Trends and dynamics of changes in calcification score over the 1-year observation period in patients on peritoneal dialysis

Stompór, Tomasz; Pasowicz, Mieczysław; Sułowicz, Władysław; Dembińska-Kieć, A.; Janda, Katarzyna; Wójcik, Katarzyna; Tracz, Wiesława; Zdzienicka, Anna; Konieczyńska, Małgorzata; Klimeczek, Piotr

doi:10.1016/s0272-6386(04)00820-0

Cited by 37 publications

(35 citation statements)

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“…Previous studies have reported progressive CAC in 45-100% of subjects with ESRD over 11-22 months of follow-up ( Table 5); progression of CAC in 80% of our middle-aged diabetic subjects who progressed to ESRD are consistent with these findings (Table 5) [1,2,11,12]. The rate of progression in our study subjects that progressed to ESRD is also similar to that reported earlier (Table 5) [1,2,11,12].…”

Section: Discussionsupporting

confidence: 91%

“…The rate of progression in our study subjects that progressed to ESRD is also similar to that reported earlier (Table 5) [1,2,11,12]. Upon controlling for nephropathy status and progression to ESRD, serum creatinine emerged as a significant predictor of the magnitude of increase in CAC scores and there was a significant interaction between progression to ESRD and serum creatinine.…”

Section: Discussionsupporting

confidence: 89%

“…It is apparent that the proportion of patients with progressive CAC is significantly lower than after attaining ESRD (Table 5) [1,2,11,12]. Conversely, CAC seems to progress over a short period of time in a significant proportion of subjects with DN even before the need for dialysis, a finding heretofore not previously reported.…”

Section: Discussionmentioning

confidence: 65%

“…In addition to cross-sectional studies, several longitudinal studies have documented rapid progression of CAC among individuals with ESRD and have attempted to define the risk factors associated with this rapid progression [1,2,11,12]. Moreover, at least two therapeutic interventions have been shown to slow the rate of progression of vascular calcification among individuals with ESRD [4,13].…”

mentioning

confidence: 99%

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Progression of coronary artery calcification in diabetics with and without chronic kidney disease

Mehrotra¹,

Budoff²,

Hokanson³

et al. 2005

Kidney International

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 65%

mentioning

confidence: 99%

See 2 more Smart Citations

Progression of coronary artery calcification in diabetics with and without chronic kidney disease

Mehrotra¹,

Budoff²,

Hokanson³

et al. 2005

Kidney International

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show abstract

“…The incidence of medial calcification is markedly increased in patients with higher age, chronic kidney disease and diabetes [4,5,6]. While serum calcium and phosphate concentrations have been reported to correlate with the progression of vascular calcification in dialysis patients [7,8,9], they only partly account for vascular calcification. We previously reported that medial calcification of the hand arteries in hemodialysis patients is advanced in patients with higher age, longer hemodialysis duration, poor glycemic control, and increased inflammatory state [10,11].…”

Section: Introductionmentioning

confidence: 99%

Significant Association Between Bone-Specific Alkaline Phosphatase and Vascular Calcification of the Hand Arteries in Male Hemodialysis Patients

Ishimura

Okuno²,

Okazaki³

et al. 2014

Kidney Blood Press Res

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Background/Aims: Bone-specific alkaline phosphatase (BAP) hydrolyzes pyrophosphate, which inhibits vascular calcification. We examined association between serum BAP and vascular calcification of male hemodialysis patients. Methods: Hand roentgenography of 167 male maintenance hemodialysis patients was conducted, and visible vascular calcification of the hand arteries was evaluated. Serum levels of 3 bone formation markers (BAP, osteocalcin, and N-terminal propeptide of type I collagen) and 2 bone resorption markers (C-terminal telopeptide of type I collagen, and cross-linked N-telopeptide of type I collagen) were measured, along with serum intact parathyroid hormone (PTH). Results: Of 167 patients, visible vascular calcification was seen in 37 patients. Among the bone formation and resorption markers, serum BAP was significantly higher in patients with vascular calcification than in those without (p<0.05); although the other 5 serum bone markers were not significantly different between them. Multivariate logistic regression analyses revealed that log [BAP] was significantly associated with vascular calcification after adjustment for age, hemodialysis duration, presence of diabetes, log [intact PTH] and each of the other 5 bone markers (p<0.0001). Conclusions: Higher serum BAP, but not other bone markers, is significantly associated with the presence of vascular calcification in male hemodialysis patients.

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Osteo‐renal regulation of systemic phosphate metabolism

Razzaque

2011

IUBMB Life

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Summary Impaired kidney function and subsequent skeletal responses play a critical role in disrupting phosphate balance in chronic kidney disease (CKD) patients with mineral and bone disorder (CKD-MBD). In patients with CKD-MBD, the inability of the kidney to maintain normal mineral ion balance affects bone remodeling to induce skeletal fracture and extraskeletal vascular calcification. In physiological conditions, bone-derived fibroblast growth factor 23 (FGF23) acts on the kidney to reduce serum phosphate and 1,25-dihydroxyvitamin D levels. In humans, increased bioactivity of FGF23 leads to increased urinary phosphate excretion, which induces hypophosphatemic diseases (e.g., rickets/osteomalacia). However, reduced FGF23 activity is associated with hyperphosphatemic diseases (e.g., tumoral calcinosis). In patients with CKD, high serum levels of FGF23 fail to reduce serum phosphate levels and lead to numerous complications, including vascular calcification, one of the important determinants of mortality of CKD-MBD patients. Of particular significance, molecular, biochemical and morphological changes in patients with CKD-MBD are mostly due to osteo-renal dysregulation of mineral ion metabolism. Furthermore, hyperphosphatemia can partly contribute to the development of secondary hyperparathyroidism in patients with CKD-MBD. Relatively new pharmacological agents including sevelamer hydrochloride, calcitriol analogs and cinacalcet hydrochloride are used either alone, or in combination, to minimize hyperphosphatemia and hyperparathyroidism associated complications to improve morbidity and mortality of CKD-MBD patients. This article will briefly summarize how osteo-renal miscommunication can induce phosphate toxicity, resulting in extensive tissue injuries.

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Trends and dynamics of changes in calcification score over the 1-year observation period in patients on peritoneal dialysis

Abstract: Chronic nonspecific inflammation does not directly attribute to progression in CaScs. Calcium-phosphate balance abnormalities appear to be the only important factors promoting CAC, although a permissive or promoting role of inflammation cannot be ruled out.

Cited by 37 publications

References 0 publications

Progression of coronary artery calcification in diabetics with and without chronic kidney disease

Progression of coronary artery calcification in diabetics with and without chronic kidney disease

Significant Association Between Bone-Specific Alkaline Phosphatase and Vascular Calcification of the Hand Arteries in Male Hemodialysis Patients

Osteo‐renal regulation of systemic phosphate metabolism

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