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ABSTRACT: Bone loss in renal transplant (RT) patients is a problem that begins during end-stage kidney disease and persists after transplantation. Suppression of parathyroid hormone (PTH) may decrease bone loss and improve fracture rate.
A single-group prospective intervention study involving 30 patients was performed at a large RT unit. Investigations included dual-emission X-ray absorptiometry scan, vertebral X-ray, calcium absorption test, 24-h urinary calcium and serum measurements of total and ionized calcium, PTH, C-telopeptide cross-links (CTX), osteocalcin, alkaline phosphatase, 25 hydroxyvitamin D (25[OH]D), and 1,25-dihydroxyvitamin D3. Patients were given 500 mg elemental calcium daily for seven d, and serum measurements were repeated.
Two-tailed Wilcoxon rank-sum test showed significant decreases in PTH (p<0.01) and CTX (p<0.01) after calcium load. Dietary calcium, mean calcium absorption, and urinary calcium excretion were below desirable levels. Mean 25 hydroxyvitamin D (25(OH)D) was low, but levels of 1,25-dihydroxyvitamin D3 were normal. Calcium absorption significantly correlated with change in PTH (p<0.001), baseline 25(OH)D (p<0.001), and mycophenolate dose (p=0.024).
Calcium malabsorption is prevalent in RT recipients, contributing to bone destruction and compounded by poor dietary intake and low 25(OH)D. Calcium supplementation appears to help overcome this deficiency and acutely suppress PTH. Calcium may be an effective and inexpensive therapy for bone loss in RT recipients.
Clinical Transplantation 08/2011; 26(2):292-9. · 1.67 Impact Factor
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Dennis H Lau,
Lorraine Mackenzie,
Darren J Kelly,
Peter J Psaltis,
Anthony G Brooks,
Michael Worthington,
Arumuga Rajendram,
Douglas R Kelly,
Yuan Zhang,
Pawel Kuklik,
Adam J Nelson,
Christopher X Wong,
Stephen G Worthley,
Mohan Rao, Randall J Faull,
James Edwards,
David A Saint,
Prashanthan Sanders
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ABSTRACT: Hypertension accounts for more atrial fibrillation (AF) than any other predisposing factor.
The purpose of this study was to characterize the time course, extent, and electrostructural correlation of atrial remodeling in chronic hypertension.
Thirty-two sheep were studied: 21 with induced "one-kidney, one-clip" hypertension and 11 controls. Sequential closed-chest electrophysiologic studies were performed in 12 conscious animals (6 hypertensive, 6 controls) to evaluate progressive remodeling over 15 weeks. Additional atrial structural/functional analyses were performed in 5 controls and at 5, 10, and 15 weeks of hypertension (five per time point) via histology/cardiac magnetic resonance imaging to correlate with open-chest electrophysiologic parameters.
The hypertensive group developed a progressive increase in mean arterial pressure (P <.001). Mean effective refractory periods were uniformly higher at all time points (P <.001). Progressive biatrial hypertrophy (P = .003), left atrial dysfunction (P <.05) and greater AF inducibility were seen early with increased inflammation from 5 weeks of hypertension. In contrast, significant conduction slowing (P <.001) with increased heterogeneity (P <.001) along with increased interstitial fibrosis resulted in longer and more fractionated AF episodes only from 10 weeks of hypertension. Significant electrostructural correlation was seen in conduction abnormalities and AF inducibility with both atrial inflammation and fibrosis.
Hypertension is associated with early and progressive changes in atrial remodeling. Atrial remodeling occurs at different time domains in chronic hypertension with significant electrostructural correlation of the remodeling cascade. Early institution of antihypertensive treatment may prevent formation of substrate capable of maintaining AF.
Heart rhythm: the official journal of the Heart Rhythm Society 05/2010; 7(9):1282-90. · 4.56 Impact Factor
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Dennis H Lau,
Lorraine Mackenzie,
Arumuga Rajendram,
Peter J Psaltis,
Douglas R Kelly,
Peter Spyropoulos,
Yuan Zhang,
Santosh A Olakkengil,
Christine H Russell,
Anthony G Brooks, Randall J Faull,
David A Saint,
Darren J Kelly,
M Mohan Rao,
Stephen G Worthley,
Prashanthan Sanders
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ABSTRACT: The aim of this study is to characterize cardiac remodeling in a large animal model of hypertension.
23 sheep were subjected to unilateral nephrectomy followed by clamping of the remaining renal artery to 60% ("one kidney-one clip", 1K1C) 3 weeks later. Blood pressure (BP) was monitored invasively over 73+/-28 days. Cardiac function was assessed with magnetic resonance imaging and compared with 12 size-matched controls. Detailed atrial histopathological analysis was performed.
In the 1K1C animals, BP rose from baseline to reach a plateau by 4 weeks (systolic BP: 107+/-12 to 169+/-27, diastolic BP: 71+/-10 to 118+/-29 mmHg, both p< 0.0001); cardiac hypertrophy was significant when compared with controls with increased left ventricular weight [left ventricular (LV)/body wt: 2.7+/-0.5 vs 2.1+/-0.2 g/kg, p=0.01] as well as bi-atrial enlargement (right atrial, RA: 22.9+/-4.9 vs 15.7+/-2.8g, p=0.003; left atrial, LA: 35.5+/-6.7 vs 20.9+/-4.1g, p=0.0003); cardiac magnetic imaging demonstrated significantly increased LA volumes (end-diastolic volume: 42.9+/-6.8 vs 28.7+/-6.3 ml, p< 0.0001) and reduced LA ejection fraction (24.1+/-3.6 vs 31.6+/-3.0%, p=0.001) while LV function was relatively preserved (42.3+/-4.7 vs 46.4+/-4.1%, p=0.1); degeneration and necrosis of atrial myocytes were evident with increased atrial lymphocytic infiltration and interstitial fibrosis.
The ovine 1K1C model produces reliable and reproducible hypertension with demonstrable cardiac end-organ damage.
Blood pressure 04/2010; 19(2):119-25. · 1.26 Impact Factor
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ABSTRACT: Antineutrophil cytoplasmic antibody-associated vasculitis is an autoimmune disease involving small to medium blood vessels. It is an uncommon illness, but can have devastating consequences, particularly on kidney function and other vital organs. Exciting progress has been made in the treatment of the disease largely because of international collaboration in randomised clinical trials. Patient survival has improved dramatically with advancements in disease diagnosis and medical treatment. The long-term morbidity from the disease, although improving, remains substantial with up to 10% of survivors requiring dialysis or kidney transplantation. Clinical trials are underway using more specifically targeted immunosuppressants in the hope to improve the long-term patient outcomes. Advancements are also being made in understanding the pathogenesis of the disease and this will further assist disease treatment and outcomes in the future.
International Journal of Evidence-Based Healthcare 03/2010; 8(1):18-27.
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Dennis H Lau,
Lorraine Mackenzie,
Darren J Kelly,
Peter J Psaltis,
Michael Worthington,
Arumuga Rajendram,
Douglas R Kelly,
Adam J Nelson,
Yuan Zhang,
Pawel Kuklik,
Anthony G Brooks,
Stephen G Worthley, Randall J Faull,
Mohan Rao,
James Edwards,
David A Saint,
Prashanthan Sanders
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ABSTRACT: Hypertension is frequently complicated by the development of atrial fibrillation (AF). However, the mechanisms of this link remain poorly understood. In addition, whether short-term hypertension can result in a substrate for AF is not known.
The purpose of this study was to characterize the atrial substrate predisposing to AF due to short-duration hypertension.
Sixteen sheep were studied: 10 had induced hypertension for 7 +/- 4 weeks via the "one-kidney, one-clip" model, and six were controls. Cardiac magnetic resonance imaging was used to assess functional changes. Open-chest electrophysiological study was performed using a custom-made 128-electrode epicardial plaque applied to both right (RA) and left atria (LA), including the Bachmann's bundle, to determine effective refractory periods (ERPs) and conduction velocity at four pacing cycle lengths from six sites. Tissue specimens were harvested for structural analysis.
The hypertensive group demonstrated the following compared with controls: higher blood pressure (P <.0001), enlarged LA (P <.05), reduced LA ejection fraction (P <.05), uniformly higher mean ERP (P <.001), slower mean conduction velocity (P <.001), higher conduction heterogeneity index (P <.0001), greater AF inducibility (P = .03), and increased AF durations (P = .04). Picrosirius red staining of atrial tissues revealed increased interstitial fibrosis (P <.0001). There was also evidence of increased inflammatory cell infiltrates (P <.0001).
Short-duration hypertension is associated with significant atrial remodeling characterized by atrial enlargement/dysfunction, interstitial fibrosis, inflammation, slowed/heterogeneous conduction, increased ERP, and greater propensity for AF.
Heart rhythm: the official journal of the Heart Rhythm Society 03/2010; 7(3):396-404. · 4.56 Impact Factor
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ABSTRACT: Anaemia is a common complication associated with haemodialysis and is usually managed by treatment with recombinant human erythropoietin (rHuEPO). However, many patients remain hyporesponsive to rHuEPO treatment despite adequate iron therapy. The effect of L-carnitine administration on rHuEPO dose and/or haematocrit in haemodialysis patients has been previously reported with equivocal results. This study examined the relationship between endogenous carnitine pool composition and rHuEPO requirements in long-term haemodialysis patients.
Pre-dialysis blood samples were collected from 87 patients and analysed for plasma L-carnitine and individual acylcarnitine levels by LCMS/MS. As an indication of rHuEPO responsiveness, erythropoietin resistance index (ERI) was calculated as rHuEPO dose/kg/week normalized for haemoglobin levels.
A significant negative correlation between L-carnitine levels and ERI was found (P = 0.0421). All patients categorized as high ERI (>0.02 microg/kg/week/gHb) exhibited subnormal L-carnitine levels (<30 microM); conversely, patients with normal L-carnitine levels (>30 microM) displayed low ERI values (<0.02 microg/kg/week/gHb). More importantly, the ratio of non-acetyl acylcarnitines/total carnitine was significantly positively correlated with ERI (P = 0.0062).
These data illustrate the relationship between carnitine levels and response to rHuEPO treatment in haemodialysis patients, in particular, the importance of the proportion of long-chain acylcarnitines within the plasma carnitine pool. This proportion may be more indicative of the response to L-carnitine supplementation than absolute L-carnitine levels alone.
Nephrology Dialysis Transplantation 12/2008; 24(3):990-6. · 3.40 Impact Factor
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Nephrology 11/2008; 13(5):448-9. · 1.31 Impact Factor
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ABSTRACT: It has been widely established that patients with end-stage renal disease undergoing chronic haemodialysis therapy exhibit low endogenous levels of L-carnitine and elevated acylcarnitine levels; however, the clinical implication of this altered carnitine profile is not as clear. It has been suggested that these disturbances in carnitine homeostasis may be associated with a number of clinical problems common in this patient population, including erythropoietin-resistant anaemia, cardiac dysfunction, and dialytic complications such as hypotension, cramps and fatigue. In January 2003, the Centers for Medicare and Medicaid Services (USA) implemented coverage of intravenous L-carnitine for the treatment of erythropoietin-resistant anaemia and/or intradialytic hypotension in patients with low endogenous L-carnitine concentrations. It has been estimated that in the period of 1998-2003, 3.8-7.2% of all haemodialysis patients in the USA received at least one dose of L-carnitine, with 2.7-5.2% of patients receiving at least 3 months of supplementation for one or both of these conditions. The use of L-carnitine within Australia is virtually non-existent, which leads us to the question: Are Australian haemodialysis patients missing out? This review examines the previous research associated with L-carnitine administration to chronic dialysis patients for the treatment of anaemia, cardiac dysfunction, dyslipidaemia and/or dialytic symptoms, and discusses whether supplementation is warranted within the Australian setting.
Nephrology 03/2008; 13(1):3-16. · 1.31 Impact Factor
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Nephrology 09/2007; 12(4):420-1. · 1.31 Impact Factor
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ABSTRACT: The aim of this pilot study was to test the effect of pravastatin on serum levels of high-sensitivity CRP (hs-CRP), IL-6 and the soluble adhesion molecules sVCAM-1, sICAM-1 and sE-selectin in chronic dialysis patients.
At the commencement of the study, serum levels of lipids, liver function tests and endothelial markers (CRP, IL-6, sICAM-1, sVCAM-1, sE-selectin) were measured. Patients then commenced 1 month of 10 mg of pravastatin per day, and if tolerated, then 4 months of 40 mg of pravastatin per day. Serum levels of lipids, liver function tests and endothelial markers were repeated after the total of 5 months of pravastatin therapy.
Thirty-nine patients were enrolled, and 25 (male/female 17/8; 21 haemodialysis, 4 peritoneal dialysis) patients completed the study. Pravastatin therapy significantly improved the patients' lipid profiles, but had no significant effect on the levels of CRP, IL-6, sICAM-1, sVCAM-1, or sE-selectin.
Short-term (5 months) treatment with pravastatin in patients receiving chronic dialysis improved their lipid profile, but had no significant effect on surrogate markers of endothelial activation.
Nephrology 07/2007; 12(3):234-8. · 1.31 Impact Factor
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ABSTRACT: Patients with end-stage renal disease (ESRD) undergoing long-term haemodialysis exhibit low L-carnitine and elevated acylcarnitine concentrations. This study evaluated endogenous concentrations of an array of acylcarnitines (carbon chain length up to 18) in healthy individuals and ESRD patients receiving haemodialysis, and examined the impact of a single haemodialysis session on acylcarnitine concentrations.
Blood samples were collected from 60 healthy subjects and 50 ESRD patients undergoing haemodialysis (pre- and post-dialysis samples). Plasma samples were analysed for individual acylcarnitine concentrations by electrospray MS/MS.
Of the 31 acylcarnitines, 29 were significantly (P<0.05) elevated in ESRD patients compared with healthy controls; in particular, C5 and C8:1 concentrations were substantially elevated. For acylcarnitines with a carbon chain length less than eight, plasma acylcarnitine concentrations decreased significantly over the course of a single dialysis session; however, post-dialysis concentrations invariably remained significantly higher than those in healthy subjects. Dialytic removal of acylcarnitines diminished once the acyl chain length exceeded eight carbons.
The accumulation of acylcarnitines during long-term haemodialysis suggests that removal by haemodialysis is less efficient than removal from the body by the healthy kidney. Removal is significantly correlated to acyl chain length, most likely due to the increased molecular weight and lipophilicity that accompanies increased chain length.
Annals of Clinical Biochemistry 10/2005; 42(Pt 5):387-93. · 2.17 Impact Factor
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ABSTRACT: Lymphoproliferative disease is a common and serious complication of organ transplantation. It is well documented that the risk of its development increases with the level of immunosuppression. Less is known about its incidence, prevalence, timing, and prognosis.
The authors conducted a retrospective review of all patients with lymphoproliferative disease after renal transplantation documented in the Australia and New Zealand Dialysis and Transplant Registry from 1970 to March 2003.
One hundred ninety-seven cases of lymphoproliferative disease occurred in 15,930 allografts in 13,516 recipients. There has been a steady increase in its incidence and prevalence each decade since 1970. Cases cluster into an early group (<2 years after transplantation) and a late group (5-10 years after transplantation). Risk factors include exposure to a calcineurin inhibitor, but there was no increased risk in those treated with anti-T-lymphocyte antibodies. Patient survival was poor: 51% at 1 year and 39% at 5 years.
Lymphoproliferative disease is an increasingly common problem after renal transplantation, and the outcome is poor. Measures to reduce its incidence might include reduction of long-term immunosuppression exposure. Established disease has a high short-term mortality, and new treatment options, such as anti-B-lymphocyte monoclonal antibodies, should be aggressively pursued.
Transplantation 07/2005; 80(2):193-7. · 4.00 Impact Factor
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Randall J Faull
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ABSTRACT: Progressive peritoneal membrane fibrosis, and associated loss of ultrafiltration and dialysis capacity, is an increasingly limiting problem with time on peritoneal dialysis. The primary culprit is the composition of the peritoneal dialysate, although episodes of peritonitis can hasten the process. At a molecular level, there is increasing evidence that several growth factors play key roles in the development of peritoneal membrane fibrosis. Transforming growth factor (TGF)-beta is widely implicated in pathological fibrosis, and a considerable body of evidence favours a similar role in the peritoneal membrane. Connective tissue growth factor (CTGF), a downstream mediator of TGF-beta-induced fibrosis, has more recently been implicated in peritoneal membrane scarring. In contrast to the pleiotropic effects of TGF-beta, CTGF more specifically targets the fibrosis pathway, and so is an attractive candidate for inhibiting the damage to the membrane. Heparin-binding epidermal growth factor-like growth factor (HB-EGF) has also been found in the peritoneal cavity, but its effect on peritoneal mesothelial cells suggests that it has a positive role in guiding membrane repair and avoiding pathological fibrosis. In the future, it is hoped that changes in peritoneal dialysis technology will create a better balance between the bad and good effects of these growth factors, which in turn will lead to more successful long-term outcomes for this major renal replacement therapy.
Nephrology 07/2005; 10(3):234-9. · 1.31 Impact Factor
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ABSTRACT: End-stage renal disease (ESRD) patients undergoing hemodialysis treatment have reduced plasma L-carnitine levels; however, the relationship between dialysis age and carnitine status is poorly understood. This study examined the relationship between duration of dialysis and plasma and skeletal muscle concentrations of L-carnitine and its esters in ESRD patients.
Blood samples were collected from 21 patients at baseline and throughout the first 12 months of hemodialysis. In 5 patients, muscle samples were obtained after 0, 6, and 12 months of hemodialysis. Blood and muscle samples were collected from an additional 20 patients with a mean dialysis age of 5.10 years. L-carnitine, acetyl-L-carnitine, and total L-carnitine were measured by high-performance liquid chromatography (HPLC).
The mean +/- SD plasma L-carnitine concentration in ESRD patients who had not yet started hemodialysis was 50.6 +/- 20.0 micromol/L. Significantly lower concentrations were observed after 12 months (29.7 +/- 10.5 micromol/L) and >12 months (22.0 +/- 5.4 micromol/L) of hemodialysis treatment. Acetyl-L-carnitine also declined with dialysis age, while plasma nonacetylated acylcarnitines continued to increase with the progression of hemodialysis therapy. An inverse relationship between dialysis age and muscle L-carnitine concentrations was observed.
Long-term hemodialysis treatment is associated with a significant reduction in endogenous plasma and muscle L-carnitine levels and a significant increase in plasma acylcarnitines. The majority of the change in plasma L-carnitine concentrations occurs within the first few months of hemodialysis, while muscle levels continue to decline after 12 months of treatment.
Kidney International 10/2004; 66(4):1527-34. · 6.61 Impact Factor
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ABSTRACT: Connective tissue growth factor (CTGF) is a fibrogenic cytokine that is highly expressed in wound healing and fibrotic lesions. The role of transforming growth factor-beta (TGF-beta) in fibrosis is well documented, and the emerging understanding that its fibrogenic actions are mediated through CTGF has provided an attractive target molecule for the modulation of matrix overproduction in fibrotic disease. The involvement of CTGF in the pathogenesis of peritoneal membrane fibrosis in peritoneal dialysis (PD) patients has not been investigated, and so the aim of this study was to ascertain whether CTGF is produced in the peritoneal cavity of PD patients and to investigate its regulation by cytokines.
Reverse transcription-polymerase chain reaction (RT-PCR), Northern blotting, and Western blotting were used to study CTGF expression by cultured human peritoneal mesothelial cells (HPMC) from peritoneal dialysis patients. Western blotting was used to detect CTGF expression in spent peritoneal dialysate from patients with and without peritonitis.
RT-PCR analysis demonstrated the expression of CTGF mRNA in cultured primay HPMCs isolated from spent peritoneal effluent. The production of the major 36 to 38 kD CTGF protein doublet by HPMC in addition to a 23 to 25 kD proteolytically processed form was confirmed by Western blotting. Several molecular weight forms of CTGF (18 to 38 kD) were also detected by Western blotting in peritoneal dialysate, with levels markedly elevated during episodes of peritonitis. Northern and Western blot analysis revealed that CTGF mRNA and protein production by HPMC was up-regulated by TGF-beta, with mRNA levels significantly increasing above the control (P < 0.01). In contrast, platelet-derived growth factor (PDGF), epidermal growth factor (EGF), and tumor necrosis factor-alpha (TNF-alpha) had no measurable effects on CTGF mRNA expression.
These results are the first to demonstrate the production of CTGF by HPMC and its presence in the peritoneal cavity of PD patients. The marked increase in CTGF levels by factors implicated in the development of peritoneal membrane fibrosis suggests its involvement in the underlying pathophysiologic mechanism(s).
Kidney International 08/2003; 64(1):331-8. · 6.61 Impact Factor
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Nephrology Dialysis Transplantation 06/2003; 18(5):1013-4. · 3.40 Impact Factor
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ABSTRACT: Since 1994 we have placed all peritoneal dialysis (Tenckhoff) catheters at our hospital laparoscopically using a technique that incorporates suture fixation into the pelvis. The purpose of this study was to determine the long-term outcome of this approach.
Perioperative and follow-up data for all patients undergoing placement of a peritoneal dialysis catheter at the Royal Adelaide Hospital were collected prospectively and managed on unit specific and hospital wide computerized databases. A total of 148 procedures were carried out in 123 patients from March 1994 to November 2001. Follow-up ranged from 3 to 68 months (median, 42 months). All procedures were undertaken or supervised by one surgeon, and catheters were routinely sutured into the pelvis at laparoscopy.
There was no perioperative mortality in this series, and only one catheter could not be placed laparoscopically. This was in a patient with extensive intra-abdominal adhesions. Mean operative time was 27 min (range, 10-100 min), and mean postoperative stay was 2.8 days (range, 1-12 days). Seven (5%) patients experienced peri/postoperative haemorrhage, and four of these underwent surgical re-exploration. Twenty-five (17%) catheters are still used for dialysis. Thirty-four (23%) catheters were removed when the recipient received a subsequent renal transplant, and 42 (28%) patients died during follow-up. Forty-six (31%) patients required catheter revision or removal because of technical problems; 26 (18%) recurrent peritonitis or exit site infection; and 20 (14%) catheter blockage. Twenty-eight reinsertion procedures were carried out in 25 patients. Ten (7%) patients developed port site hernias at late follow-up, and required hernioplasty. Catheter migration leading to malfunction (poor drainage) occurred in eight (5%) patients only.
Laparoscopic placement of peritoneal dialysis catheters is a safe and effective procedure. The majority of patients will dialyse successfully using this technique. Suturing the catheter tip into the pelvis is associated with a low rate of catheter migration.
ANZ Journal of Surgery 04/2003; 73(3):109-11. · 1.25 Impact Factor
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ABSTRACT: Tertiary hyperparathyroidism, manifesting as hypercalcaemia, is common after renal transplantation. It often resolves within the first few years, but in previous studies has been associated with bone, renal and cardiovascular pathology. There have been no large studies in the last 10 years, or in patients treated predominantly with Cyclosporin A, that have examined the long-term effect of this condition on patient or transplant outcomes. A retrospective analysis was conducted of 171 consecutive renal transplant recipients with at least 1 year of graft survival from 1984 to 1996. Measurement was made of current and past incidence of hypercalcaemia, the natural history of post-transplant hypercalcaemia, and its effect on graft survival and function, and patient mortality. The incidence of hypercalcaemia was 26% and did not change significantly during the time frame of the study. The average serum calcium increased until 6 months post-transplantation, and then steadily decreased over the next 7 years. There was a significant variation in the rate of decrease between subjects. No long-term effect on patient or graft survival or function was detected. Post-transplant hypercalcaemia usually represents a benign condition that resolves with time. A conservative approach is recommended in the management of most patients in this group.
Nephrology 12/2001; 5(1‐2):133 - 138. · 1.31 Impact Factor
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Randall J Faull
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ABSTRACT: The linkage between bone parameters (calcium, phosphate, parathyroid hormone) and cardiovascular death in dialysis patients has led to a major resurgence in interest in this area of nephrological practice. Two major groups have recently published extensive guidelines for clinical practice in this area--the National Kidney Foundation's Kidney Disease Outcomes and Quality Initiative from the United States, and the Caring for Australasians with Renal Impairment group from Australia and New Zealand. There are some important differences in their recommendations, which reflect variations in local clinical practice, reimbursement systems, and interpretation of the medical literature. Two areas of divergence are highlighted in this editorial--use of vitamin D and its analogs, and use of phosphate binders. Readers of guidelines such as these need to be careful to interpret such recommendations in the context of the realities of their local clinical practice and availability of therapies.
Seminars in Dialysis 20(3):191-4. · 2.27 Impact Factor
