Pulmonary Calcification in Chronic Dialysis Patients

Conger, John D.; Hammond, William S.; Alfrey, Allen C.; Contiguglia, Sebastian R.; Stanford, Ray E.; Huffer, William E.

doi:10.7326/0003-4819-83-3-330

Cited by 215 publications

(151 citation statements)

References 15 publications

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“…18 -21 In patients with uremia, whitlockite has been described as a preliminary stage in soft tissue calcifications but not in vascular calcifications. 8,22,23 Most studies so far have exclusively detected hydroxyapatite or carbonated apatite in uremic vascular calcifications 7,8 -except for one study, which reported brushite in arteriovenous fistulas. 9 Whitlockite has been described only once as a chemical compound in the nonuremic human aorta 24 ; however, in this context, it has to be mentioned that hydroxyapatite rarely exists in its pure form in biologic systems but occurs often as carbonated apatite, which may also contain magnesium.…”

Section: Discussionmentioning

confidence: 99%

Ultrastructural Analysis of Vascular Calcifications in Uremia

Schlieper¹,

Aretz²,

Verberckmoes³

et al. 2010

Journal of the American Society of Nephrology

151

138

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Accelerated intimal and medial calcification and sclerosis accompany the increased cardiovascular mortality of dialysis patients, but the pathomechanisms initiating microcalcifications of the media are largely unknown. In this study, we systematically investigated the ultrastructural properties of medial calcifications from patients with uremia. We collected iliac artery segments from 30 dialysis patients before kidney transplantation and studied them by radiography, microcomputed tomography, light microscopy, and transmission electron microscopy including electron energy loss spectrometry, energy dispersive spectroscopy, and electron diffraction. In addition, we performed synchrotron x-ray analyses and immunogold labeling to detect inhibitors of calcification. Von Kossa staining revealed calcification of 53% of the arteries. The diameter of these microcalcifications ranged from 20 to 500 nm, with a core-shell structure consisting of up to three layers (subshells). Many of the calcifications consisted of 2-to 10-nm nanocrystals and showed a hydroxyapatite and whitlockite crystalline structure and mineral phase. Immunogold labeling of calcification foci revealed the calcification inhibitors fetuin-A, osteopontin, and matrix gla protein. These observations suggest that uremic microcalcifications originate from nanocrystals, are chemically diverse, and intimately associate with proteinaceous inhibitors of calcification. Furthermore, considering the core-shell structure of the calcifications, apoptotic bodies or matrix vesicles may serve as a calcification nidus.

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Section: Discussionmentioning

confidence: 99%

Ultrastructural Analysis of Vascular Calcifications in Uremia

Schlieper¹,

Aretz²,

Verberckmoes³

et al. 2010

Journal of the American Society of Nephrology

151

138

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“…Metastatic pulmonary calcifications have been shown to be present in 60-80% of autopsied haemodialysis patients, although rarely recognized during life [6], their extent is usually reflected in the survival of the patient Although many patients remain asymptomatic, some develop severe respiratory symptoms which are related to the extent of calcification. Restrictive lung diseases with progressive decrease in TL,CO, VC and hypoxaemia may be associated with rising levels of pulmonary calcium levels [3].…”

Section: Discussionmentioning

confidence: 99%

Metastatic pulmonary calcification after renal transplantation

Murris-Espin

Lacassagne²,

Didier³

et al. 1997

Eur Respir J

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Metastatic pulmonary calcifications, unlike dystrophic calcifications, occur in the normal healthy lung. The radiological pattern is quite specific. The disease is commonly described in chronic renal failure with calcium disorders. The prognosis is totally unpredictable.In 1992, a 50 yr old man underwent a successful renal transplantation during the final stage of chronic renal failure. He subsequently developed asymptomatic diffuse nodular opacities, that were discovered in 1995. An open lung biopsy confirmed the diagnosis of metastatic pulmonary calcification. There was no calcium disorder in this patient.In contrast to the benign course of pulmonary calcification in most patients, some fulminant pulmonary calcifications complicating renal transplantation or hypercalcaemia have been described. Radiographic identification of such entities is important to permit correction of calcium disorders. Otherwise, the condition is a potentially progressive and fatal cause of respiratory failure.

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“…Hemodialysis has been in clinical use years (36), but some of its diverse and u complications have only recently becom (37,38). The acute leukopenia of hemod described 8 yr ago (1, 2), but its mechani mained obscure (39).…”

Section: Discussionmentioning

confidence: 99%

Hemodialysis leukopenia. Pulmonary vascular leukostasis resulting from complement activation by dialyzer cellophane membranes.

Craddock

Fehr

Dalmasso³

et al. 1977

J. Clin. Invest.

980

315

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A B S T R A C T Acute leukopenia occurs in all patients during the first hour of hemodialysis with cellophanemembrane equipment. This transient cytopenia specifically involves granulocytes and monocytes, cells which share plasma membrane reactivity towards activated complement components. The present studies document that complement is activated during exposure of plasma to dialyzer cellophane, and that upon reinfusion of this plasma into the venous circulation, granulocyte and monocyte entrapment in the pulmonary vasculature is induced. During early dialysis, conversion of both C3 and factor B can be demonstrated in plasma as it leaves the dialyzer. Moreover, simple incubation of human plasma with dialyzer cellophane causes conversion of C3 and factor B, accompanied by depletion of total hemolytic complement and C3 but sparing of hemolytic C1. Reinfusion of autologous, cellophane-incubated plasma into rabbits produces selective granulocytopenia and monocytopenia identical to that seen in dialyzed patients. Lungs from such animals reveal striking pulmonary vessel engorgement with granuloThis work was presented in part at

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Pulmonary Calcification in Chronic Dialysis Patients

Cited by 215 publications

References 15 publications

Ultrastructural Analysis of Vascular Calcifications in Uremia

Ultrastructural Analysis of Vascular Calcifications in Uremia

Metastatic pulmonary calcification after renal transplantation

Hemodialysis leukopenia. Pulmonary vascular leukostasis resulting from complement activation by dialyzer cellophane membranes.

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