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PubMed2005

A novel prognostic index for mortality in renal transplant recipients after hospitalization.

BACKGROUND: Prognostic indices that estimate long-term mortality are essential not only to compare different clinical studies and populations but also to perform the most appropriate therapeutic interventions. All-cause mortality is high after renal transplantation (RTx), but no prognostic index has focused on predicting mortality in RTx. We developed and tested a prognostic index for mortality in RTx after hospitalization. METHODS: We retrospectively analyzed survival in 1,293 RTx recipients who were randomly assigned to two groups: a modeling population (n=646), used to create the new index, and a testing population (n=647), used to test this index. Patients were stratified into three risk groups (low, medium, and high) by combining peritransplant risk factors for mortality (beta-coefficient), using a simple eight-point check list: age, pretransplant cardiovascular disease, renal dysfunction at discharge, cardiac hypertrophy, vascular calcification, diabetes, time on dialysis, and acute tubular necrosis. RESULTS: Overall lower survival rates were observed with increasing risk classes in the testing population (log-rank test=18; P=0.0001). The 8-year survival rates ranged from 94% in the lowest-risk group to 59% in the highest-risk group. The area under the receiver operating characteristic curve was 0.63. Mortality risk (Cox analysis) significantly increased with increasing risk classes (medium risk: relative risk=3.8, 95% confidence interval=1.5-9.5, P=0.004; high risk: relative risk=6.3, 95% confidence interval=2.4-16.2, P=0.0001). CONCLUSIONS: This simple prognostic index applicable at the bedside may accurately predict survival in RTx recipients after discharge. Consequently, targeted treatment interventions may be indicated for minimizing mortality, especially in high-risk groups.

Adult↗

PubMed2006

Cinacalcet chloride is efficient and safe in renal transplant recipients with posttransplant hyperparathyroidism.

BACKGROUND: Persistent hyperparathyroidism (HPT) is observed in approximately 50% of kidney transplant recipients one year after transplantation. It may result in hypercalcemia, hypophosphatemia, bone demineralization, vascular calcification, lithiasis, and participate in chronic allograft nephropathy. We evaluated the use of the calcimimetic cinacalcet chloride to correct chronic hypercalcemia in posttransplant HPT, in a prospective single-center study. METHODS: Nine patients with persistent hypercalcemia (>2.6 mmol/L) and stable graft function were treated with cinacalcet (30 mg/day, thereafter adapted to obtain normal serum Ca levels) for six months. Their immunosuppressive schedule included mycophenolate mofetil (MMF), steroids, and cyclosporine A (4), tacrolimus (4), or sirolimus (2). RESULTS: Serum Ca levels significantly decreased from 2.75+/-0.15 to 2.59+/-0.10, 2.42+/-0.29 and 2.44+/-0.25 mmol/L by one, two, and six months, respectively (P<0.02, Wilcoxon test for paired data, for all the data points). Parathyroid hormone (PTH) serum levels decreased from 171+/-102 to 134+/-63 pg/ml by two months (P<0.05) and stabilized thereafter (148+/-99 pg/ml at six months; NS). No changes in glomerular filtration rate (49.8+/-18.6 and 51.3+/-19 ml/min at initiation and six months, respectively) and no variation in serum concentration of the immunosuppressive drugs were observed. Three patients withdrew the treatment because gastrointestinal intolerance. CONCLUSION: Cinacalcet allows the correction of hypercalcemia with no interference in immunosuppressive treatment or renal function. However, whether the increased intolerance observed was due to the association of cinacalcet chloride with other drugs required in renal transplantation (e.g., MMF) needs to be assessed.

Calcium↗

PubMed2024

Multiple urinary peptides are associated with hypertension: a link to molecular pathophysiology.

OBJECTIVES: Hypertension is a common condition worldwide; however, its underlying mechanisms remain largely unknown. This study aimed to identify urinary peptides associated with hypertension to further explore the relevant molecular pathophysiology. METHODS: Peptidome data from 2876 individuals without end-organ damage were retrieved from the Human Urinary Proteome Database, belonging to general population (discovery) or type 2 diabetic (validation) cohorts. Participants were divided based on systolic blood pressure (SBP) and diastolic BP (DBP) into hypertensive (SBP ≥140 mmHg and/or DBP ≥90 mmHg) and normotensive (SBP <120 mmHg and DBP <80 mmHg, without antihypertensive treatment) groups. Differences in peptide abundance between the two groups were confirmed using an external cohort ( n  = 420) of participants without end-organ damage, matched for age, BMI, eGFR, sex, and the presence of diabetes. Furthermore, the association of the peptides with BP as a continuous variable was investigated. The findings were compared with peptide biomarkers of chronic diseases and bioinformatic analyses were conducted to highlight the underlying molecular mechanisms. RESULTS: Between hypertensive and normotensive individuals, 96 (mostly COL1A1 and COL3A1) peptides were found to be significantly different in both the discovery (adjusted) and validation (nominal significance) cohorts, with consistent regulation. Of these, 83 were consistently regulated in the matched cohort. A weak, yet significant, association between their abundance and standardized BP was also observed. CONCLUSION: Hypertension is associated with an altered urinary peptide profile with evident differential regulation of collagen-derived peptides. Peptides related to vascular calcification and sodium regulation were also affected. Whether these modifications reflect the pathophysiology of hypertension and/or early subclinical organ damage requires further investigation.

Humans↗

PubMed2025

Enhancer-targeting CRISPR screens at coronary artery disease loci suggest shared mechanisms of disease risk.

To systematically identify causal genetic mechanisms that confer risk for coronary artery disease (CAD) in GWAS loci, we mapped genome-wide variant-to-enhancer-to-gene (V2E2G) links in vascular smooth muscle cells (SMC). Enhancers identified by active chromatin features, and further prioritized by base-resolution deep learning models of chromatin accessibility in 108 CAD loci, were studied with CRISPRi targeting and Direct-Capture Targeted Perturb-seq (DC-TAP-seq) evaluation of 470 genes. Seventy-six V2E2G links were identified for 59 candidate CAD genes representing gene programs including epithelial-mesenchymal transformation, ubiquitination, and protein folding as well as BMP and TGFB signaling. Similar methods employed with an independent focused screen targeting one candidate locus at 9p21.3 identified 10 enhancers regulating expression of multiple genes at this location. Detailed molecular studies revealed that two enhancers mediating transcription factor binding and transcriptional regulation contribute to ancestry-specific and sex-specific risk for CAD and the surrogate biomarker vascular calcification. Together, these studies advance our identification of GWAS CAD V2E2G links across the genome, and specific mechanisms of risk at the complex 9p21.3 locus.

Journal Article↗

PubMed2003

Comparison of intravenous coronary angiography using synchrotron radiation with selective coronary angiography.

Intravenous coronary angiography with synchrotron radiation is a novel and minimally invasive technique for coronary imaging. At the Hamburger Synchrotronstrahlungslabor HASYLAB at DESY, a dedicated angiography system has been developed, which has been shown to provide detailed images of coronary artery segments. For each scan, two monochromatic X-ray images below and above the K-edge of iodine were recorded simultaneously. The two images were subtracted logarithmically to produce a maximal contrast enhancement of the iodine. To date, the procedure has been carried out on 379 outpatients. No complications occurred during or after the angiographic procedure, and hospitalization was not required in any subject. The acceptance by patient is extremely high. Five outside reviewers, blinded as to the clinical data or prior angiographic interpretation, reviewed the images for the presence or absence of 70% or more occlusion of a vessel. They reached a sensitivity of 79% and a specificity of 99%. The study has demonstrated that the synchrotron method has satisfactory sensitivity and very high specificity for severe stenoses. The new method has several advantages over magnetic resonance imaging (MRI), electron beam computed tomography (EBCT), and multi-slice computed tomography (MSCT). Neither vascular calcification (CT) nor the presence of metal stents (MRI) impairs the evaluation of perfusion of segments of the coronary arteries. Furthermore, the spatial resolution is three or four times higher using synchrotron angiography, and problems due to respiratory motion are eliminated.

Adult↗

PubMed2001

Fulminant and relentless cutaneous necrosis with excruciating pain caused by calciphylaxis developing in a patient undergoing peritoneal dialysis.

A 50-year-old Japanese female with chronic renal failure who had been on continuous ambulatory peritoneal dialysis developed fulminant systemic cutaneous necrosis that began as painful livedo reticularis-like skin lesions on her thighs. Because of disseminated vascular calcification within the muscular layer of her lower limbs, we eventually diagnosed her with calciphylaxis. The skin necrosis progressed rapidly, and she died of sepsis and pneumonia on the 53rd hospital day. In addition to her long-lasting severe hyperparathyroidism and extremely elevated serum phosphorus and calcium levels, mechanical, frictional stimulation inflicted on the local skin and administration of corticosteroids were suspected to have precipitated the calciphylaxis. Our lack of awareness of this disease in its early stages resulted in our missing the chance to do a parathyroidectomy that might have changed the course. It is important to know the clinical features of this rare disease in order to make a diagnosis as early as possible.

Calciphylaxis↗

PubMed2005

End-stage renal disease--not an equal opportunity disease: the role of genetic polymorphisms.

Despite several decades of development in renal replacement therapy, end-stage renal disease (ESRD) patients continue to have markedly increased morbidity and mortality especially caused by cardiovascular disease (CVD). This shows that current strategies, e.g. the focus on dialysis adequacy, to improve the clinical outcome in ESRD patients have to be complemented by novel approaches. Although traditional risk factors are common in dialysis patients they cannot alone explain the unacceptably high prevalence of CVD in this patient group. Much recent interest has therefore focused on the role of various nontraditional cardiovascular risk factors, such as inflammation, vascular calcification and oxidative stress. Recent studies show that genetic factors, such as DNA single nucleotide polymorphisms, may significantly influence the immune response, the levels of inflammatory markers, as well as the prevalence of atherosclerosis in this patient group. To elucidate the respective roles of DNA polymorphisms in genes that encode inflammatory markers (such as IL-10, IL-6 and TNF-alpha) and other factors that may affect the development of atherosclerosis (such as apolipoprotein E, transforming growth factor and fetuin-A), sufficiently powered studies are needed in which genotype, the protein product and the specific phenotype all are analysed in relation to outcome. The recent developments in the field of genetics have opened up entirely new possibilities to understand the impact of genotype on disease development and progress and thus offer new options and strategies for treatment. It seems conceivable that in the near future, prognostic or predictive multigene DNA assays will provide the nephrological community with a more precise approach for the identification of "high-risk" ESRD patients and the development of accurate individual treatment strategies. For this purpose, integrative studies on genotype-phenotype associations and impact on clinical outcome are needed.

Arteriosclerosis↗

PubMed1997

Distal penile gangrene in a patient with chronic renal failure.

To date, only 10 cases of distal penile gangrene in patients with chronic renal failure have been reported. This rare condition is believed to result from progressive vascular calcification due to secondary hyperparathyroidism in patients with chronic renal failure. We report an additional case of distal penile gangrene in a 41-year-old man who presented with chronic renal disease and pulmonary tuberculosis. Since some authors have emphasized that aggressive surgical treatment in such cases has a significant mortality rate, we took a more conservative approach to treatment.

Adult↗

PubMed1975

What is tertiary hyperparathyroidism?

Five patients who had gross abnormalities of calcium and phosphorus metabolism due to long standing renal failure are described to illustrate the difficulties with the term "tertiary hyperparathyroidism". One patient who had unequivocal biochemical tertiary hyperparathyroidism was found histologically to have nodular hyperplasia of all four glands even though one gland weighed twice as much (12g) as the combined weight of the other three. Another patient was not hypercalcaemic but had all the other features of the condition including rapid onset of osteitis fibrosa, vascular calcification and a probable parathyroid adenoma, with hyperplasia of the three glands. The other three had hypercalcaemia only after a reduction in the plasma inorganic phosphorus due either to renal transplantation or aluminum hydroxide therapy. The bone histology of the five patients varied from severe osteomalacia to severe osteitis fibrosa. A consideration of the factors involved in causing hypercalcaemia in these patients and a review of the literature leads to the conclusion that the term tertiary hyperparathyroidism is often misleading and best avoided.

Adenoma↗

PubMed2004

Tamm-Horsfall protein is a critical renal defense factor protecting against calcium oxalate crystal formation.

BACKGROUND: The tubular fluid of the mammalian kidney is often supersaturated with mineral salts, but crystallization rarely occurs under normal conditions. The unique ability of the kidney to avoid harmful crystal formation has long been attributed to the inhibitory activity of the urinary macromolecules, although few in vivo studies have been carried out to examine this hypothesis. Here we examined the role of Tamm-Horsfall protein (THP), the principal urinary protein, in urinary defense against renal calcium crystal formation, using a THP knockout model that we recently developed. METHODS: Wild-type and THP knockout mice were examined for the spontaneous formation of renal calcium crystals using von Kossa staining. The susceptibility of these mice to experimentally induced renal crystal formation was evaluated by administering mice with ethylene glycol, a precursor of oxalate, and vitamin D(3), which increases calcium absorption. Renal calcium crystals were visualized by von Kossa stain, dark field microscopy with polarized light and scanning electron microscopy. RESULTS: Inactivating the THP gene in mouse embryonic stem cells results in spontaneous formation of calcium crystals in adult kidneys. Excessive intake of calcium and oxalate, precursors of the most common type of human renal stones, dramatically increases both the frequency and the severity of renal calcium crystal formation in THP-deficient, but not in wild-type mice. Under high calcium/oxalate conditions, the absence of THP triggers a marked, adaptive induction in renal epithelial cells of osteopontin (OPN), a potent inhibitor of bone mineralization and vascular calcification. Thus, OPN may serve as an inducible inhibitor of calcium crystallization, whereas THP can serve as a constitutive and apparently more effective inhibitor. CONCLUSION: These results provide the first in vivo evidence that THP is a critical urinary defense factor and suggest that its deficiency could be an important contributing factor in human nephrolithiasis, a condition afflicting tens of millions of people in the world annually.

Animals↗

PubMed2004

Survival following parathyroidectomy among United States dialysis patients.

BACKGROUND: Secondary hyperparathyroidism (SHPTH) is highly prevalent among persons with end-stage renal disease (ESRD). SHPTH has been linked to uremic bone disease, vascular calcification, and a higher risk of death. Parathyroidectomy (PTX) can dramatically reduce parathyroid hormone (PTH) and phosphate levels; however, the relationship between PTX and survival is not known. METHODS: We conducted an observational matched cohort study utilizing data from the United States Renal Database System (USRDS) in which 4558 patients undergoing a first PTX while on hemodialysis or peritoneal dialysis were individually matched by age, race, gender, cause of ESRD, dialysis duration, prior transplantation status, and dialysis modality to 4558 control patients who did not undergo PTX. Patients were followed from the date of PTX until they died or were lost to follow-up. RESULTS: The 30-day postoperative mortality rate following PTX was 3.1%. Long-term relative risks of death among patients undergoing PTX were estimated to be 10% to 15% lower than those of matched control patients not undergoing surgery. Survival curves between the 2 groups crossed 587 days following PTX. Median survival was 53.4 months (95% CI: 51.2-56.4) in the PTX group, and 46.8 months (95% CI: 44.7-48.9) in the control group. CONCLUSION: PTX was associated with higher short-term, and lower long-term, mortality rates among U.S. patients receiving chronic dialysis. Measures to attenuate SHPTH may play an important role in reducing mortality among patients with end-stage renal disease.

Adult↗

PubMedDate not supplied

Lanthanum: a safe phosphate binder.

Accumulation of inorganic phosphate due to renal functional impairment contributes to the increased cardiovascular mortality observed in dialysis patients. Phosphate plays a causative role in the development of vascular calcification in renal failure; treatment with calcium-based phosphate binders and vitamin D can further increase the Ca x PO(4) product and add to the risk of ectopic mineralization. The new generation of calcium-free phosphate binders, sevelamer and lanthanum, can control hyperphosphatemia without adding to the patients calcium load. In this article, the metabolism of lanthanum carbonate and its effects in bone, liver and brain are discussed. Although lanthanum is a metal cation its effects are not comparable to those of aluminum. Indeed, in clinical studies no toxic effects of lanthanum have been reported after up to four years of follow-up. The bioavailability of lanthanum is extremely low. The effects observed in bone are due to phosphate depletion, with no signs of direct bone toxicity yet observed in rats or humans. The liver is the main route of excretion for lanthanum carbonate, which can be localized in the lysosomes of hepatocytes. No lanthanum could be detected in brain tissue.

Animals↗

PubMedDate not supplied

Fatal childhood calciphylaxis in a 10-year-old and literature review.

Calciphylaxis is a rare but highly morbid disorder of vascular calcification and skin necrosis, affecting 1% to 4% of adults with end-stage renal disease. Only three affected children have previously been described. We report an unusual instance of fatal calciphylaxis involving a 10-year-old boy, in the setting of sarcoidosis-induced end-stage renal disease. A review of pediatric calciphylaxis cases suggests: (a) increased risk in boys with end-stage renal disease and secondary hyperparathyroidism; (b) frequent distal extremity and visceral organ involvement, (c) worse prognosis with acral necrosis, and (d) possible increased resistance to medical treatment compared to adult patients. Hyperesthetic pain is a common sentinel symptom, and soft tissue x-rays or xeroradiography or both may aid in the diagnosis of pediatric calciphylaxis. Parathyroidectomy in combination with supportive medical management may be the best treatment option in stopping the progression of disease in the pediatric population.

Calciphylaxis↗

PubMed2005

Management of calcium, phosphorus and bone metabolism in dialysis patients using sevelamer hydrochloride and vitamin D therapy.

Abnormalities of mineral metabolism, including those of calcium (Ca), phosphorus (P), and parathyroid hormone (PTH) in patients on maintenance hemodialysis induce severe bone involvement, which manifests as renal osteodystrophy. Recently, vascular calcification caused by abnormal mineral metabolism has been attracting attention because cardiovascular diseases (CVD) are a major cause of death in hemodialysis patients. Since 2000, the treatment standard for overt secondary hyperparathyroidism (SHPT) in our facilities has shifted from conventional or pulse therapy with oral vitamin D3 (VitD) to intravenous pulse therapy with maxacalcitriol or calcitriol. After selecting the criterion of overt SHPT as intact-PTH>500 pg/mL, the proportion of overt SHPT cases among all hemodialysis patients decreased from 12% at the start of intravenous pulse treatment to 6.4% after 4 years' treatment. However, the number of patients who had an interruption to pulse treatment because of hypercalcemia and/or hyperphosphatemia was high and it became a bottleneck for the continuation of the therapy. The major cause of hypercalcemia is considered to be Ca load derived from oral calcium carbonate. In Japan, sevelamer hydrochrolide (SH), which does not contain Ca, has been available commercially since 2003 and potentially should enable a reduction in the incidence of overt SHPT during long-term intravenous treatment when combined with careful adjustment of the dose of VitD and strict monitoring of Ca and P level concentrations. In this study, we found that the proportion of patients who satisfy the recommended serum concentrations of Ca and P reported by K/DOQI guideline was low irrespective of the serum concentration of intact-PTH. The aortic calcification index was high in the patient group with lower intact-PTH level concentration, probably because of reduced Ca and P buffering ability associated with reduced bone turnover. We consider that VitD treatment with SH might give better control of the intact-PTH level concentration within the range recommended by the K/DOQI guideline.

Bone Density Conservation Agents↗

PubMedDate not supplied

The developing role of the renal diabetes nurse.

Diabetes as a chronic disease is often complicated in its management, particularly when combined with chronic and end-stage renal failure. Patients, carers and health care professionals are unfortunately often confused by either too little or conflicting advice provided by the two specialist teams. Within this context, the Renal Diabetes Nurse (RDN) role serves to bridge the gap by ensuring effective links and communication. Currently, renal referrals are made from surrounding secondary care settings and primary care GP practices. The expansion of renal outreach clinics, the appointment of new consultant nephrologists and the emergence of nurse-led clinics, reflects our continuous growth to meet the demand for renal services. The number of patients with renal failure and diabetes is set to increase as the acceptance criteria are clarified and referral routes made explicit. An ageing population with 21-62% of the renal population over the age of 65 (depending on the location of the renal unit), coupled with an increase in the Asian and African-Caribbean population all contribute to increased patient numbers. It is now well recognised that these patients often experience associated generalised atheroma and vascular calcification from inadequately managed hypertension and diabetes over a number of years. Consequently, this group of patients are often "high maintenance" requiring input from the multidisciplinary team on a continuing basis.

Diabetic Nephropathies↗

PubMed2005

Different routes bridging calcium in Japanese hemodialysis patients.

There is growing evidence that not only serum calcium concentration but also excess calcium load is associated with vascular calcification and mortality in hemodialysis patients. Calcium load in hemodialysis patients cumulatively comes from three different routes: oral intake of calcium including calcium-based phosphate binders, traffic of calcium from/to dialysate, and calcemic action of vitamin D. The K/DOQI guidelines recommend sevelamer hydrochloride instead of calcium-containing phosphate binders to control serum phosphate concentration. However, in Japan, both kinds of phosphate binders are used concomitantly, mainly because Japanese patients are prone to a higher incidence of sevelamer-associated adverse events such as gastrointestinal symptoms. Regarding the calcium concentration of dialysate (D-Ca) in Japan, 3.0 mEq/L is more popular than 2.5 mEq/L. Calcium loaded through 3.0 mEq/L dialysate may lead to metastatic calcification rather than to bone formation because serum phosphate concentration rebounds several hours after the end of each hemodialysis session when plasma pH is still high. In contrast, use of 2.5 mEq/L dialysate may result in an unfavorable increase of intact parathyroid hormone particularly when the amount of oral calcium intake is reduced. Although a higher dose of vitamin D is required to counteract the stimulation of parathyroid glands, hypercalcemia is less likely with 2.5 mEq/L dialysate. As the new K/DOQI guidelines are released, it is time to discuss the appropriate D-Ca as well as doses and kinds of phosphate binders and vitamin D for the comprehensive management of Japanese hemodialysis patients.

Bone and Bones↗

PubMed2005

Combination therapy with sevelamer hydrochloride and calcium carbonate in Japanese patients with long-term hemodialysis: alternative approach for optimal mineral management.

Calcium (Ca) overload by Ca-containing phosphorus (P) binder has been suggested to be implicated in the pathogenesis of soft tissue and vascular calcification, which contribute to increased morbidity and mortality of cardiovascular disease in patients undergoing dialysis. Recently, a noncalcium P binder, sevelamer hydrochloride (sevelamer), has become available in Japan. However, Japanese patients undergoing dialysis might be less tolerant of sevelamer treatment, and it is likely to cause hypocalcemia because their dietary Ca intake is less than that in European and American patients. We evaluated the effects of combination therapy with sevelamer and calcium carbonate (CC) on mineral metabolism in Japanese hemodialysis patients, as an alternative form of P management. A total of 210 hemodialysis patients were enrolled, and were given a small dose of sevelamer (0.75-1.5 g/day) on CC treatment. Sevelamer dose was gradually increased, while CC decreased during 24 weeks. Five patients discontinued sevelamer treatment because of severe constipation, anorexia, and parathyroidectomy for severe secondary hyperparathyroidism. After 24 weeks, the dose of sevelamer was significantly increased to 3.29 g/day (initial dose: 1.47 g/day), while CC was decreased by 54%. Adjusted serum Ca significantly decreased (9.63 +/- 0.57-9.45 +/- 0.67 mg/dL; P = 0.0012), although serum P increased (5.89 +/- 1.32-6.25 +/- 1.32 mg/dL; P = 0.017). Serum intact PTH (iPTH) significantly increased in patients with a low or normal iPTH level (< or =300 pg/mL), while it did not change in patients with secondary hyperparathyroidism (>300 pg/mL). The results suggest that the therapeutic regimen is more tolerant and reduces Ca load in Japanese hemodialysis patients while avoiding hypocalcemia. In addition, the mitigated Ca overload could improve PTH hyposecretion in patients with adynamic bone disease, which is associated with soft tissue calcification and higher mortality in uremia.

Antacids↗

PubMed1978

Osteomalacic dialysis osteodystrophy: a trial of phosphate-enriched dialysis fluid.

To assess whether phosphate depletion is an aetiological factor in osteomalacic dialysis osteodystrophy we undertook a prospective trial of phosphate-enriched dialysis fluid, in association with oral 1alpha-hydroxycholecalciferol, for this condition. Thirty patients started the trial; of the 27 who completed more than 6 months' treatment, 14 had iliac crest bone biopsies at the beginning and end of the treatment period. Side effects included pruritus, stiffness, and increase in corneal and vascular calcification. Only one patient showed histological improvement of osteomalacia, and eight deteriorated; in seven the osteitis fibrosa worsened. Myopathy showed some improvement in four patients, but became worse in four. This treatment does not seem to have a place in the routine management of non-hypophosphataemic patients on dialysis.

Adolescent↗