Consequences of hyperphosphatemia and elevated levels of the calcium-phosphorus product in dialysis patients

Levin, Nathan W.; Hoenich, Nicholas A.

doi:10.1097/00041552-200109000-00003

Cited by 74 publications

(48 citation statements)

References 20 publications

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“…58 -61 Pi overload accelerates calcification in CKD, and control of Pi reduces calcification in CKD. [62][63][64] Klotho exerts its phosphaturic effects by inhibiting renal NaPi-2a and NaPi-2c in the renal proximal tubule. 25,38 Maintenance of high Klotho in CKD preserves phosphaturia and lessens phosphate retention.…”

Section: Pathogenic Role Of Klotho In Progression Of Ckd and Its Compmentioning

confidence: 99%

Klotho Deficiency Causes Vascular Calcification in Chronic Kidney Disease

Hu¹,

Shi²,

Zhang³

et al. 2011

Journal of the American Society of Nephrology

823

877

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Soft-tissue calcification is a prominent feature in both chronic kidney disease (CKD) and experimental Klotho deficiency, but whether Klotho deficiency is responsible for the calcification in CKD is unknown. Here, wild-type mice with CKD had very low renal, plasma, and urinary levels of Klotho. In humans, we observed a graded reduction in urinary Klotho starting at an early stage of CKD and progressing with loss of renal function. Despite induction of CKD, transgenic mice that overexpressed Klotho had preserved levels of Klotho, enhanced phosphaturia, better renal function, and much less calcification compared with wild-type mice with CKD. Conversely, Klotho-haploinsufficient mice with CKD had undetectable levels of Klotho, worse renal function, and severe calcification. The beneficial effect of Klotho on vascular calcification was a result of more than its effect on renal function and phosphatemia, suggesting a direct effect of Klotho on the vasculature. In vitro, Klotho suppressed Na ϩ -dependent uptake of phosphate and mineralization induced by high phosphate and preserved differentiation in vascular smooth muscle cells. In summary, Klotho is an early biomarker for CKD, and Klotho deficiency contributes to soft-tissue calcification in CKD. Klotho ameliorates vascular calcification by enhancing phosphaturia, preserving glomerular filtration, and directly inhibiting phosphate uptake by vascular smooth muscle. Replacement of Klotho may have therapeutic potential for CKD.

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Section: Pathogenic Role Of Klotho In Progression Of Ckd and Its Compmentioning

confidence: 99%

Klotho Deficiency Causes Vascular Calcification in Chronic Kidney Disease

Hu¹,

Shi²,

Zhang³

et al. 2011

Journal of the American Society of Nephrology

823

877

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“…In addition, uncontrolled hyperphosphatemia is an established risk factor for cardiovascular calcifications [22]. Elevated Ca × P product was predictive parameter for VC in studies of Maher et al, and Salgueira et al [11,18].…”

Section: Discussionmentioning

confidence: 99%

Cardiac valve calcifications and predictive parameters in hemodialysis patients

et al. 2007

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AbstractCardiac valvular calcification is frequent among hemodialysis (HD) patients. The presence of valvular calcification can help identify HD patients with a higher risk for cardiovascular diseases. Our aim was to determine the prevalence of valvular calcification (VC) in our maintenance hemodialysis (HD) population and to examine some possible etiologic factors for its occurrence. We studied forty-four patients on hemodialysis (23 women and 21 men; mean age 57 ± 18 year; mean HD duration 34 ± 28 months). Valvular calcification (VC) was observed in 21 patients (48%). Of these patients, 6 patients (13%) had mitral valvular calcification, 9 patients (20%) had aortic valvular calcification, and 6 patients (13%) had calcification of both valves. The patients with VC were older than patients without VC (66±14 vs. 50±18). The patients with aortic calcification had longer HD duration than others (48±29 vs. 27±24 months). Patients with VC had higher systolic and diastolic blood pressures than patients without VC. The patients with mitral calcification had higher C-reactive protein (CRP) levels (14 ± 13 vs. 7 ± 7). No significant differences were found with respect to calcium, phosphorus, parathyroid hormone, alkaline phosphatase and mean Ca × P product. Our study confirmed that there is an increased prevalence of VC in HD patients. Age is a risk factor for cardiac VC in HD patients. Longer HD duration was associated with aortic valve calcification. In addition, elevated level of CRP is associated with mitral valve calcification in HD patients.

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“…On the other hand, elevated levels of the calcium-phosphorus product play a pivotal role in vascular calcification, calciphylaxis, and cardiovascular morbidity and mortality. A lowering of levels such that the calcium-phosphorus product is below 55 mg 2 /dl 2 might well be one of the therapeutic management strategies in patients with renal failure (Levin and Hoenich 2001). Therefore, assembling calcium, phosphorus, and calcium-phosphorus product provides an adequate merging utilization of input variables in building the model.…”

Section: Discussionmentioning

confidence: 99%