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Ingela Fehrman-Ekholm

Publications and source records attributed to Ingela Fehrman-Ekholm.

6 recordsLinked to original sources

Incidence of end-stage renal disease among live kidney donors.

BACKGROUND: The increasing use of living kidney donors requires knowledge about long-term effects, especially number and causes of donors with end-stage renal disease (ESRD). METHODS: A retrospective data analysis of 1,112 consecutive living kidney donors who underwent nephrectomy from 1965 until 2005 at Sahlgrenska University Hospital. Case reports were sought with help from nephrologists in the region and data from Swedish Registry of Active Uremic Treatment (SRAU). RESULTS: The number of cases with end stage kidney failure among living kidney donors was 6/1112, that is 0.5%. The donors had reached ESRD during the years 2001-2006, that means 36-41 years after start of the living donor program. The donors were 45-89 years old, median 77 years, and five of six were males. Time since donation was 14-27 years, median 20 years, for the donors developing ESRD. The diagnoses were nephrosclerosis (4 cases), postrenal failure (1 case), and renal carcinoma (1 case). The expected incidence for development of ESRD according to incidence in the general population would have been two donors but we found six. However, considering the high age of the donors in this follow up, the age-matched incidence is calculated to be closer to six donors due to higher incidence in the aged. CONCLUSION: In all 0.5% of the donors developed ESRD. Due to high age of the uremic donors, there seems to be no increased incidence.

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Renal function in the elderly (>70 years old) measured by means of iohexol clearance, serum creatinine, serum urea and estimated clearance.

OBJECTIVE: A survey revealed that kidney donors live longer than non-donors. When measured using an injection technique in elderly former kidney donors, the glomerular filtration rate (GFR) was found to be markedly decreased. The aim of this study was to determine the relationship between GFR and age in a cohort of elderly controls with two kidneys. We were also interested to find out whether GFR estimated using different equations correlated with the exact measurements. MATERIAL AND METHODS: Renal function was determined using the iohexol technique in 52 elderly "healthy" persons aged 70-110 years. Blood tests were done at the same time. Estimated clearance was determined using the equations of Cockroft-Gault, Walser and Levey. RESULTS: GFR showed a strong correlation with age (p = 0.0002), with an annual decline of 1.05 ml/min. Using formulas for estimation of clearance, the best correlation was found with that of Levey. Probably the most widely-used formula, that of Cockroft-Gault, underestimated the clearance, the mean value being 46.2 +/- 11.3 ml/min/1.73 m2, compared to the measured mean value of 67.7 +/- 10.8 ml/min/1.73 m2. Serum (s)-creatinine did not correlate with age (p = 0.3997). However, s-urea increased with age (p = 0.0019), while s-albumin (p = 0.0018), blood haemoglobin (p = 0.0060) and s-ferritin (p = 0.0243) decreased with age. A total of 21/52 (30%) of the elderly subjects had a GFR >70 ml/min/1.73 m2, but none of these persons was aged >90 years. Of the 21 subjects with good function, eight seemed to be quite healthy, with normal test values. CONCLUSION: GFR decreases by approximately 1.05 ml/min per year in very old persons. S-urea seems to be more sensitive than s-creatinine for indicating renal function in the elderly. The best formula for estimation of clearance is that of Levey. The Cockroft-Gault formula seems to underestimate GFR.

Age Factors↗

Associations between circulating inflammatory markers and residual renal function in CRF patients.

BACKGROUND: Circulating levels of cytokines and other inflammation markers are markedly elevated in patients with chronic renal failure. This could be caused by increased generation, decreased removal, or both. However, it is not well established to what extent renal function per se contributes to the uremic proinflammatory milieu. The aim of the present study is to analyze the relationship between inflammation and glomerular filtration rate (GFR) in 176 patients (age, 52 +/- 1 years; GFR, 6.5 +/- 0.1 mL/min) close to the initiation of renal replacement therapy. METHODS: Circulating levels of high-sensitivity C-reactive protein (hsCRP), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), hyaluronan, and neopterin were measured after an overnight fast. Patients subsequently were subdivided into two groups according to median GFR (6.5 mL/min). RESULTS: Despite the narrow range of GFR (1.8 to 16.5 mL/min), hsCRP, hyaluronan, and neopterin levels were significantly greater in the subgroup with lower GFRs, and significant negative correlations were noted between GFR and IL-6 (rho = -0.18; P < 0.05), hyaluronan (rho = -0.25; P < 0.001), and neopterin (rho = -0.32; P < 0.0005). In multivariate analysis, although age and GFR were associated with inflammation, cardiovascular disease and diabetes mellitus were not. CONCLUSION: These results show that a low GFR per se is associated with an inflammatory state, suggesting impaired renal elimination of proinflammatory cytokines, increased generation of cytokines in uremia, or an adverse effect of inflammation on renal function.

Biomarkers↗

Plasma pentosidine is associated with inflammation and malnutrition in end-stage renal disease patients starting on dialysis therapy.

Pentosidine is an advanced glycation end-product (AGE), formed by glycosylation and oxidation, that accumulates markedly in end-stage renal disease (ESRD). It has been speculated that AGE and carbonyl stress contributes to long-term complications such as cardiovascular disease (CVD) in ESRD patients. This study determined plasma levels of pentosidine as well as the presence of inflammation (CRP > or = 10 mg/L), clinical CVD (CVD(clin)), and malnutrition (subjective global assessment [SGA] > 1) in a cohort of 191 ESRD patients, median age of 55 yr (range, 23 to 70 yr) and median GFR = 7 ml/min (range, 2 to 17 ml/min), close to start of renal replacement therapy. Fifty-one elderly subjects, median age of 82 yr (range, 71 to 110 yr), with mild renal impairment, median GFR = 67 ml/min (range, 38 to 113 ml/min), were also studied for comparative analysis of plasma pentosidine. The plasma pentosidine content was elevated in all patients compared with the levels in the elderly subjects and were negatively correlated with GFR both in the ESRD patients (Rho = -0.24; P < 0.01; n = 159) and in the elderly subjects (Rho = -0.31; P < 0.05). Moreover, the plasma pentosidine content was correlated with age in the ESRD patients (Rho = 0.26; P < 0.001) and in the elderly subjects (Rho = 0.44; P < 0.001). The 63 malnourished ESRD patients (35%) had a significantly higher (P < 0.05) median plasma pentosidine than the well-nourished patients (39 versus 27 pmol/mg albumin). Similarly, 73 inflamed patients (38%) had a significantly higher (P < 0.001) median pentosidine content compared with 118 non-inflamed patients (37 versus 24 pmol/mg albumin). Also, the plasma pentosidine content showed weak but significant positive correlations with CRP (Rho = 0.28; P < 0.0001), fibrinogen (Rho = 0.23; P < 0.01; n = 126), IL-6 (Rho = 0.22; P < 0.01; n = 169), and soluble vascular cellular adhesion molecule-1 (Rho = 0.38; P < 0.001; n = 74). On the other hand, no significant differences in plasma pentosidine content were noted between the patients with and those without CVD(clin) (32 versus 27 pmol/mg albumin, respectively). Analyses of all-cause mortality, by Kaplan-Meier, showed that mortality was not linked to the plasma pentosidine content. Moreover, survival analysis by the Cox regression model showed that age (P < 0.001), diabetes mellitus (P < 0.01), malnutrition (P < 0.01), and CVD(clin) (P < 0.01) independently predicted poor outcome, whereas an elevated plasma pentosidine content did not. The present study shows that an elevated plasma pentosidine content in ESRD patients is significantly associated with both inflammation and malnutrition and confirms that low residual renal function and high age further contribute to an increased plasma pentosidine content. However, in this small cohort, the plasma pentosidine content did not predict outcome. Thus, accumulation of plasma pentosidine is unlikely to be an appropriate clinically useful marker to predict mortality in ESRD patients.

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