Major Cause Of Chronic Kidney Disease Research Articles

EFFECT OF RENAL DENERVATION ON BLOOD PRESSURE IN PATIENTS WITH CHRONIC KIDNEY DISEASE AND UNCONTROLLED HYPERTENSION: RESULTS OF A PROSPECTIVE RANDOMIZED SHAM-CONTROLLED STUDY

Objective: The activity of the sympathetic nervous system (SNS) is increased in patients with chronic kidney disease (CKD) and endovascular renal denervation (RDN) offers the opportunity to modulate SNS activity and thereby blood pressure. Hypothesis: In patients with CKD stage 3 and uncontrolled hypertension, endovascular ultrasound-based RDN (uRDN) reduces 24-hour ambulatory BP without adverse safety events. Design and method: In a multicenter prospective randomized clinical trial, following the criteria of a blinded sham-controlled design, patients with CKD stage 3 and uncontrolled hypertension despite prescription of 1-5 antihypertensive medications were enrolled. Patients were randomly allocated to either endovascular uRDN using the Paradise™ Renal Denervation System (ReCor Medical, Inc., Palo Alto, CA, USA) or a sham procedure restricted to renal angiopgraphy alone. The primary endpoint was the change in mean 24-hour ambulatory systolic BP at 6 months while on stable medication. Secondary endpoints were changes of other 24h ambulatory BP values, office BP and safety parameters of uRDN. Blinding was to be maintained through 6 months. Due to slow recruitment through 2 years, the trial was prematurely stopped. Results: Of 25 randomized patients (mean age 67yrs), 20 subjects had a 6 month visit per protocol. Major cause of CKD was hypertension and/or type-2 diabetes (N=13). There was no difference in clinical characteristics (eGFR, UACR, BMI, HbA1c, comorbidities), pretreatment 24 hour/day/night ambulatory and office BP between the uRDN (N=10) and the sham group (N=10). After 6 months the decrease in 24h(and day) ambulatory diastolic BP was significantly greater in the RDN compared with the sham group (p=0.035 (and 0.030)). Within the uRDN group, 24 hour (and day) ambulatory diastolic BP decreased over time compared to pretreatment values, whereas in the sham group no changes occurred. Systolic ambulatory BP decreased numerically in the uRDN group, but was not significant. No safety concerns related to uRDN emerged. Conclusions: In this randomized sham-controlled blinded study, despite its premature stop leading to a small study cohort, we observed a decrease of diastolic BP after endovascular uRDN and no safety signals in these hypertensive patients with CKD.

Preventive and healing effect of high dosing grape seed flour on CKD patients of various stages and aetiologies

ABSTRACT Introduction Chronic kidney disease (CKD) is a worldwide public health concern characterised by a progressive alteration of renal function, and obesity, diabetes and hypertension are major risk factors. Oxidative stress is commonly observed in CKD patients resulting from an imbalance between overproduction of reactive oxygen species (ROS) and impairment of defense mechanisms. Therefore, strategies that alleviate oxidative stress may have major clinical implications towards improving vascular health and reducing the burden of CKD. Also, CKD worsens the quality of life of patients, therefore it is fundamental to implement new therapeutic strategies aimed at slowing down its progression. Materials and methods This interventional study is a randomised placebo-controlled clinical trial consisting at the daily oral supplementation with high dosing grape seed flour (GSF ≈ 1 g/kg) for experimental (n = 30) or starch for placebo (n = 10) to patients suffering from CKD of various stages and aetiologies. Blood and urine samples were collected at baseline and after a six-month-long supplementation period to follow up the disease evolution through the determination of renal function biomarkers, as well as antioxidant, anti-inflammatory and blood parameters. Results Supplementation with high dosing GSF was safe and well tolerated during the entire period of investigation. GSF clearly improved the main renal function biomarkers as GFR, proteinuria, blood pressure, oxidative stress and inflammation as well as the overall patient welfare as indicated by several blood parameters. Conclusion Most importantly high dosing GSF specifically halted and even reversed the progression of diabetic nephropathy a major cause of CKD and end stage renal disease.

Kidney failure, CKD progression and mortality after nephrectomy

PurposeThis study tested the hypothesis that progression of chronic kidney disease (CKD) is less aggressive in patients whose primary cause of CKD was nephrectomy, compared with non-surgical causes.MethodsA sample of 5983 patients from five specialist nephrology practices was ascertained from the Queensland CKD Registry. Rates of kidney failure/death were compared on primary aetiology of CKD using multivariable Cox proportional hazards models. CKD progression was compared using multivariable linear and logistic regression analyses.ResultsOf 235 patients with an acquired single kidney as their primary cause of CKD, 24 (10%) and 38 (17%) developed kidney failure or died at median [IQR] follow-up times of 12.9 [2.5–31.0] and 33.6 [18.0–57.9] months after recruitment. Among patients with an eGFR < 45 mL/min per 1.73m2 at recruitment, patients with diabetic nephropathy and PCKD had the highest rates (per 1000 person-years) of kidney failure (107.8, 95% CI 71.0–163.8; 75.5, 95% CI 65.6–87.1); whereas, patients with glomerulonephritis and an acquired single kidney had lower rates (52.9, 95% CI 38.8–72.1; 34.6, 95% CI 20.5–58.4, respectively). Among patients with an eGFR ≥ 45 mL/min per 1.73m2, those with diabetic nephropathy had the highest rates of kidney failure (16.6, 95% CI 92.5–117.3); whereas, those with glomerulonephritis, PCKD and acquired single kidney had a lower risk (11.3, 95% CI 7.1–17.9; 11.7, 95% CI 3.8–36.2; 10.7, 95% CI 4.0–28.4, respectively).ConclusionPatients who developed CKD after nephrectomy had similar rates of adverse events to most other causes of CKD, except for diabetic nephropathy which was consistently associated with worse outcomes. While CKD after nephrectomy is not the most aggressive cause of kidney disease, it is by no means benign, and is associated with a tangible risk of kidney failure and death, which is comparable to other major causes of CKD.

Early detection of kidney diseases in diabetic patients with serum cystatin-C

Background: Prevalence of chronic kidney disease (CKD) is increased worldwide. According to Kidney Disease Improving Global Outcomes guidelines, CKD is defined as abnormalities of kidney structure or function, present for >3 months with implications for health. In individuals with Type-2 diabetes, assessment of kidney function is mandatory, as diabetic nephropathy constitutes the major cause of CKD which leads to end-stage renal disease in diabetic patients. Cystatin-“C”, an alternative biomarker of kidney function, is a better predictor of CKD and is less affected by age, race, or muscle mass. Hence, the presence of elevated serum cystatin C is directly linked with risk of developing a progressive form of CKD. Aim and Objectives: This study aims to evaluate the importance of serum cystatin C as a marker for early detection of CKD in diabetic and non-diabetic patients. Materials and Methods: A total of 25 non-diabetics with CKD (Group-I) and 25 diabetics with CKD (Group-II) were included in the study. Cystatin C and glucose were estimated in the serum sample. Latex-enhanced immunoturbidimetric assay method was used for the estimation of serum cystatin-C. Random blood glucose was estimated using glucose oxidase-peroxidase method. Student’s t-test was used for comparison between CKD with non-diabetics and CKD with diabetics by SPSS statistical package version 20.0. “P” < 0.05 was considered as statistically significant. The results of the two groups are expressed as Mean ± SD. Results: Serum cystatin-C levels were significantly increased (P < 0.001) in Group-I when compared to Group-II. There was a significant negative correlation (r = –0.447, P < 0.001) between serum cystatin C and estimating glomerular filtration rate was observed, which indicates that there is a possibility of renal damage in non-diabetic subjects. Conclusion: Cystatin C can be used as a good alternative marker compared to creatinine for assessing severe kidney damage.

Brain dysfunction in tubular and tubulointerstitial kidney diseases.

ABSTRACTKidney function has two important elements: glomerular filtration and tubular function (secretion and reabsorption). A persistent decrease in glomerular filtration rate (GFR), with or without proteinuria, is diagnostic of chronic kidney disease (CKD). While glomerular injury or disease is a major cause of CKD and usually associated with proteinuria, predominant tubular injury, with or without tubulointerstitial disease, is typically non-proteinuric. CKD has been linked with cognitive impairment, but it is unclear how much this depends on a decreased GFR, altered tubular function or the presence of proteinuria. Since CKD is often accompanied by tubular and interstitial dysfunction, we explore here for the first time the potential role of the tubular and tubulointerstitial compartments in cognitive dysfunction. To help address this issue we selected a group of primary tubular diseases with preserved GFR in which to review the evidence for any association with brain dysfunction. Cognition, mood, neurosensory and motor disturbances are not well characterized in tubular diseases, possibly because they are subclinical and less prominent than other clinical manifestations. The available literature suggests that brain dysfunction in tubular and tubulointerstitial diseases is usually mild and is more often seen in disorders of water handling. Brain dysfunction may occur when severe electrolyte and water disorders in young children persist over a long period of time before the diagnosis is made. We have chosen Bartter and Gitelman syndromes and nephrogenic diabetes insipidus as examples to highlight this topic. We discuss current published findings, some unanswered questions and propose topics for future research.

Strategies for preventing end stage kidney disease: The impact of kidney stone disease on Chronic Kidney Disease in Pakistan.

Chronic Kidney Disease (CKD) is one of the major noncommunicable diseases that have social and economic impacts along with day-to-day health-related problems. Kidney stone disease is still one of the major causes of CKD in Pakistan. Kidney stone disease is a preventable cause of renal failure, if detected and treated early. Kidney stone is prevalent in the stone belt areas in our country which are located in rural areas. The treatment is very costly, and mostly available only in large cities. The treatment requires tertiary care setup and expertise. Therefore, there is a need to focus on the preventive strategies which are mainly dietary and lifestyle modifications, along with public awareness programmes. Nephrologists and urologists along with the government should take interest and give priority to CKD due to stone disease.

Ketoanalogue supplements reduce mortality in patients with pre-dialysis advanced diabetic kidney disease: A nationwide population-based study

Metabolism dysregulation and protein energy wasting occur in patients with chronic kidney disease (CKD) and are associated with poor survival, especially in patients prior to starting dialysis. Accumulating evidence indicates that dietary supplementation with ketoanalogues (KAs, a mixture of branched-chain amino acids) exerts a variety of beneficial effects for patients with CKD. However, the role of KAs in diabetic kidney disease (DKD), one of the major causes of CKD, is still controversial. The aim of this study was to explore the impact of KA supplements on survival in patients with stage 5 DKD who have not yet started dialysis (DKD-5-ND). We analyzed a nationwide cohort retrieved from the National Health Insurance Research Database in Taiwan to study the long-term impact of KA supplements in patients with DKD-5-ND. We enrolled 15,782 incident pre-dialysis DKD patients between January 1, 2004 and December 31, 2007. Landmark analysis was used to eliminate immortal bias, and overlap weighting was used to balance differences between the KA users and nonusers in the beginning. The primary study endpoint was all-cause mortality, and the occurrence of permanent dialysis (presenting the end-stage renal disease, ESRD) and major adverse cardiovascular events (MACEs) was also evaluated. All patients were followed for five years or until death. The prevalence of KA usage in the DKD-5-ND patients was 6.3%. The 5-year all-cause mortality rate in the KA users was lower than that in the nonusers (34.7% vs 42.7%). After adjusting for known covariates, the KA users still had a lower risk of mortality (adjusted hazard ratio [aHR]: 0.73, 95% confidence interval [CI]: 0.66-0.82). In addition, the incidence of ESRD was also slightly lower among the KA users (90.9% for users vs 91.2% for nonusers, adjusted cause-specific hazard ratio [aCSHR]: 0.65, 95% CI: 0.61-0.69), and the occurrence of MACEs was lower (adjusted incidence rate ratios [aIRR]: 0.76, 95% CI: 0.67-0.86). Although the all-cause mortality was higher among patientsolder than 70 years (60.5% for KA users vs 46.5% for nonusers) the risk reduction seemed prominent among older patients (aHR: 0.65, 95% CI: 0.56-0.76 for patients aged ≥70 years; aHR: 0.82, 95% CI: 0.71-0.96 for patients aged<70 years). The reduction in risks of mortality was consistent in subgroup analysis and sensitivity tests. The use of KA supplements seemed to be beneficial for patients with DKD-5-ND; further in-depth analysis of using KA for these patients is warranted.

Chronic kidney disease: Definition, updated epidemiology, staging, and mechanisms of increased cardiovascular risk.

Chronic kidney disease: Definition, updated epidemiology, staging, and mechanisms of increased cardiovascular risk.

Anemia in patients of diabetic kidney disease.

Anemia is the major complication resulting from chronic kidney disease (CKD) and also a risk factor for cardiovascular events and a poor quality of life (QoL). Diabetic kidney disease (DKD) is the major cause of CKD. Initially, insulin resistance has been reported to increase erythropoiesis, but it might be a minor issue. DKD-related anemia developed earlier and was more severe than non-DKD-related anemia based on more complicated mechanisms, including greater bleeding tendency associated with antiplatelet effect, less O2 sensing due to autonomic neuropathy or renin-angiotensin-aldosterone system inhibitor use, inhibitory effect of inflammatory cytokines, urinary loss of erythropoietin (EPO), and poor response to EPO. In DKD patients, prompt correction of anemia allows for a better cardiovascular outcome and QoL, which are similar to the promising effect of anemia correction in CKD patients. However, current evidence recommended that the avoidance of a high or normalized hemoglobin (Hb) level has been suggested in the treatment of anemia in DKD patients. Despite that EPO has a pleotropic effect on renal protection from animal studies, the renal benefit was less evident in CKD and DKD patients. Recently, the antidiabetic agent, sodium glucose cotransporter-2 inhibitors (SGLT2i), has been reported to exhibit the renal benefits due to the tubulo-glomerular feedback in addition to sugar control. It may also be due to less renal ischemic through higher EPO levels, followed by higher Hb levels. More studies are needed to clarify the link between the renal benefit of SGLT2i and EPO production.

Raising awareness, screening and prevention of chronic kidney disease: It takes more than a village.

Chronic kidney disease (CKD) is a major public health problem worldwide. Its prevalence and incidence are increasing, particularly among the ethnic minority populations. Diabetes, hypertension and obesity have been the three major aetiologies for CKD in all developed countries. While diabetes and hypertension remain the major causes of CKD in developing countries, environmental pollution, pesticides, water, analgesic abuse and herbal medications are common causes in these regions. Rapid urbanization and globalization are thought to be the contributing factors to rising prevalence and incidents of CKD. Despite the rising prevalence of CKD, disease awareness remains profoundly low. Worldwide, only 6% of the general population and 10% of the high-risk population are aware of their CKD statuses. Health screenings have been shown to be effective in improving the incidence of ESRD. However, currently there is no effective tool to assess and evaluate the awareness objectively.

Medical Nutrition Therapy for Patients with Non–Dialysis-Dependent Chronic Kidney Disease: Barriers and Solutions

Medical Nutrition Therapy for Patients with Non–Dialysis-Dependent Chronic Kidney Disease: Barriers and Solutions

Erythropoietic Response to Anaemia of Dialysis Naïve Patients with Chronic Kidney Disease in Zaria, North-West Nigeria.

Chronic kidney disease (CKD) is a global health problem with an increasing prevalence worldwide. Anemia is one of its consistent and severe hematological complications although its mechanism is not fully elucidated. The primary defect could manifest as serum erythropoietin (sEPO) deficiency or EPO resistance. We set out to determine the erythropoietic response to anemia of patients with CKD and its relationship with their iron status in a cross-sectional descriptive study of 91 patients in various stages of CKD. Materials and Methods: Soluble transferrin receptor (sTfR), sEpo, and serum ferritin levels were determined using ELISA method (Diagnostic Automation Inc and WKEA med supplies corp.). Data generated were analyzed using Epi Info version 3.5.3 and level of statistical significance was set at ≤0.05. Results: Participants comprised of 50 females (54.9%) and 41 (45.1%) males with an overall mean age of 47 ± 15 years. The major causes of CKD were hypertension (HTN) (50.54%), diabetes mellitus (DM) (6.59%), and HTN + DM (19.78%). The mean hemoglobin (Hb) concentration of the participants was 10.97 ± 2.28 g/dl; the red cell indices were within normal ranges except for Red cell distribution width-Coefficient of variation (%) which was elevated (16.29%). The mean serum ferritin, sTfR, and sEpo were 70.58 ± 46.44 ng/ml (interquartile range [IQR] 82.00), 22.9 ± 49.7 ng/ml (IQR 15.00), and 12.49 ± 33.47 IU/L (IQR 6.00), respectively, with a high variance. Serum ferritin and sTfR are consistently low across the stages of CKD (range between 54.54 ng/ml and 88.64 ng/ml), but sEPO for stage 3 and 4 showed a 2-fold increase when compared to normal level at Hb 10.97 g/dl (29.54 IU/L and 38.83 IU/L, respectively). Correlation between sTfR and sEpo (r2 = 0.96, P = 0.001), while between sEpo and serum ferritin (r2 = 0.02, P = 0.185), and between Hb and stage of CKD undulating (r2 = 0.41, P = 0.001). In contrast to some existing literature, this study has demonstrated that EPO resistance and iron deficiency contributes to anemia in CKD and serum ferritin can be used to assess the iron level of dialysis naïve CKD patients at every stage of the disease.

Clinical analysis of 108 cases with chronic kidney disease at stage 2 to 5 in children

Objective To analyze the pathogenesis, initially diagnosed symptoms and clinical manifestations of children with chronic kidney disease(CKD) at stage 2 to 5. Methods The data of 108 children who were hospitalized in Children′s Hospital Affiliated to Capital Institute of Pediatrics from September 2007 to April 2016 with CKD stage 2 to 5 were retrospectively analyzed.The etiologies, clinical manifestations and examinations were summarized, and the clinical manifestations were compared between the congenital hereditary urinary diseases group and the acquired urinary diseases group. Results (1) In the 108 cases collected, 66 cases were male, 42 cases were female, aged from 3 months to 15 years and 1 month old.Twenty-four cases were diagnosed at stage 2, 26 cases at stage 3, 35 cases at stage 4, and 23 cases at stage 5.(2)Twenty-eight kinds of illness were involved in the cause of CKD.Among them, 57 cases(52.8%) had congenital anomalies of the kidney and urinary tract, 5 cases(4.6%) had hereditary kidney diseases, 41 cases(38.0%) had other primary or secondary kidney diseases, and in 5 cases(4.6%) the causes of disease were unknown.(3) For the initially diagnosed symptoms, 29 cases(26.9%) were due to complaints associated with kidney disease, 36 cases(33.3%) were of other outside kidney symptoms, and 43 cases(39.8%) were of negative symptoms.The results of urinary ultrasound were abnormal in 79 cases(73.1%) and 87 cases(80.6%) showed abnormality in urinary analysis.There were 105 cases (97.2%) with abnormal manifestations either in urinary tract ultrasound or in urinary analysis.(4)The ages on diagnosis as CKD in children with congenital hereditary urinary diseases(5.89 years old) were younger than that of children with acquired urinary diseases(9.20 years old), and the difference was significant(Z=-3.434, P=0.001). The frequency of cases with short stature or lower-weight in group of congenital hereditary urinary diseases[66.1%(41/62 cases), 64.5%(40/62 cases)] were significantly higher than those of the acquired urinary diseases group[43.9%(18/41cases), 43.9%(18/41 cases)], and the differences were statistically significant(χ2=4.983, 4.263, P=0.026, 0.039). Conclusions The causes of CKD are complicated, and the congenital anomalies of kidney and urinary tract are the major causes of CKD at stage 2 to 5 in the cases.The initially diagnosed symptoms of CKD are insidious and atypical.The children with congenital hereditary urinary diseases tend to have more serious growth retardation.Urinary analysis and ultrasound may have an important significance for early diagnosis of CKD in children. Key words: Chronic kidney disease; Child; Etiology; Clinical manifestation

African origins and chronic kidney disease susceptibility in the human immunodeficiency virus era.

Chronic kidney disease (CKD) is a major public health problem worldwide with the estimated incidence growing by approximately 6% annually. There are striking ethnic differences in the prevalence of CKD such that, in the United States, African Americans have the highest prevalence of CKD, four times the incidence of end stage renal disease when compared to Americans of European ancestry suggestive of genetic predisposition. Diabetes mellitus, hypertension and human immunodeficiency virus (HIV) infection are the major causes of CKD. HIV-associated nephropathy (HIVAN) is an irreversible form of CKD with considerable morbidity and mortality and is present predominantly in people of African ancestry. The APOL1 G1 and G2 alleles were more strongly associated with the risk for CKD than the previously examined MYH9 E1 risk haplotype in individuals of African ancestry. A strong association was reported in HIVAN, suggesting that 50% of African Americans with two APOL1 risk alleles, if untreated, would develop HIVAN. However these two variants are not enough to cause disease. The prevailing belief is that modifying factors or second hits (including genetic hits) underlie the pathogenesis of kidney disease. This work reviews the history of genetic susceptibility of CKD and outlines current theories regarding the role for APOL1 in CKD in the HIV era.

Sustained Activation of EGFR Triggers Renal Fibrogenesis after Acute Kidney Injury

Severe acute kidney injury (AKI) is frequently accompanied by maladaptive repair and renal fibrogenesis; however, the molecular mechanisms that mediate these acute and chronic consequences of AKI remain poorly understood. In this study, we examined the role of epidermal growth factor receptor (EGFR) in these processes using waved-2 (Wa-2) mice, which have reduced EGFR activity, and their wild-type (WT) littermates after renal ischemia. Renal EGFR phosphorylation was induced within 2 days after ischemia, increased over time, and remained elevated at 28 days in WT mice, but this was diminished in Wa-2 mice. At the early stage of postischemia (2 days), Wa-2 mice developed more severe acute renal tubular damage with less reparative responses as indicated by enhanced tubular cell apoptosis, and reduced dedifferentiation and proliferation as compared to WT animals. At the late stage of postischemia (28 days), Wa-2 mice exhibited a less severe renal interstitial fibrosis as shown by reduced activation/proliferation of renal myofibroblasts and decreased deposition of extracellular matrix proteins. EGFR activation also contributed to cell cycle arrest at the G2/M phase, a cellular event associated with production of profibrogenetic factors, in the injured kidney. Collectively, these results indicate that severe AKI results in sustained activation of EGFR, which is required for reparative response of renal tubular cells initially, but eventually leads to fibrogenesis.

Urinary transglutaminase 2 as a potential biomarker of chronic kidney disease detection and progression

BackgroundThis study aimed to determine whether urinary transglutaminase 2 (TG2) has the potential to act as an early biomarker of chronic kidney disease (CKD) and whether it can predict the rate of progression better than can albuminuria. MethodsUrine samples were collected prospectively from 292 patients with CKD at the Sheffield Kidney Institute and 33 controls and followed for a minimum of 3 years. The cohort consisted of 61·7% men of whom 89% were white. Major causes of CKD were: diabetic nephropathy (29·05%), chronic glomerulonephritis (23·01%), hypertensive nephrosclerosis (16·6%), atherosclerotic renovascular disease (8·3%), chronic interstitial nephritis (6·41%), and autosomal dominant polycystic kidney disease (4·52%). Urinary TG2 was measured by an in-house sandwich ELISA. One-way ANOVA with Bonferroni correction was applied to estimate differences between groups. Area under the curve for receiver operating characteristic (ROC) analysis was used to determine prediction accuracy. A p value of less than 0·05 was considered statistically significant. FindingsUrine TG2 was 41 times higher in CKD patients than in healthy individuals (mean 3381 ng/mL [SD 135·36] vs 81·6 [4·18], p<0·001). Levels were elevated 17 fold by CKD stage 2. The largest increase in urine TG2 was observed in patients with diabetic nephropathy (7005 ng/mL [376]) with a 85-fold rise in CKD compared with healthy individuals, followed by hypertensive nephrosclerosis (3899 ng/mL [277]). TG2:creatinine ratio was 9·72 ng/mmoL [1·29] in controls versus 605·77 ng/mmoL [81·07] in patients with CKD (p<0·001). TG2 excretion was elevated in those patients with progressive (estimated glomerular fitration rate decline 2–5 mL/min/1·73m2 per year, 8997·91 ng/mL) or rapidly progressive CKD (>5 mL/min/year, 17650·195 ng/mL) compared with non-progressors (<2 mL/min/1·73m2 per year, 2764 ng/mL; p>0·05). There was no correlation between TG2 and total proteinuria (r=0·02808, 95% CI −0·09814 to 0·1534; p=0·6632). ROC curve analysis determined an 81·1% accurate prediction of progression for the TG2:creatinine ratio compared with just 71·4% for the albumin:creatinine ratio. InterpretationUrinary TG2 was significantly increased in all causes of CKD. ROC curve analysis demonstrated that TG2:creatinine ratio is a better predictor of patients with progressive CKD than albumin:creatinine ratio indicating its potential as a non-invasive biomarker of progressive kidney scarring. FundingUniversity of Sheffield and Pfizer.

English

BACKGROUND OF THE STUDY : The chronic kidney disease (CKD) is a known end result of type2 Diabetes mellitus and hypertension in recent times. It is associated with many features like hyperkalemia,hypocalcemia,hyponatremia,anaemia, hypoalbuminemia,multidrug resistant high blood pressure etc.So if we detect all these features early,we can extend the quality life of CKD patients. OBJECTIVES: The present study is undertaken with the following objective, to assess the clinical profile , biochemical profile and to determine the aetiology of chronic kidney disease, wherever possible at the time of presentation. MATERIALS AND METHODS : This is a descriptive study in which 50 patients with chronic kidney disease (CKD) ,who admitted at Chigateri General Hospital and Bapuji Hospital, attached to J.J.M. Medical College, Davangere, between year 2009 to 2011 were included.They were all fulfilled the criteria set by the National Kidney Foundations, Kidney Disease outcome quality initiative for diagnosing CKD by subjecting them to clinical assessment, laboratory analysis and ultrasonography of the abdomen and pelvis.The descriptives were reported based on frequencies and percentages (statistical method). RESULTS: The aetiology of CRF in our patients were found to be diabetic nephropathy in 38%, hypertensive nephropathy in 28%, chronic glomerulonephritis in 24%, obstructive uropathy in 6%, polycystic kidney disease in 2% and chronic pyelonephritis in 2%. The abnormality in the laboratory profile of the patients were found to be anaemia in 90%, hypocalcemia in 46%, hypoalbuminaemia in 34%, pedal edema in 78% and oliguria in 76%. The commonest clinical signs were high blood pressure in 92% and pallor in 90% of patients. CONCLUSIONS: The following conclusions can be drawn by our study, 1. The major symptoms were swelling of feet,oliguria and breathlessness, the major signs were pallor and persistent high blood pressure. 2. The major causes of CKD in descending order were, type2 diabetes mellitus,hypertension,chronic glomerulonephritis,and obstructive uropathy. 3. The lab features which commonly seen in our study were hypocalcemia, hyponatremia , hyperkalemia, anaemia and hypoalbuminemia in significant number of patients.

Are Physicians Ready to Prevent Osteoporotic Fractures in Hemodialysis Patients?

Dear Editor, Chronic kidney disease (CKD) is associated with many adverse outcomes including mineral and bone disorders. The prevalence of fractures among patients with CKD exceeds that of the general population, due to impairments in bone quantity, bone quality, and abnormalities of neuromuscular function with profound effects on morbidity and mortality (1). Type 2 diabetes mellitus (T2DM), that is a major cause of CKD, appears per se associated with an increased fracture risk despite a higher bone mineral density (BMD). The heavy burden of fractures in T2DM is much more due to poor bone quality than BMD, and bone quality is not detected by common diagnostic tools such as dual energy X-ray absorptiometry (2). Little is known about the efficacy of antiosteoporotic drugs in subjects undergoing hemodialysis, as these patients are often excluded in large randomized controlled trials. Raloxifene, a selective estrogen receptor modulator, prevents bone loss in postmenopausal women and reduces risk of vertebral fracture (3). Although the effects on bone density and biochemical markers were about half those observed in women treated with alendronate, the reduction in vertebral fracture risk was similar to alendronate, suggesting that other factors, beyond BMD, contribute to prevention of fractures. Saito et al. have recently reported the effects of one year raloxifene treatment on bone metabolism in hemodialysis women with and without T2DM (4). Data from Saito et al. evidence a significant increase of bone density evaluated by calcaneal quantitative ultrasound and a slight not significant reduction of the bone resorption marker NTx, both in T2DM and non T2DM women treated with raloxifene. Raloxifene is metabolized in the liver, and the resulting glucuronides are excreted in the bile, thus CKD is expected not to affect the pharmacokinetics of raloxifene. Hemodialysis patients with T2DM usually show low bone turnover rate, therefore raloxifene, that is only a mild bone resorption inhibitor seems a valid choice. Raloxifene, differently from hormone replacement therapy (HRT), reduces also the incidence of breast cancer, but, as to HRT, increases the incidence of venous thromboembolic events, thus caution is advised for the treatment of patients with high cardiovascular risk such as in CKD. Moreover, data on the possible effects of raloxifene on the insulin-glucose homeostasis are few, but raloxifene does not significantly affect glycemic control (5). The longer life expectancy obtained through hemodialytic programs in patients with CKD, should encourage researchers to look forward to bone health and reduction of the fracture risk. Unfortunately, to date, there are limited data on fracture risk assessment and fracture preventions with antiosteoporotic drugs in the hemodialytic population. What has been shown by Saito et al. on surrogate markers of bone strength (BMD and bone turnover) is encouraging for further prospective intervention studies to verify the long term safety and antifracture efficacy of raloxifene in T2DM hemodialysis patients.

Obesity and the kidney

Obesity represents an important risk factor for the development of chronic kidney disease (CKD), due to its known strong association with diabetes mellitus and hypertension, the two major causes of CKD, but also as an independent renal risk factor. This direct relationship between obesity and kidney injury has been undervalued. The aim of this revisión is to point out the mechanisms of kidney injury induced by obesity, underline the importance of this association and alert for the prevention, education and treatment of the obese patient, as a way to control this heavy modifiable risk factor.

Estudo epidemiológico da doença renal crônica terminal no oeste do Paraná: uma experiência de 878 casos atendidos em 25 anos

The incidence and prevalence of treated end-stage chronic kidney disease (CKD) patients continue to grow throughout the world. Renal transplantation remains the preferred form of renal substitutive therapy, but given the limited number of donors, dialytic therapies are the most common modalities. To assess a registry of patients admitted for renal substitutive therapy at a single centre from 1984 to 2009. This is a retrospective epidemiological study. The following were analyzed: demographic and clinical characteristics; incidence of CKD; underlying kidney disease; dialysis modalities; mortality; and causes of death. The variables were compared by using the chi-square test, Student t test, ANOVA, and Tukey test. Kaplan-Meier curves were used to estimate patient's survival. A p value < 0.05 was considered statistically significant. In the period studied, 878 patients were admitted to dialysis. Their mean age was 47.0 ± 16.2 years, 549 (62.5%) were males, and 712 (81.1%) were white. The major cause of CKD was hypertension in 351 (40.0%) patients, diabetic nephropathy in 174 (19.8%), and chronic glomerulonephritis in 180 (20.5%) patients. The main dialytic modality was hemodialysis. The one-year mortality rate was 10.4%. The most common cause of death was cardiovascular, affecting 126 (34.6%) patients. The cohort of patients studied had a low mortality rate. Cardiovascular disease remains the most common cause of death in end-stage chronic kidney disease. Screening for cardiovascular disease is highly recommended for those patients.