Early Stages Of Renal Failure Research Articles

A CLINICAL STUDY THROUGH AYURVEDA IN THE MANAGEMENT OF MUTRAGHATA W.S.R. CHRONIC KIDNEY DISEASE (CKD) – A CASE STUDY

Chronic Kidney Disease itself indicates chronicity with irreversible damage to the kidneys due to main leading factor in many cases nowadays as a major cause which is Hypertension and Diabetes mellitus type 2, which clinically presents as symptomless sometimes in initial stages and further presents with pedal oedema, decreased appetite, nausea, difficulty in micturition/decreased urine output, frothy/foamy urine, fatigue. Usually it is manifested through various lab investigations such as kidney function test in which increase in serum urea levels, serum creatinine and other are seen i.e., a waste product made by our muscles, also Kidney’s one of the vital function is production of erythropoietin.Ayurveda has played an essential role in the early stages of renal failure in the hunt for this effective and safe treatment. Mutra is a kleda product, according to Ayurveda. Acharya Sushruta, a worldrenowned surgeon, has a good description of Mutrapravrutti.Creatine and Creatinine are not the same substances. Creatine from liver transported to other tissues. Creatine are 98% present in skeletol and heart muscles.in these muscles it gets converted to high energy source creatine phosphate. In skeletol muscle approximately 1/4th of Creatine exists as free Creatine and 3/4th exists as Creatine phosphate compound. It acts as a storage form of energy in the muscle. The amount of C. phosphate in the body is proportional to the muscle mass

A Case Studyof Chronic Kidney Disease

Chronic Renal/Kidney Failure is another name for chronic kidney disease. Kidney illness is becoming more common in India as a result of changing lifestyles, dietary habits, hypertension, and uncontrolled diabetes. It is a silent assassin. Hemodialysis and peritoneal dialysis are the most common treatments for chronic kidney failure, followed by kidney transplantation. Kidney failure treatment is highly costly and out of reach for most Indians. Ayurveda has played an essential role in the early stages of renal failure in the hunt for this effective and safe treatment. A 35-year-old male patient with pitting edoema on his legs, eyes, and face, as well as dyspnea, frothy urine, anorexia, and constipation, is the subject of this case study. Chronic Kidney Disease has been diagnosed. Hemodialysis was recommended, but the patient refused, instead he had Ayurvedic treatment with Punarnava Mandur, Vrukkadoshantak Vati,ArkPunarnavaArk Makoe. Symptoms and investigation have improved. The purpose of this case study is to investigate Chronic Kidney Disease from an Ayurvedic perspective, as well as to examine the results of Ayurvedic therapy in Chronic Kidney Disease as a symptom and modern parameter investigation.

Holistic vision of the patient with chronic kidney disease in a universalistic healthcare system.

Chronic kidney disease (CKD) is an increasing public health problem. Aging is one of the leading causes, particularly in Western countries, but several comorbidities, such as hypertension and diabetes are involved in its pathogenesis. Thus, the treatment of CKD patient is very complex and requires an integrated strategy. In this context, the holistic approach to the CKD patient and not to the disease itself should be the answer. General practitioners, specialists, voluntary associations, and nonprofit organizations, in addition to the family of the patient, all contribute to the patient care. Moreover, due to the low sensitivity of creatinine values in the early stages of renal failure, its diagnosis often occurs in the advanced phases of the disease. Therefore, the health costs for CKD patients are hardly sustainable by health systems. The reorganization of economic and epidemiological data through new models is necessary to allow the sustainability of the system and to ensure medical care for all patients. In this review, we aim to deal with all the issues about patient care, standards of care, and the impact of chronicity from a global perspective in light of the current state of the Italian healthcare system.

Inflammation both increases and causes resistance to FGF23 in normal and uremic rats.

Fibroblast growth factor 23 (FGF23) increases phosphorus excretion and decreases calcitriol (1,25(OH)2D) levels. FGF23 increases from early stages of renal failure. We evaluated whether strict control of phosphorus intake in renal failure prevents the increase in FGF23 and to what extent inflammation impairs regulation of FGF23. The study was performed in 5/6 nephrectomized (Nx) Wistar rats fed diets containing 0.2-1.2% phosphorus for 3 or 15 days. FGF23 levels significantly increased in all Nx groups in the short-term (3-day) experiment. However, at 15 days, FGF23 increased in all Nx rats except in those fed 0.2% phosphorus. In a second experiment, Nx rats fed low phosphorus diets (0.2 and 0.4%) for 15 days received daily intraperitoneal lipopolysaccharide (LPS) injections to induce inflammation. In these rats, FGF23 increased despite the low phosphorus diets. Thus, higher FGF23 levels were needed to maintain phosphaturia and normal serum phosphorus values. Renal Klotho expression was preserved in Nx rats on a 0.2% phosphorus diet, reduced on a 0.4% phosphorus diet, and markedly reduced in Nx rats receiving LPS. In ex vivo experiments, high phosphorus and LPS increased nuclear β-catenin and p65-NFκB and decreased Klotho. Inhibition of inflammation and Wnt signaling activation resulted in decreased FGF23 levels and increased renal Klotho. In conclusion, strict control of phosphorus intake prevented the increase in FGF23 in renal failure, whereas inflammation independently increased FGF23 values. Decreased Klotho may explain the renal resistance to FGF23 in inflammation. These effects are likely mediated by the activation of NFkB and Wnt/β-catenin signaling.

Early Detection of Active Glomerular Lesions in Dogs and Cats Using Podocin.

In veterinary medicine, sensitive and specific markers of the early stages of renal failure still remain to be established. Podocytes could be a promising diagnostic tool in veterinary nephrology, especially in the differentiation of active pathological disease and glomerulopathies. Podocin is one of the robust proteins exploitable in detection of podocyturia. This article presents podocyte detection in urine for diagnostic purposes in veterinary medicine using a variety of methods. We describe the advantages and disadvantages of the immunohistochemical technique currently used, and of scanning microscopy, chromatography, and immunostaining. The identification of podocin-positive cells is a promising diagnostic tool in the detection of the early stages of glomerular basement membrane damage. The detection of renal failure prior to the occurrence of azotaemia is of high clinical importance from the clinical and scientific points of view.

Role of diffusion weighted MRI in characterization of renal diseases

Background: MRI has the unique ability to show both structure and function objectively without any radiation exposure to the patient. Apparent diffusion coefficient (ADC) is a quantitative parameter that combines the effects of capillary perfusion and water diffusion. Renal parameters have shown inverse relationship with the ADC values in these studies. So, ADC values have a potential to serve as a marker of renal function. The aim of the present endeavor was to study the role of DW MRI in characterization of renal function and to find out the clinical use of DW MRI in renal diseases; and establish the relationship between renal function assessed by eGFR and that by DW MRI calculated in terms of ADC values in various renal diseasesMethods: Total 30 patients were included in the study. The study was carried out in department of radiodiagnosis at Dr. RPMGC Kangra. 1.5 Tesla MRI machine was used. The ADC value was calculated at upper, mid and lower pole of each kidney and the mean was taken. Then the mean of right and left kidneys was taken to calculate the mean ADC of the patient.Results: Serum creatinine in present study ranged from 0.67 to 13.9mg/dl, with mean value of 7.28mg/d. Serum urea ranged from 22 to 293mg/dl with the mean of 119.6mg/dl. There was significant inverse correlation occurred between ADC values and serum urea (r=-0.43, p=0.02). There was significant inverse correlation between ADC values and serum creatinine (p=0.01) and a positive correlation between eGFR and ADC values (r=0.14, p=0.47).Conclusions: ADC values consistently decreased with increasing stage of renal failure, so these can be used as an indirect maker of renal function. Authors conclude that lower would be the ADC value more advanced would be the stage of renal failure. DW MRI can also be detect early stages of renal failure even when the serum maker are within normal range.

Determination of NF-κB and RANKL levels in peripheral blood osteoclast precursor cells in chronic kidney disease patients.

Chronic kidney disease (CKD) is a progressive condition characterized by irreversible loss of functional nephron mass due to variety of causes; an inevitable complication of CKD is metabolic bone disease, and this pathology is called as renal osteodystrophy (ROD). In this study, we aimed to determine the levels of serum sRANKL and intracellular NF-κB levels in peripheral blood osteoclast precursor cells in patients with stage 3 CKD. Forty-one male patients aged 35-60 with CKD identified as stage 3 according to GFR calculated on the basis of creatinine values and 27 healthy male subjects with age ranging from 40 to 60 as control group were included in this study. Levels of biochemical parameters, vitamin D3, parathyroid hormone, bone mineral density, sRANKL and NF-κB were determined by using photometric, electrochemiluminescence, HPLC, ELISA and flow cytometric methods in control and patient groups, respectively. When stage 3 CKD patients were compared with controls, patients with stage 3 CKD had statistically significantly higher iPTH levels, but they had statistically significantly lower vitamin D3 levels. However, the other biochemical parameters, bone mineral density, sRANKL and NF-κB levels did not reveal any significance. In conclusion, vitamin D3 and iPTH levels seem to be important parameters for evaluating the early stages of ROD. The lack of statistically significant differences in the levels of sRANKL and NF-κB suggests that these parameters are not sufficient in the evaluation of bone metabolism in the early stages of renal failure.

Early renal failure as a cardiovascular disease: Focus on lipoprotein(a) and prothrombotic state.

Patients with renal failure are at increased risk of cardiovascular events even at the earliest stages of disease. In addition to many classic cardiovascular risk factors, many conditions that are commonly identified as emerging risk factors might contribute to occurrence of cardiovascular disease. Changes in circulating levels of many of these emerging risk factors have been demonstrated in patients with early stages of renal failure caused by different types of renal disease and have been associated with detection of cardiovascular complications. However, for most of these factors evidence of benefits of correction on cardiovascular outcome is missing. In this article, we comment on the role of lipoprotein(a) and prothrombotic factors as potential contributors to cardiovascular events in patients with early renal failure.

Serum total p-cresylsulfate level is associated with abnormal QTc interval in stable angina patients with early stage of renal failure

Backgroundp-Cresylsulfate (PCS), a protein-bound uraemic retention solute, is known to cause endothelial dysfunction and possibly plays a role in coronary atherosclerosis. Furthermore, the association among serum total PCS, major adverse cardiovascular events, and all-cause mortality were also found in previous studies. However, little is known about the relationship between total PCS level and prolonged QT interval. We assessed whether serum total PCS level is related with prolonged QT interval by measuring 12-lead electrocardiogram (ECG) recording in stable angina patients with early stage of renal failure. MethodsSerum total PCS concentrations were measured by using the Ultra Performance LC System in 154 consecutive stable angina patients. A 12-lead ECG recording was obtained from each subject. ResultsPatients with abnormal corrected QT (QTc) interval have higher median serum total PCS levels than patients with normal QTc interval. Statistically significant associations were observed between the serum total PCS levels and the QTc interval (r=0.217, P=0.007). Using multivariate and trend analyses, serum total PCS level was independently associated with QTc prolongation. ConclusionsThis study indicates that serum total PCS levels are significantly higher in the presence of abnormal QTc interval and are associated with the QTc prolongation. Whether total PCS plays a role in the pathogenesis of QTc prolongation requires future investigation.

Is IL-33 useful to detect early stage of renal failure?

IL-33 is a proinflammatory cytokine that is a member of IL-1 family. Previously the effect of IL-33 on kidney injury is showed in animal models. In this study, we searched if we can use IL-33 to show the early stage of kidney injury in diabetic patients. Three groups are identified: 26 patients in Group 1: Healthy group, that do not have any chronic diseases and not taking any medication; 42 patients in Group 2: DM (diabetes mellitus) group without any known kidney disease and with normal kidney functions; 32 patients in Group 3: DM + MA (microalbuminuria) group that are assumed to have nephropathy. IL-33 level of DM patient group is greater than healthy group; also IL-33 level of DM + MA patient group is greater than healthy group; but there is not any difference between DM and DM + MA group. The increase in IL-33 levels in diabetic nephropathy is not associated with kidney injury but the increase could be resulting because of diabetes. So IL-33 cannot be used in early recognition of diabetic nephropathy.

Insulin Resistance in the Early Stages of Renal Failure: Implications for Cardiovascular Risk

An elevated risk of cardiovascular events is present in patients with mild-to-moderate renal function impairment. Similar to patients with end-stage renal disease, this elevated risk can be accounted for by high prevalence of classic and emergent cardiovascular risk factors and additional conditions that are more specifically related to the organ failure, such as anemia and electrolyte disturbances. Among emergent cardiovascular risk factors, insulin resistance has been demonstrated to contribute significantly to the cardiovascular risk in the general population and it is known that abnormalities of glucose metabolism and hyperinsulinemia due to insulin resistance are present in patients with renal failure. Because patients with more advanced disease stage have several abnormalities that might affect the cellular action of insulin acting as important confounders, the relationship between insulin sensitivity and renal function should be better evaluated in the early stages of renal failure. This article overviews the evidence supporting the presence of increased cardiovascular morbidity and mortality in patients with early stages of renal disease, and examines the potential for insulin resistance to contribute to cardiovascular risk in these patients.

Isoelectric focusing of urinary transferrin for detection of early stages of diabetic nephropathy

Urinary albumin (ALB) and transferrin (TF) are useful markers for impaired renal function. Compared to ALB, TF is more readily excreted into urine from an early stage of renal failure because of its smaller number of negative charges. However, few evidence of a change in isoelectric point (pI) value of urinary TF in nephropathy patients has been reported. We analyzed pI values of urinary TF by an isoelectric focusing, and compared the results in normal subjects with those in diabetic patients at various stages of nephropathy. Urine samples of diabetics were randomly collected from 24 patients and 7 healthy volunteers. An apotransferrin with a high pI value was detected in samples of healthy subjects. However, the pI value of TF bands derived from diabetic patients shifted to the lower side, and the more nephropathy stages progressed, greater change of pI value was detected. In addition, TF with low iron-binding capacity was detected in some samples from diabetics. These results suggest that determination of the pI value of urinary TF in diabetic patients may be useful diagnostic markers for an early detection of diabetic nephropathy.

Keishibukuryogan Reduces Renal Injury in the Early Stage of Renal Failure in the Remnant Kidney Model

The effects of keishibukuryogan on the early stage of progressive renal failure were examined in rats subjected to 5/6 nephrectomy. Keishibukuryogan, one of the traditional herbal formulations, was given orally at a dose of 1% (w/w) and 3% (w/w) in chow. Administration of keishibukuryogan was started at 1 week after 5/6 nephrectomy and was continued for 4 weeks. At the end of the experiment, Azan staining did not reveal any severe histological changes in the kidneys of the nephrectomized rats. On the other hand, significant increases in mRNA expressions of transforming growth factor-β 1 and fibronectin related to tissue fibrosis, as examined by Reverse Transcriptase-Polymerase Chain Reaction, were observed in nephrectomized rats, and they were significantly suppressed by 3% keishibukuryogan treatment. Against gene expressions related to macrophage infiltration, 3% keishibukuryogan treatment significantly suppressed osteopontin mRNA levels, and monocyte chemoattractant protein-1 and vascular cell adhesion molecule-1 mRNA levels showed a tendency to decrease, but without statistical significance. It was also observed that 3% keishibukuryogan attenuated serum urea nitrogen and urinary protein excretion levels. From these results, it was suggested that keishibukuryogan exerts beneficial effects that result in slowing the progression of chronic renal failure.

Drug Therapy in Patients With Chronic Renal Failure

Roughly 20% of patients in hospital have impaired kidney function. This is frequently overlooked because of the creatinine-blind range in which early stages of renal failure are often hidden. Chronic kidney disease is divided into 5 stages (CKD 1 to 5). Selective literature search. Methotrexate, enoxaparin and metformin are examples of drugs that should no longer be prescribed if the glomerular filtration rate (GFR) is 60 mL/min or less. With antidiabetic (e.g. glibenclamide), cardiovascular (e.g. atenolol) or anticonvulsive (e.g. gabapentin) drugs, the advice is to use alternative preparations such as gliquidone, metoprolol or carbamazepine which are independent of kidney function. Drug dose adjustment should be considered with antimicrobial (e.g. ampicillin, cefazolin), antiviral (e.g. aciclovir, oseltamivir) and, most recently, also for half of all chemotherapeutic and cytotoxic drugs in patients with impaired kidney function (with e.g. cisplatin, for instance, but not with paclitaxel). Decisions concerning drug dose adjustment must be based on the pharmacokinetics but this is an adequate prerequisite only in conjunction with the pharmacodynamics. There are two different dose adjustment rules: proportional dose reduction according to Luzius Dettli, and the half dosage rule according to Calvin Kunin. The latter leads to higher trough concentrations but is probably more efficient for anti-infective therapy.

Serum levels of total p-cresylsulphate are associated with angiographic coronary atherosclerosis severity in stable angina patients with early stage of renal failure

Objective p-Cresylsulphate (PCS), a protein-bound uraemic retention solute, is known to cause endothelial dysfunction and possibly plays a role in coronary atherosclerosis. We aimed to investigate the relationship of total PCS with traditional biomarkers associated with chronic coronary atherosclerosis. In addition, the relationship between serum total PCS levels and the severity of coronary artery stenosis was also explored. Methods and results Serum total PCS concentrations were measured by using the Ultra Performance LC System in 202 consecutive stable angina patients, and their associations with angiographic indexes of the number of diseased vessels and modified Gensini score were estimated. Patients with significant coronary artery stenosis have higher median serum total PCS levels than patients with normal coronary arteries. Statistically significant associations were observed between the serum total PCS levels and the number of diseased vessels ( β = 0.261, p = 0.0002), and modified Gensini score ( β = 0.171, p = 0.016). Using multivariate analysis, serum total PCS level was independently associated with the presence and severity of CAD. Conclusions This study indicates that serum total PCS levels are significantly higher in the presence of CAD and are correlated with the severity of the disease, which suggest that increased serum total PCS may be involved in the pathogenesis of coronary atherosclerosis.

Early renal failure detection by cystatin C in Type 2 diabetes mellitus: varying patterns of renal analyte expression

The early stages of renal failure are poorly diagnosed by current routine tests. We studied cystatin C and routine renal analyte patterns in Type 2 diabetes mellitus. Type 2 diabetes mellitus patients (n = 48) were tested for serum cystatin C, urine albumin, haemoglobin A1c, serum creatinine, serum urea, urine creatinine, glucose, triglycerides and low density lipoproteins (LDL). Glomerular filtration rate (GFR) estimates were made using Cockroft-Gault and Modification of Diet in Renal Disease formulae. The cystatin C (95%CI) reference range was 0.78-0.86 mg/L. While serum cystatin C showed general correlation with routine renal tests, a plateau was observed in analytes measured against cystatin C. Cystatin C improved sensitivity led to detection of renal abnormality in 19% of patients not diagnosed by routine tests. Cystatin C is a more sensitive marker of renal disease in Type 2 diabetes mellitus where estimated GFR is unreported at >60 mL/min and where antihypertensive medications render microalbuminuria detection unreliable. Its incorporation into a panel of renal function tests is highly recommended.

Importance of Recognizing Occult Renal Disease in Hypertensive Patients

Occult renal disease (ORD) is a condition that characterizes the early stages of renal failure and which cannot be detected by routine monitoring. The aims of this study were to determine the prevalence of ORD in hypertensive patients attending cardiology outpatient clinics and to identify its relationship with specific cardiovascular risk factors or treatment. A cross-sectional, retrospective, multicenter observational study was carried out in 1214 hypertensive patients attending cardiology outpatient clinics. Data from 1190 patients (98%) were analyzed. In 11%, the glomerular filtration rate (GFR) was calculated by the attending cardiologist using the Modification of Diet in Renal Disease equation. Overall, 9.5% of patients were found to have ORD. Affected patients were more likely to be female, to be older, to have a history of dyslipidemia, diabetes, a sedentary lifestyle or atrial fibrillation or a long history of hypertension compared with those without ORD, but were less likely to have a history of dyslipidemia, diabetes or a sedentary lifestyle than those with renal failure. There was no significant difference in treatment. Moreover, ORD was observed in 2.9% (two of 68) of those aged under 50 years, in 3.3% (seven of 210) aged 50-60 years, in 9.3% (37 out of 398) aged 60-70 years and in 13.5% (70 out of 518) aged over 70 years. Almost 10% of hypertensive patients reviewed by a cardiologist had moderate renal dysfunction that had not been investigated. They represent an unrecognized population with an intermediate cardiovascular risk. Consequently, it is recommended that the GFR should be calculated, especially in women and older patients.

Presentation and role of transplantation in adult patients with type 1 primary hyperoxaluria and the I244T AGXT mutation: Single-center experience

Primary hyperoxaluria type 1 (PH1) is a rare genetic disorder characterized by allelic and clinical heterogeneity. We aim to describe the presentation and full single-center experience of the management of PH1 patients bearing the mutation described in our community (I244T mutation+polymorphism P11L). Since 1983, 12 patients with recurrent renal lithiasis have been diagnosed with PH1 and renal failure in the Canary Islands, Spain. Diagnostic confirmation was based on the presence of oxalosis in undecalcified bone or kidney allograft biopsy, reduced alanine:glyoxylate aminotransferase activity in liver biopsy, and blood DNA analysis. Patients underwent different treatment modalities depending on individual clinical circumstances and therapeutic possibilities at the time of diagnosis: hemodialysis, isolated kidney, simultaneous liver-kidney, or pre-emptive liver transplantation. In all cases, the presentation of advanced renal disease was relatively late (>13 years) and no cases were reported during lactancy or childhood. The eight patients treated with hemodialysis or isolated kidney transplantation showed unfavorable evolution leading to death over a variable period of time. In contrast, the four patients undergoing liver transplantation (three liver+kidney and one pre-emptive liver alone) showed favorable long-term allograft and patient survival (up to 12 years follow-up). In conclusion, in this PH1 population, all bearing the I244T mutation, the development of end-stage renal disease was distinctive during late adolescence or adulthood. Our long-term results support pre-emptive liver transplantation at early stages of renal failure, and kidney-liver transplantation for those with advanced renal disease.

1,25-Dihydroxyvitamin D downregulation of TGFα/EGFR expression and growth signaling: a mechanism for the antiproliferative actions of the sterol in parathyroid hyperplasia of renal failure

Elevated serum levels of parathyroid hormone (PTH) contribute to the increased morbidity and mortality in renal failure patients. Parathyroid gland hyperplasia is a major cause of high serum PTH. The present studies used the rat model of renal failure to address the mechanisms underlying uremia-induced parathyroid hyperplasia and the antiproliferative properties of vitamin D therapy (1,25-dihydroxyvitamin D (1,25(OH) 2D 3) or its less calcemic analogs). Enhanced TGFα/EGFR co-expression is the major mitogenic signal in uremic parathyroid glands. At early stages of renal failure, vitamin D therapy efficiently counteracts uremia- and high phosphorus-induced hyperplasia by inhibiting the increases in parathyroid-TGFα/EGFR co-expression. In established hyperparathyroidism, characterized by highly enhanced-TGFα/EGFR co-expression, vitamin D therapy arrests growth by suppressing EGFR-growth signals from the plasma membrane and nuclear EGFR actions as a transactivator of the cyclin D1 gene, an important contributor to parathyroid hyperplasia in humans. In advanced renal failure, reduced-parathyroid vitamin D receptor levels limits the antiproliferative efficacy of vitamin D therapy. However, non-antiproliferative doses of 1,25-dihydroxyvitamin D enhance the anti-EGFR actions of EGFR–tyrosine kinase inhibitors (TKI). In fact, combined 1,25-dihydroxyvitamin D/TKI therapy inhibits parathyroid hyperplasia more efficiently than phosphorus restriction, the most powerful promoter of parathyroid growth arrest available at present.

The importance of bone health in end-stage renal disease: out of the frying pan, into the fire?

In the early stages of renal failure, hyperparathyroidism develops as a compensatory mechanism to control serum levels of calcium, phosphorus and calcitriol. As kidney disease progresses, this ability to maintain mineral homeostasis is lost, leading to the development of renal osteodystrophy (ROD). Over the past decade, the pattern of ROD seen in patients with chronic kidney disease (CKD) has changed. Previously, the majority of patients had mixed uraemic osteodystrophy or aluminium-related osteomalacia. The decreased use of aluminium-based phosphate binders, coupled with improvements in the management of hyperphosphataemia, led to a reduction in the prevalence of these types of ROD. Since the mid-1990s, there has been an increase in the prevalence of adynamic bone disease as a result of increased suppression of parathyroid hormone through the use of calcium-based phosphate binders and calcitriol therapy. Adynamic bone disease is also associated with several clinical factors, such as older age, use of continuous ambulatory peritoneal dialysis and the presence of diabetes mellitus, as well as the use of calcitriol therapy. Studies of calcium metabolism in patients with CKD have shown that adynamic bone disease is a distinct clinical condition that leads to hypercalcaemia via mechanisms different from that seen in high-turnover bone disease. As high calcium x phosphorus product has been associated with soft tissue and vascular calcifications, and increased mortality, optimizing bone health may be an important way of reducing cardiovascular risk in patients with CKD. To do this, novel, effective, non-calcium, non-aluminium phosphate binders will be necessary.