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Introduction: Chronic kidney disease (CKD) risk staging is based on estimated glomerular filtration rate (eGFR) and albumin-creatinine ratio (ACR). However, the relationship between all-cause hospitalization risk and the current CKD staging system has not been well studied among older adults, despite a high prevalence of CKD and a high risk of hospitalization in old age., Methods: Among 4,766 participants of the Atherosclerosis Risk in Communities study, CKD was staged according to Kidney Disease Improving Global Outcomes (KDIGO) criteria, using creatinine-based eGFR (eGFRcr) and ACR. Incidence rates of all-cause hospitalization associated with each CKD risk group were analyzed using negative binomial regression. Additionally, cause-specific hospitalization risks for cardiovascular, infectious, kidney, and other diseases were estimated. The impacts of using cystatin C-based eGFR (eGFRcys) to estimate the prevalence of CKD and risks of hospitalization were also quantified., Results: Participants experienced 5,548 hospitalizations and 29% had CKD. Hospitalization rates per 1,000 person-years according to KDIGO risk categories were 208-223 ("low risk"), 288-376 ("moderately increased risk"), 363-548 ("high risk"), and 499-1083 ("very high risk"). The increased risk associated with low eGFR and high ACR persisted in adjusted analyses, examinations of cause-specific hospitalizations, and when CKD was staged by eGFRcys or eGFRcr-cys, a combined equation based on both creatinine and cystatin C. In comparison to eGFRcr, staging by eGFRcys increased the prevalence of CKD to 50%, but hospitalization risks remained similarly high., Discussion/conclusion: In older adults, decreased eGFR, increased ACR, and KDIGO risk stages based on a combination of these measures, were strong risk factors for hospitalization. These relationships were consistent, regardless of the marker used to estimate GFR, but the use of cystatin C resulted in a substantially higher prevalence of CKD than the use of creatinine. Older adults in the population with very high risk stages of CKD have hospitalization rates exceeding 500 per 1,000 person-years., (© 2019 S. Karger AG, Basel.)

Background: Prior studies suggest that certain aspects of the diet related to magnesium intake, such as dietary acid load, protein intake and dietary patterns rich in fruits and vegetables, may impact kidney disease risk. We hypothesized that lower dietary magnesium intake would be prospectively associated with more rapid kidney function decline., Methods: Among participants in the Healthy Aging in Neighborhoods of Diversity across the Life Span study with estimated glomerular filtration rate (eGFR) ≥60 ml/min/1.73 m2 at baseline (2004-2009), dietary magnesium intake was calculated from two 24-hour dietary recalls. Rapid decline was defined as ≥3% eGFR decline per year., Results: Median (25th-75th percentile) dietary magnesium intake was 116 (96-356) mg/1,000 kcal. Among 1,252 participants, those with lower dietary magnesium intake were younger, and were more likely to be African-American men. A total of 177 participants (14.1%) experienced rapid eGFR decline over a median follow-up of 5 years. Lower dietary magnesium intake was significantly associated with a greater odds of rapid eGFR decline (OR for tertile 1 vs. 3: 2.02, 95% CI 1.05-3.86, p value for trend across tertiles = 0.02) in analyses adjusted for sociodemographics (age, sex, race, education level, health insurance status, poverty status), kidney disease risk factors (smoking status, diabetes, hemoglobin A1c, hypertension, body mass index), baseline eGFR and dietary factors (total energy intake; diet quality; dietary intake of fiber, sodium, calcium, potassium and phosphorus)., Conclusions: In this urban population, lower dietary magnesium intake was independently associated with greater odds of rapid kidney function decline., Competing Interests: The authors have no relevant conflicts of interest to report., (© 2016 S. Karger AG, Basel.)

Background: Higher dietary acid load can result in metabolic acidosis and is associated with faster kidney disease progression in patients with chronic kidney disease (CKD). However, the relationship between dietary acid load and incident CKD has not been evaluated., Methods: We conducted prospective analyses of the Atherosclerosis Risk in Communities study participants without CKD at baseline (1987-1989, n = 15,055). Dietary acid load was estimated using the equation for potential renal acid load by Remer and Manz, incorporating dietary intake data from a food frequency questionnaire. Incident CKD was assessed from baseline through 2010 and defined as estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m2 accompanied by 25% eGFR decline, CKD-related hospitalization or death or end-stage renal disease identified by linkage to the US Renal Data System registry., Results: In the overall study population, 55% were female, 26% were African-American and mean age at baseline was 54 years. During a median follow-up of 21 years, there were 2,351 (15.6%) incident CKD cases. After adjusting for demographics (age, sex, race-center), established risk factors (diabetes status, hypertension status, overweight/obese status, smoking status, education level, physical activity), caloric intake and baseline eGFR, higher dietary acid load were associated with higher risk of incident CKD (hazard ratio [HR] for quartile 4 vs. 1: 1.13, 95% CI 1.01-1.28, p for trend = 0.02; HR per interquartile range increase: 1.06, 95% CI 1.00-1.11, p = 0.04)., Conclusion: Dietary acid load is associated with incident CKD in a population-based sample. These data suggest a potential avenue for CKD risk reduction through diet., (© 2016 S. Karger AG, Basel.)

Background/aims: Plasma fluorescent oxidation products (FLOP) constitute a stable and easily measured biomarker of cumulative oxidative stress. However, their association with chronic kidney disease (CKD) has not been studied., Methods: We examined the association of FLOP and CKD in 201 CKD patients and 201 controls without CKD from the community. CKD was defined as an estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m(2) or the presence of albuminuria., Results: Adjusted median (interquartile range) FLOP levels were significantly higher in patients with CKD than in controls [FLOP1 (lipid oxidation products): 215.2 (181.3-268.7) vs. 156.6 (139.6-177.3) fluorescent intensity units/ml, p < 0.0001; FLOP2 (DNA oxidation products): 534.8 (379.3-842.4) vs. 269.9 (232.4-410.5) fluorescent intensity units/ml, p < 0.0001; FLOP3 (protein and phospholipid oxidation products): 51.4 (44.4-66.0) vs. 45.2 (38.3-51.7) fluorescent intensity units/ml, p = 0.002]. Compared with those with a FLOP level below the 75th percentile, participants with a FLOP level above the 75th percentile had increased odds of CKD after adjustment for covariables (FLOP1: odds ratio 13.1, 95% confidence interval 6.2-27.6; FLOP2: odds ratio 5.7, 95% confidence interval 2.9-11.1; FLOP3: odds ratio 2.4, 95% confidence interval 1.2-4.7). Levels of FLOP1, FLOP2 and FLOP3 were related to eGFR (p < 0.0001 for all) and log-transformed urine albumin (p < 0.005 for all) in multivariable-adjusted linear regression models., Conclusion: These data indicate that an elevated FLOP level is associated with CKD status and severity. Future studies are warranted to elucidate its role in the development and progression of CKD., (Copyright © 2012 S. Karger AG, Basel.)