pyrophosphate and Kidney-Failure--Chronic

Treatment of anemia remains an integral component in the care of patients with end stage kidney disease receiving dialysis. Currently, both erythropoiesis stimulating agents and iron replacement agents remain important anemia management strategies for patients undergoing hemodialysis (HD). Ferric pyrophosphate citrate (FPC) was approved by the U.S. Food and Drug Administration in January 2015 as an iron replacement product in adult patients receiving long-term maintenance HD. FPC is administered to patients on HD through the dialysate. Multicenter randomized, placebo-controlled phase three clinical studies (CRUISE 1 and 2) have found dialysate FPC to maintain hemoglobin level and iron balance in patients receiving chronic HD. Adverse events were similar in both the dialysate FPC-treated and placebo groups. Another study showed a significant reduction in the prescribed erythropoietin-stimulating agents dose at the end of treatment in the dialysate FPC-treated group compared with placebo. These studies have shown that dialysate FPC is efficacious and well tolerated. In this article, we review clinical studies evaluating the efficacy and safety of FPC and also propose a protocol for iron replacement in HD units where dialysate FPC is to be used.

Topics: Anemia; Clinical Trials as Topic; Diphosphates; Hematinics; Humans; Iron; Kidney Failure, Chronic; Renal Dialysis

Management of anemia remains an integral component in the care of patients with chronic kidney disease undergoing hemodialysis. In addition to erythropoiesis-stimulating agents, iron-replacement agents remain a key strategy for anemia treatment in this patient population. Ferric pyrophosphate citrate (FPC), a novel iron-replacement agent, was approved by the US Food and Drug Administration in January 2015 for use in adult patients receiving chronic hemodialysis (HD). This iron product is administered to patients on HD via the dialysate. The recently published, multicenter, randomized, placebo-controlled, phase 3 clinical trials found FPC to maintain hemoglobin level and iron balance in patients undergoing chronic HD. The mean hemoglobin level in these phase 3 clinical studies was maintained from baseline to the end of the treatment in the dialysate iron (FPC-treated) group, however, it decreased by 0.4 g/dL in the control group (P < 0.001). Adverse and serious adverse events were similar in both groups. Another recent study showed a significant reduction in the prescribed ESA dose at the end of treatment in the FPC-treated group compared with placebo. These studies have shown that FPC administered via the dialysate is efficacious and apparently well tolerated. In this article, in addition to reviewing the clinical studies evaluating the efficacy and safety of FPC, we propose a protocol for iron management in HD centers where FPC is to be used.

Topics: Anemia, Iron-Deficiency; Dialysis Solutions; Diphosphates; Ferric Compounds; Hematinics; Humans; Iron; Kidney Failure, Chronic; Renal Dialysis

Patients with chronic kidney disease have increased cardiovascular mortality from a combination of increased atherosclerotic disease, left ventricular hypertrophy and increased prevalence of vascular calcification (VC). Previously VC was thought to be a passive process which involved the deposition of calcium and phosphate into the vessel wall. However, recent studies have shown that VC is a highly regulated, cell-mediated process similar to bone formation, in that it is associated with expression of bone-related proteins, such as type I collagen and alkaline phosphatase. Animal and in vitro models of VC have shown that a multitude of factors including phosphate, matrix gla protein (MGP) and fetuin are involved in regulating VC. Certain factors induce calcification whereas others inhibit the process. Despite these insights, it is still not fully known how VC is regulated and a treatment for VC remains elusive. Ongoing research will hopefully elucidate these mechanisms and thereby produce targets for future therapeutic intervention. This review will highlight some of the scientific models of VC and how they have increased the understanding of this complex process.

Topics: Alkaline Phosphatase; alpha-Fetoproteins; Animals; Apoptosis; Atherosclerosis; Calcinosis; Calcium-Binding Proteins; Cardiovascular Diseases; Collagen Type I; Diphosphates; Disease Models, Animal; Extracellular Matrix Proteins; Humans; Hypertrophy, Left Ventricular; Inflammation; Kidney Failure, Chronic; Matrix Gla Protein; Mice; Osteopontin; Phosphorus; Prevalence; Risk Factors; Vascular Diseases; Vitamin D; Vitamins

In the last decade, the nephrology community has focused its attention on the main cause of morbidity and mortality in chronic renal failure patients: cardiovascular disease. In addition, recent studies pointed out that vascular calcification (VC) is a major cause of cardiovascular disease in the dialysis population. Interestingly, the pathogenesis of VC and soft tissue calcification in chronic kidney disease (CKD) has been extensively investigated. Nowadays we know that VC is associated not only with passive calcium phosphate deposition, but also with an active, cell-mediated process. To better understand the pathogenesis of VC in CKD, numerous regulatory proteins have been studied, because of their ability to inhibit mineral deposition in the vessels. We here examine the state of the art of those substances recognized as regulatory key factors in preventing VC in uremic conditions, such as fetuin A (alpha2-Heremans-Schmid glycoprotein), matrix gamma-carboxyglutamic acid protein, pyrophosphate, osteoprotegerin and bone morphogenetic protein. We conclude that at present it is too early to introduce these novel markers into clinical practice.

Topics: 1-Carboxyglutamic Acid; alpha-Fetoproteins; Bone Morphogenetic Protein 7; Bone Morphogenetic Proteins; Calcinosis; Diphosphates; Humans; Kidney Failure, Chronic; Models, Biological; Osteoprotegerin; Risk Factors; Transforming Growth Factor beta; Uremia; Vascular Diseases

Topics: Animals; Calcium; Cholecalciferol; Diphosphates; Glomerular Filtration Rate; Humans; Hydroxycholecalciferols; Hypercalcemia; Kidney Failure, Chronic; Mitochondria, Liver; Parathyroid Glands; Parathyroid Hormone; Phosphates; Rats

Topics: Absorption; Acidosis, Renal Tubular; Alkalies; Aluminum; Biopsy; Bone Diseases; Calcium; Diphosphates; Humans; Hydroxides; Hyperparathyroidism; Hypocalcemia; Kidney Failure, Chronic; Kidney Glomerulus; Magnesium; Ossification, Heterotopic; Osteitis Fibrosa Cystica; Osteomalacia; Osteoporosis; Osteosclerosis; Parathyroid Glands; Phosphates; Radiography; Renal Dialysis; Vitamin D

Topics: Animals; Bone Diseases; Bone Resorption; Calcinosis; Calcium; Diphosphates; Homeostasis; Humans; Hydroxyapatites; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Organophosphonates; Osteogenesis; Osteomalacia; Rats; Renal Dialysis; Uremia

Ferric pyrophosphate citrate (FPC) is indicated to maintain hemoglobin in patients with stage 5 hemodialysis-dependent chronic kidney disease on chronic hemodialysis by addition to the dialysate. An intravenous (IV) FPC presentation containing 6.75 mg of iron in 4.5 mL was developed. The objective was to establish the equivalence of iron delivery via dialysate and IV infusion using a pharmacokinetic approach. An open-label, randomized, multiple-period, single-dose, crossover study was conducted in 27 patients with CKD-5HD. Each patient received (1) a basal iron profile over 12 hours, (2) FPC 6.75 mg Fe IV predialyzer, (3) FPC 6.75 mg Fe IV postdialyzer, and (4) FPC 2 μM (110 μg Fe/L of hemodialysate). Serum and plasma iron was analyzed for total Fe and transferrin bound iron (TBI). Equivalence was determined by comparing maximum observed concentration and area under the concentration-time curve from time 0 to the last observation of 110 μg Fe/L of hemodialysate (reference) and test treatments Fe predialyzer and postdialyzer iron profiles. The main outcome measure was the measurement of bioequivalence between the reference and test treatments. Bioequivalence parameters showed that infusion of FPC iron IV, predialyzer and postdialyzer delivered equivalent iron as via hemodialysate. The increment in serum total Fe from predialysis to postdialysis was the same as observed in the long-term clinical studies of FPC. FPC IV was well tolerated. IV infusion of 6.75 mg iron as FPC during 3 hours of HD delivers an equivalent amount of iron as when Triferic is delivered via hemodialysate. The IV presentation of FPC extends the ability to provide FPC iron to all patients receiving hemodialysis or hemodiafiltration.

Topics: Administration, Intravenous; Citric Acid; Cross-Over Studies; Dialysis Solutions; Diphosphates; Hematinics; Humans; Iron; Kidney Failure, Chronic; Renal Dialysis

Soluble iron salts are toxic for parenteral administration because free iron catalyzes free radical generation. Pyrophosphate strongly complexes iron and enhances iron transport between transferrin, ferritin, and tissues. Hemodialysis patients need iron to replenish ongoing losses. We evaluated the short-term safety and efficacy of infusing soluble ferric pyrophosphate by dialysate.. Maintenance hemodialysis patients receiving erythropoietin were stabilized on regular doses of intravenous (i.v.) iron dextran after oral iron supplements were discontinued. During the treatment phase, 10 patients received ferric pyrophosphate via hemodialysis as monthly dialysate iron concentrations were progressively increased from 2, 4, 8, to 12 micrograms/dl and were then sustained for two additional months at 12 micrograms/dl (dialysate iron group); 11 control patients were continued on i.v. iron dextran (i.v. iron group).. Hemoglobin, serum iron parameters, and the erythropoietin dose did not change significantly from month 0 to month 6, both within and between the two groups. The weekly dose of i.v. iron (mean +/- SD) needed to maintain iron balance during month 6 was 56 +/- 37 mg in the i.v. iron group compared with 10 +/- 23 mg in the dialysate iron group (P = 0.001). Intravenous iron was required by all 11 patients in the i.v. iron group compared with only 2 of the 10 patients receiving 12 micrograms/dl dialysate iron. The incidence of adverse effects was similar in both groups.. Slow infusion of soluble iron pyrophosphate by hemodialysis may be a safe and effective alternative to the i.v. administration of colloidal iron dextran in maintenance hemodialysis patients.

Topics: Adult; Aged; Aged, 80 and over; Anemia, Iron-Deficiency; Dialysis Solutions; Diphosphates; Drug Administration Routes; Erythropoietin; Female; Ferritins; Hemoglobins; Humans; Iron; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis; Solubility; Transferrin

To evaluate the potential ethnic differences of ferric pyrophosphate citrate (FPC, Triferic) in healthy subjects and patients with hemodialysis-dependent stage 5 chronic kidney disease (CKD-5HD) and identify covariates that may influence pharmacokinetics (PK) of FPC.. Data were collected from 2 Asian and 4 non-Asian clinical studies involving healthy subjects and CKD-5HD patients. Three population PK models were developed: M1 for intravenous (IV) administration of FPC in healthy subjects; M2 for dialysate administration of FPC in CKD-5HD patients; M3 for pre-dialyzer administration of FPC in CKD-5HD patients. All the models were fitted to concentration versus time data of FPC using the nonlinear mixed effect approach with the NONMEM. In total, 26 Asians and 65 non-Asians were included in the final model analysis database. Forty healthy subjects were administered FPC via intravenous (IV) route and 51 patients with CKD-5HD via dialysate (N = 50) and pre-dialyzer blood circuit administration (N = 51). The PK parameters of FPC IV were similar. The population PK model showed good parameter precision and reliability as shown by model evaluation, and no relevant influence of ethnicity on PK parameters was observed. In healthy subjects, the maximum observed plasma concentration (C. The population pharmacokinetics model successfully described the PK parameters of FPC in healthy subjects and CKD-5HD patients and were comparable between Asian and non-Asian populations.

Topics: Citrates; Dialysis Solutions; Diphosphates; Ethnicity; Hematinics; Humans; Iron; Kidney Failure, Chronic; Reproducibility of Results

Patients with end-stage renal disease (ESRD) are at elevated risk of acquiring infectious diseases, including tuberculosis (TB). Inflammation and uremia negatively impact immune function in this population, but specific pathways involved in TB immunity have not been identified. Although γδ T cells are known to contribute to protection from TB, their phenotype and function in patients with ESRD is relatively unknown. To determine this we recruited 20 patients with and 20 without ESRD (controls), with or without latent TB infection to assess γδ T cell frequency, surface phenotype, and cytokine production by flow cytometry in response to stimulation. γδ T cells derived from patients with ESRD exhibited significantly lower expression of CCR5, CXCR3, and CD26 compared to controls. Furthermore, patients with ESRD, particularly the group with latent TB infection, exhibited poor IFNγ, TNFα, and GMCSF responses to stimulation with either phosphoantigen HMB-PP, IL-12/IL-18, E. coli, or phorbol myristate acetate and ionomycin. Similar dysfunctional responses were observed in patients with active TB. Surprisingly, neither the γδ phenotype nor its function was associated with plasma markers of inflammation or microbial translocation. Thus, there is significant perturbation of the γδ T-cell population in patients with ESRD, particularly in those with latent TB infection.

Topics: Adult; Aged; Cytokines; Diphosphates; Disease Susceptibility; Female; Flow Cytometry; Humans; Intraepithelial Lymphocytes; Kidney Failure, Chronic; Latent Tuberculosis; Lymphocyte Activation; Male; Middle Aged; Mycobacterium tuberculosis; Uremia

Vascular calcification is a major risk factor of cardiovascular mortality, particularly for patients with end-stage renal disease and diabetes. Although chronic inflammation is one of the etiologic factors, the underlying mechanism is not fully understood. To clarify this, we studied how nuclear factor-kappa B (NF-κB) induction, a mediator of inflammation, might promote vascular calcification. Activation of NF-κB by tumor necrosis factor (TNF) promoted inorganic phosphate-induced calcification in human aortic smooth muscle cells. Pyrophosphate (an inhibitor of calcification) efflux to the extracellular matrix was suppressed along with the decreased expression of ankylosis protein homolog (ANKH), a transmembrane protein that controls pyrophosphate efflux of cells. The restoration of ANKH expression in these cells overcame the decreased pyrophosphate efflux and calcification. Tristetraprolin, a downstream product of NF-κB activation, may mediate destabilization of ANKH mRNA as its knockdown by shRNA increased ANKH expression and decreased calcification. Furthermore, a rat chronic renal failure model, with increased serum TNF levels, activated NF-κB and decreased ANKH levels. In contrast, the inhibition of NF-κB maintained ANKH expression and attenuated vascular calcification both in vivo and in vitro. Both human calcified atherosclerotic lesions and arteries from patients with chronic kidney disease had activated NF-κB and decreased ANKH expression. Thus, TNF-activated NF-κB promotes inflammation-accelerated vascular calcification by inhibiting ankylosis protein homolog expression and consequent pyrophosphate secretion.

Topics: Animals; Atherosclerosis; Diphosphates; Disease Models, Animal; Disease Progression; Down-Regulation; Genes, Reporter; HEK293 Cells; Humans; I-kappa B Proteins; Inflammation Mediators; Kidney Failure, Chronic; Male; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; NF-kappa B; NF-KappaB Inhibitor alpha; Osteogenesis; Phosphate Transport Proteins; Promoter Regions, Genetic; Rats; Rats, Wistar; RNA Interference; RNA Stability; Signal Transduction; Time Factors; Transfection; Tristetraprolin; Tumor Necrosis Factor-alpha; Vascular Calcification

Pyrophosphate (PPi) is a potent inhibitor of vascular calcification and may be deficient in renal failure. We sought to determine whether plasma PPi is affected by dialysis or the mode of dialysis and whether it correlates with vascular calcification.. PPi was measured in plasma samples stored from a recent study of vascular calcification in 54 HD patients, 23 peritoneal dialysis (PD) patients and 38 patients with stage 4 chronic kidney disease (CKD). Calcification was quantified in a standardized section of the superficial femoral artery using computed tomography, and PPi was measured by enzyme assay, at both baseline and 1 year.. Baseline plasma PPi was weakly correlated with age and serum phosphate, but not with alkaline phosphatase activity or other biochemical parameters, and did not differ between HD, PD and CKD patients. Both baseline calcification score and change in the calcification score at 1 year decreased with increasing quartiles of plasma PPi. In a multivariate analysis, plasma PPi was independently correlated with baseline calcification (P = 0.039) and the change in calcification (P = 0.029).. Plasma PPi is negatively associated with vascular calcification in end-stage renal disease (ESRD) and CKD but is not affected by dialysis, the mode of dialysis or nutritional or inflammatory status. Although these data are consistent with an inhibitory effect of PPi on vascular calcification, further studies are needed to establish a causal role.

Topics: Aged; Calcinosis; Chronic Disease; Diphosphates; Female; Femoral Artery; Humans; Kidney Diseases; Kidney Failure, Chronic; Male; Middle Aged; Multivariate Analysis; Peritoneal Dialysis; Renal Dialysis; Tomography, X-Ray Computed

Pyrophosphate (PPi) is a known inhibitor of hydroxyapatite formation and has been shown to inhibit medial vascular calcification in vitamin D-toxic rats. It was demonstrated recently that endogenous production of PPi prevents calcification of rat aorta that are cultured in high concentrations of calcium and phosphate. For determining whether PPi metabolism is altered in hemodialysis patients, plasma levels and dialytic clearance of PPi were measured in stable hemodialysis patients. Predialysis plasma [PPi] was 2.26 +/- 0.19 microM in 38 clinically stable hemodialysis patients compared with 3.26 +/- 0.17 in 36 normal subjects (P < 0.01). Approximately 30% of plasma PPi was protein bound, and this was not altered in dialysis patients. There was a weak inverse correlation with age in normal individuals but not in dialysis patients. Plasma [PPi] in dialysis patients was correlated with plasma [PO4(3-)] (r = 0.56) but not with [Ca2+], parathyroid hormone, or the dose of dialysis, and levels did not vary between interdialytic periods of 2 and 3 d. Plasma [PPi] decreased 32 +/- 5% after standard hemodialysis in 17 patients. In vitro clearance of PPi by a 2.1-m2 cellulose acetate dialyzer was 36%, and the mean PPi removal in five patients was 43 +/- 5 micromol, consistent with a similar in vivo clearance. Cleared PPi was greater than the plasma pool but less than the estimated extracellular fluid pool. Erythrocyte PPi content decreased 24 +/- 4%, indicating that intracellular PPi is removed as well. It is concluded that plasma [PPi] is reduced in hemodialysis patients and that PPi is cleared by dialysis. Plasma levels in some patients were below those that have previously been shown to prevent calcification of vessels in culture, suggesting that altered PPi metabolism could contribute to vascular calcification in hemodialysis patients.

Topics: Adult; Aged; Black People; Calcium; Diphosphates; Erythrocytes; Female; Humans; Hydroxyapatites; Kidney Failure, Chronic; Male; Middle Aged; Phosphates; Phosphorus; Renal Dialysis; Time Factors; Vitamin D; White People

Hypophosphatemia complicating parathyroidectomy for secondary hyperparathyroidism in renal failure is usually corrected by the oral or intravenous routes. We present a case in which those methods of treatment were not possible, and the phosphate was administered intraperitoneally. Phosphate was added as one molar sodium diphosphate solution to the dialysis fluid. In our case the procedure was well tolerated, phosphate blood levels were rapidly corrected, no alterations in calcium, magnesium or other parameters were detected and the patient was discharged in good condition. In selected cases of hungry bone syndrome after parathyroidectomy, intraperitoneal phosphate can be used safely.

Topics: Adult; Chronic Kidney Disease-Mineral and Bone Disorder; Dialysis Solutions; Diphosphates; Female; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Parathyroidectomy; Peritoneal Dialysis; Phosphates

10 patients with chronic renal failure (6 women, 4 men), 19 to 59 years of age, duration of the disease form 3 up to 21 years, treated by hemodialysis from 2 to 5 years, were examined. The scintigraphic examination of the bones with 99mTc pyrophosphate (166.5.10(6) MBq) on the third hour after the i.v. application of the radiocolloid, registered by the scanning device SELO-DS-2, allows the discovery of the initial changes of the so called renal osteodystrophy (bone disease in patients on chronic hemodialysis). The coefficient bones/soft tissues may be used as a quantitative index of the renal osteodystrophy in these patients whereas the coefficient calvaria/sternum has not the same diagnostic value.

Topics: Adolescent; Adult; Bone and Bones; Chronic Kidney Disease-Mineral and Bone Disorder; Diphosphates; Female; Humans; Kidney Diseases; Kidney Failure, Chronic; Male; Middle Aged; Radionuclide Imaging; Renal Dialysis; Technetium; Technetium Tc 99m Pyrophosphate

In a series of 28 long-term dialysis patients with musculoskeletal complaints, the radiologic findings in six cases resembled those occurring in the arthropathy of idiopathic calcium pyrophosphate dihydrate deposition (CPPD) disease. These findings included osteophytes, subchondral cysts, and cartilage loss in the metacarpophalangeal joints, patellofemoral joints, wrists, and shoulders. Chondrocalcinosis was present in three of the six cases. There were no significant differences in renal function or levels of serum calcium, phosphorus, iron, ferritin, aluminum, or parathormone between these patients and a control group matched for sex and age. Long-term dialysis may be associated with a metabolic arthritis similar to the arthritis which occurs in CPPD deposition disease. The etiology may include deposition of CPPD crystals, hydroxyapatite, or other calcium-containing substances in joints, or it may be related to a number of dialysis-induced metabolic abnormalities.

Topics: Arthritis; Arthrography; Calcinosis; Calcium Pyrophosphate; Cartilage, Articular; Cysts; Diphosphates; Hemochromatosis; Humans; Hyperparathyroidism, Secondary; Iron; Kidney Failure, Chronic; Renal Dialysis

Diagnostic potentialities of investigation of the kidneys using 99mTc-pyrophosphate were studied in 34 patients with rheumatoid arthritis (RA) for articular scintigraphy. The results obtained were compared with those of radionuclide renography with 131I-hippuran and excretory urography. A possibility of investigation of the kidneys with 99mTc-pyrophosphate for the assessment of parenchyma function and kidney urodynamics was shown. Taking into account a high prevalence of nephropathy in RA patients, dynamic renal scintigraphy and clearance registration were recommended at the first stage of articular scintigraphy with 99mTc-pyrophosphate in order to obtain information on the anatomotopographic site and accumulation-evacuatory function of the kidneys.

Topics: Adult; Aged; Arthritis, Rheumatoid; Diphosphates; Female; Humans; Iodohippuric Acid; Joints; Kidney; Kidney Failure, Chronic; Male; Middle Aged; Radioisotope Renography; Technetium; Technetium Tc 99m Pyrophosphate; Time Factors; Tomography, Emission-Computed

Two cases of chronic renal failure showing very interesting technetium-99m-pyrophosphate bone scans are presented. In both cases striking uptake of activity was shown in the left ventricle of the heart, the mucosa of the stomach and in both lungs. This picture was attributed to metastatic calcification in these organs. Cases of metastatic calcification demonstrated with bone-seeking agents have been presented previously, but have mainly shown intense uptake of activity in the lungs and in a few cases, and to a lesser degree, in the stomach. However, we believe that our cases are unique in showing especially the left ventricle of the heart as well as the mucosa of th stomach with exceptional clarity.

Topics: Adult; Bone and Bones; Calcinosis; Diphosphates; Female; Heart; Humans; Kidney Failure, Chronic; Mucous Membrane; Radionuclide Imaging; Stomach; Technetium; Technetium Tc 99m Pyrophosphate

In order to determine the place of Technetium-99m-pyrophosphate bone scintigraphy in the assessment of renal osteodystrophy, 17 patients with chronic renal failure requiring hemodialysis underwent bone scans and these were compared to results of biochemical, radiological and histologic studies. Bone histology was abnormal in all patients with most having evidence of osteomalacia and hyperparathyroid bone disease. Using semi-quantitative scan scores and regional bone-standard ratios, isotope uptake was increased in 16 patients, while 15 had elevated alkaline phosphatase levels and 7 had X-ray changes. An osteoid-osteoclast index combining histological osteomalacia and hyperparathyroid disease was derived and was found to correlate more closely with alkaline phosphatase and parathyroid hormone levels than with scan parameters. It was concluded that bone scans did not provide therapeutically useful information that could not be obtained from biochemical and radiological studies. It appeared that only bone histology could differentiate osteomalacia and hyperparathyroid bone disease.

Topics: Adult; Bone and Bones; Chronic Kidney Disease-Mineral and Bone Disorder; Diphosphates; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Radionuclide Imaging; Technetium; Technetium Tc 99m Pyrophosphate

Topics: Adult; Bone and Bones; Chronic Kidney Disease-Mineral and Bone Disorder; Diphosphates; Humans; Kidney Failure, Chronic; Kidney Transplantation; Middle Aged; Prednisone; Renal Dialysis; Whole-Body Counting

A high incidence of abnormal 99mTechnetium-tin-pyrophosphate (99mTcPPi) is reported in a population of chronic renal failure patients. Using the 5 hour bone to soft tissue ratio as a quantitative index of increased uptake, 78% of 45 long-term dialysis patients and a similar proportion of non-dialyzed chronic renal failure patients were found to have increased uptakes. In animal studies using a uremic model, similar increased uptakes of 99mTcPPi was found with evidence of increased vascularity as reflected by red cell or plasma volumes in the bone or by the uptake of concomitantly administered 45Ca. The evidence suggests that the abnormal bone scans reflect abnormalities in collagen metabolism that occurs in the uremic state and that 99mTcPPi scans are useful in the diagnosis and management of renal osteodystrophy.

Topics: Animals; Bone and Bones; Calcium; Chronic Kidney Disease-Mineral and Bone Disorder; Diphosphates; Female; Femur; Humans; Kidney Failure, Chronic; Radionuclide Imaging; Rats; Renal Dialysis; Technetium; Time Factors; Tin; Uremia

Topics: Adolescent; Adult; Aged; Alkaline Phosphatase; Calcium; Child; Chronic Kidney Disease-Mineral and Bone Disorder; Diphosphates; Female; Humans; Injections, Intravenous; Kidney Failure, Chronic; Kidney Transplantation; Male; Middle Aged; Parathyroid Glands; Phosphates; Phosphorus Isotopes; Radiography; Renal Dialysis; Transplantation, Homologous

Topics: Alkaline Phosphatase; Cellulose; Cholelithiasis; Diphosphates; Electrophoresis; Hepatitis; Humans; Hyperparathyroidism; Hyperthyroidism; Intestinal Mucosa; Isoenzymes; Jejunum; Kidney Failure, Chronic; Kinetics; Liver; Liver Cirrhosis; Neoplasm Metastasis; Organ Specificity; Osteoporosis; Pyrophosphatases; Regression Analysis; Vinyl Compounds

Topics: Arthritis; Calculi; Cartilage Diseases; Colchicine; Crystallization; Diphosphates; Female; Humans; Joint Diseases; Kidney Failure, Chronic; Knee; Male; Periarthritis; Radiography; Shoulder; Synovial Fluid; Synovitis; Wrist