concentrations; and (iii) a clear cut reduction of elevated plasma MVA levels after a single hemodialysis treatment.