Coronary Calcium Score in Renal Transplant Recipients

Bubenícek, P; Kautznerová, Dana; Sotorník, I; Adamec, M; Lánská, Věra; Teplan, Vladimı́r

doi:10.1159/000210082

Cited by 13 publications

(2 citation statements)

References 56 publications

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“…As previously mentioned, VCs not infrequently tend to progress after KTx, even though at a lower rate as compared with dialysis patients [21, 22, 40, 41]. Some of our preliminary results, produced as yet only in abstract form [23], suggested that aortic calcifications, evaluated according to Kauppila et al [42], increased in 30% of patients over the first year after KTx.…”

Section: Clinical Consequences Of Hc In Ktxsupporting

confidence: 50%

Clinical Impact of Hypercalcemia in Kidney Transplant

Cafforio

Alfieri

2011

International Journal of Nephrology

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Hypercalcemia (HC) has been variably reported in kidney transplanted (KTx) recipients (5–15%). Calcium levels peak around the 3rd month after KTx and thereafter slightly reduce and stabilize. Though many factors have been claimed to induce HC after KTx, the persistence of posttransplant hyperparathyroidism (PT-HPT) of moderate-severe degree is universally considered the first causal factor. Though not proven, there are experimental and clinical suggestions that HC can adversely affect either the graft (nephrocalcinosis) and other organs or systems (vascular calcifications, erythrocytosis, pancreatitis, etc.). However, there is no conclusive evidence that correction of serum calcium levels might avoid the occurrence of these claimed clinical effects of HC. The best way to reduce the occurrence of HC after KTx is to treat as best we can the secondary hyperparathyroidism (SHP) during the uraemic stages. The indication to Parathyroidectomy (PTX), either before or after KTx, in order to prevent or to treat, respectively, HC after KTx, is still a matter of debate which has been revived by the availability of the calcimimetic cinacalcet for the treatment of PT-HPT. However, we still need to better clarify many points as regards the potential adverse effects related to either PTX or cinacalcet use in this clinical set, and we are waiting for the results of future randomized controlled trials to achieve some more definite conclusions on this topic.

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Section: Clinical Consequences Of Hc In Ktxsupporting

confidence: 50%

Clinical Impact of Hypercalcemia in Kidney Transplant

Cafforio

Alfieri

2011

International Journal of Nephrology

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“…Studies of SNF472, sotatercept, and oral activated charcoal each reported attenuation of VC progression, whereas studies of exercise training, spironolactone, and nicotinamide did not. We did not include in our review other studies which reported effects on VC after changes in kidney replacement therapies, such as several observational studies assessing the effect of kidney transplantation on VC 120 – 125 and several evaluating changes in VC after commencement of more frequent or longer hours of hemodialysis (such as nocturnal dialysis) 123 , 126 , 127 . These studies have predominantly reported that VC progression is attenuated by both kidney transplantation and nocturnal hemodialysis when compared with continuation of conventional hemodialysis, but not all studies have consistently shown this 119 , 124 , 125 …”

Section: Discussionmentioning

confidence: 99%

Interventions To Attenuate Vascular Calcification Progression in Chronic Kidney Disease: A Systematic Review of Clinical Trials

Smith

Tiong

et al. 2022

JASN

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Background Vascular calcification is associated with cardiovascular morbidity and mortality in people with chronic kidney disease (CKD). Evidence-based interventions that may attenuate its progression in CKD remain uncertain. Methods We conducted a systematic review of prospective clinical trials of interventions to attenuate vascular calcification in people with CKD, compare with placebo, another comparator, or standard of care. We included prospective clinical trials (randomized and nonrandomized) involving participants with stage 3-5D CKD or kidney transplant recipients; the outcome was vascular calcification measured using radiological methods. Quality of evidence was determined by the Cochrane risk of bias assessment tool and the Grading of Recommendations, Assessment, Development, and Evaluations (GRADE) method. Results There were 77 trials (63 randomized) involving 6898 participants eligible for inclusion (median sample size, 50; median duration, 12 months); 58 involved participants on dialysis, 15 involved individuals with nondialysis CKD, and 4 involved kidney transplant recipients. Risk of bias was moderate over all. Trials involving magnesium and sodium thiosulfate consistently showed attenuation of vascular calcification. Trials involving intestinal phosphate binders, alterations in dialysate calcium concentration, vitamin K therapy, calcimimetics, and antiresorptive agents had conflicting or inconclusive outcomes. Trials involving vitamin D therapy and HMG-CoA reductase inhibitors did not demonstrate attenuation of vascular calcification. Mixed results were reported for single studies of exercise, vitamin E-coated or high-flux hemodialysis membranes, interdialytic sodium bicarbonate, SNF472, spironolactone, sotatercept, nicotinamide, and oral activated charcoal. Conclusions Currently, there are insufficient or conflicting data regarding interventions evaluated in clinical trials for mitigation of vascular calcification in people with CKD. Therapy involving magnesium or sodium thiosulfate appears most promising, but evaluable studies were small and of short duration.

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Progressive renal injury from transgenic expression of human carbonic anhydrase IV folding mutants is enhanced by deficiency of p58 ^IPK

Datta¹,

Shah²,

Rubbelke³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Mutations in the human carbonic anhydrase IV (hCAIV) have been associated with retinal degeneration in an autosomal-dominant form of retinitis pigmentosa (RP17). Prior in vitro cell culture studies confirmed that all of the RP17-associated hCAIV mutations cause protein misfolding, leading to endoplasmic reticulum (ER) stress–induced apoptosis in cells expressing the mutant proteins. To evaluate the physiological impacts of these folding mutants in other carbonic anhydrase IV–producing tissues, we generated two transgenic mouse lines expressing R219S or R14W hCAIV under control of the endogenous hCAIV promoter. Expression of either of these mutant proteins in kidneys caused progressive renal injury in male transgenic mice as evidenced by an age-dependent increase in the tubule cell apoptosis starting at approximately 20 weeks of age and vacuolization throughout the renal cortex in older mice. Up-regulation of the ER chaperone, BiP, was observed in the cells of the renal cortex of the male transgenic mice, suggesting ER stress as a causal factor for the renal injury. The renal injury inflicted by expression of the folding mutants was markedly enhanced by haploinsufficiency of the ER cochaperone p58 IPK . The transgenic mice expressing the hCAIV folding mutants on a p58 IPK heterozygous background showed extensive renal tubular apoptosis by approximately 10 weeks of age in both male and female mice. These data indicate that expression of the RP17-associated folding mutants of hCAIV can adversely affect tissues beyond the retina and their in vivo proteotoxicity is sensitive to modulation of the protein folding environment of the ER.

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Coronary Calcium Score in Renal Transplant Recipients

Cited by 13 publications

References 56 publications

Clinical Impact of Hypercalcemia in Kidney Transplant

Clinical Impact of Hypercalcemia in Kidney Transplant

Interventions To Attenuate Vascular Calcification Progression in Chronic Kidney Disease: A Systematic Review of Clinical Trials

Progressive renal injury from transgenic expression of human carbonic anhydrase IV folding mutants is enhanced by deficiency of p58 ^IPK

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Coronary Calcium Score in Renal Transplant Recipients

Cited by 13 publications

References 56 publications

Clinical Impact of Hypercalcemia in Kidney Transplant

Clinical Impact of Hypercalcemia in Kidney Transplant

Interventions To Attenuate Vascular Calcification Progression in Chronic Kidney Disease: A Systematic Review of Clinical Trials

Progressive renal injury from transgenic expression of human carbonic anhydrase IV folding mutants is enhanced by deficiency of p58 IPK

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Progressive renal injury from transgenic expression of human carbonic anhydrase IV folding mutants is enhanced by deficiency of p58 ^IPK