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      Do Biochemical Measures Change in Living Kidney Donors?

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          Background: Living kidney donation provides a unique opportunity to assess possible biochemical changes attributable to small decrements in glomerular filtration rate. We reviewed studies which followed 5 or more healthy donors, where changes in biochemical measures or anemia were assessed at least 4 months after nephrectomy. Methods: We searched MEDLINE, EMBASE, and Science Citation databases, and reviewed reference lists from 1966 through June 2006. We abstracted data on study and donor characteristics and biochemical outcomes of interest. Results: Eight studies examined at least one outcome of interest. The average time after donation ranged from 0.4 to 11 years, the postdonation creatinine clearance ranged from 73 to 99 ml/min, and the decrement after donation ranged from 11 to 38 ml/min. Nephrectomy did not change hemoglobin, erythropoietin, serum phosphate, calcium or C-reactive protein levels. The studies were inconsistent as to whether parathyroid hormone levels increased and 1,25-dihydroxyvitamin D levels decreased after nephrectomy. Uric acid levels increased variably post-donation. Plasma homocysteine increased in the single study included in this review. Conclusions: The mechanistic changes described above and their prognostic significance need clarification. Based on existing evidence, it is not necessary to routinely monitor living kidney donors for changes in these biochemical measures.

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          Most cited references 15

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          Prevalence of calcidiol deficiency in CKD: a cross-sectional study across latitudes in the United States.

          Recent Kidney Disease Outcomes Quality Initiative guidelines have raised concerns of 25-hydroxyvitamin D, or calcidiol, insufficiency and deficiency in patients with chronic kidney disease (CKD) not yet on dialysis therapy; however, no cross-sectional study across latitudes has been performed to support this assertion. Baseline screening data from a prospective study were used to determine calcidiol levels in subjects with moderate to severe CKD not yet on dialysis therapy from 12 geographically diverse regions of the United States. Calcidiol deficiency is defined as levels less than 10 ng/mL (< 25 nmol/L), and insufficiency, as levels of 10 to 30 ng/mL (25 to 75 nmol/L). Two hundred one subjects with a mean age 65 +/- 13 years and calculated glomerular filtration rate (GFR) of 27 +/- 11 mL/min (0.45 mL/s) were evaluated. Overall mean calcidiol level was 19.4 +/- 13.6 ng/mL (48 +/- 34 nmol/L), with a range of 0 to 65 ng/mL (0 to 162 nmol/L). Only 29% and 17% of subjects with moderate and severe CKD had sufficient levels, respectively. Mean calcidiol levels were less than sufficient levels in all geographic locations tested. Multivariate analysis found log calcidiol level correlated with calcium level (P = 0.016), log calcitriol level (P = 0.024), sex (P = 0.041), geographic location (P = 0.045), and inverse intact parathyroid hormone level (P = 0.013), but not calculated GFR or phosphorous level. Calcidiol levels changed modestly in 18 patients who had calcidiol levels measured in winter and late summer after confirmed exposure to sunlight, with mean calcidiol levels of 17.9 +/- 11.7 to 21.2 +/- 10.0 ng/mL (45 +/- 29 to 53 +/- 25 nmol/L; P = 0.015). This cross-sectional cohort study found a high prevalence of calcidiol deficiency and insufficiency in patients with moderate and severe CKD not on dialysis therapy regardless of geographic location.
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            Hyperparathyroidism and 1,25-dihydroxyvitamin D deficiency in mild, moderate, and severe renal failure.

            It has been postulated that hyperparathyroidism in chronic renal failure results from hypocalcemia, occurring, in part, from phosphate retention and/or deficient 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] synthesis. However, many studies have failed to demonstrate hyperphosphatemia or low 1,25-(OH)2D levels in patients with mild renal failure. We measured creatinine clearance (CCr), fractional excretion of phosphorus (FEP), and serum phosphorus, ionized calcium, and plasma N-terminal PTH, and 1,25-(OH)2D concentrations in 21 normal subjects and 51 patients with renal failure. Patients with mild renal failure (Ccr, greater than 40 mL/min.1.73 m2) had normal mean serum phosphorus and ionized calcium and decreased mean 1,25-(OH)2D levels compared with those in normal subjects. In patients with moderate renal failure (CCr, 20-40), the mean ionized calcium level was normal, plasma PTH levels and FEP were elevated, and the decrement in 1,25-(OH)2D was more pronounced. The mean ionized calcium level was decreased only in the group of patients with severe renal failure (CCr, less than 20). The 1,25-(OH)2D values correlated positively with CCr and negatively with the log of plasma PTH and serum phosphorus concentrations. Log of plasma PTH correlated negatively with CCr and positively with FEP. The ionized calcium concentration correlated very weakly with CCr and the log of the plasma PTH level. These data demonstrate the presence of hyperparathyroidism, normocalcemia, and 1,25-(OH)2D deficiency in renal failure and are consistent with a role for 1,25-(OH)2D in the suppression of parathyroid activity through as yet unidentified mechanisms.
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              Long-term consequences of live kidney donation follow-up in 93% of living kidney donors in a single transplant center.

              Live kidney donation is increasing rapidly. Increases of blood pressure and proteinuria but no accelerated loss of renal function in kidney donors have been described. The credibility of this research is hampered by retrieval rates of only 50-70% of donors. We studied renal function, blood pressure, proteinuria, parathyroid hormone, 1,25(OH)2 cholecalciferol and calcium and phosphate excretion in a live kidney donor cohort with a 93% retrieval rate. A comprehensive physical and laboratory examination including 24-h urine collection was conducted. None of the 152 donors had renal failure. Mean time after uninephrectomy was 11 +/- 7 (range: 1-28) years. GFR had declined by 25%. Blood pressure had increased from 125 +/- 15/79 +/- 11 to 134 +/- 19/81 +/- 9 mmHg (p 150 mg/day), but only 10% had albuminuria. Nineteen percent had increased PTH, 30% had a decreased tubular reabsorption rate of phosphate. Regarding risk factors for a higher loss of GFR, greater increases in blood pressure or proteinuria no consistent picture emerged. Because of the high incidence of proteinuria and possible changes in bone metabolism inclusion of kidney donors in registries appears worthwhile.

                Author and article information

                Nephron Clin Pract
                Nephron Clinical Practice
                S. Karger AG
                November 2007
                21 September 2007
                : 107
                : 3
                : c82-c89
                aDivision of Nephrology, University of Western Ontario, London,Ont., Canada; bRenal Unit, University of Glasgow, Glasgow, UK; cDivision of Nephrology, University of British Columbia, Vancouver, B.C., Canada; dDivision of Nephrology, University of Western Australia, Perth, Australia; eDepartment of Medicine, University of Manitoba, Winnipeg, Man., and fDepartment of Epidemiology and Biostatistics, University of Western Ontario, London, Ont., Canada
                108648 Nephron Clin Pract 2007;107:c82–c89
                © 2007 S. Karger AG, Basel

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                Figures: 1, Tables: 5, References: 32, Pages: 1
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