Time trends in reported prevalence of kidney stones in the United States: 1976–199411.See Editorial by Goldfarb, p. 1951.

Time trends in reported prevalence of kidney stones in the United States: 1976–1994.BackgroundA body of evidence establishes that the occurrence of kidney stone disease has increased in some communities of industrialized countries. Information on recent temporal trends in the United States is lacking and population-based data on epidemiologic patterns are limited.Study objective was to determine whether kidney stone disease prevalence increased in the United States over a 20-year period and the influence of region, race/ethnicity, and gender on stone disease risk.MethodsWe measured the prevalence of kidney stone disease history from the United States National Health and Nutrition Examination Survey (II and III), population-based, cross-sectional studies, involving 15,364 adult United States residents in 1976 to 1980 and 16,115 adult United States residents in 1988 to 1994.ResultsDisease prevalence among 20- to 74-year-old United States residents was greater in 1988 to 1994 than in 1976 to 1980 (5.2% vs. 3.8%, P < 0.05), greater in males than females, and increased with age in each time period. Among 1988 to 1994 adults, non-Hispanic African Americans had reduced risk of disease compared to non-Hispanic Caucasians (1.7% vs. 5.9%, P < 0.05), and Mexican Americans (1.7% vs. 2.6%, P < 0.05). Also, age-adjusted prevalence was highest in the South (6.6%) and lowest in the West (3.3%). Findings were consistent across gender and multivariate adjusted odds ratios for stone disease history, including all demographic variables, as well as diuretic use, tea or coffee consumption, and dietary intake of calcium, protein, and fat did not materially change the results.ConclusionPrevalence of kidney stone disease history in the United States population increased between 1980 and 1994. A history of stone disease was strongly associated with race/ethnicity and region of residence

Critical Role of DNA Checkpoints in Mediating Genotoxic-Stress–induced Filamentous Growth in Candida albicans

The polymorphic fungus Candida albicans switches from yeast to filamentous growth in response to a range of genotoxic insults, including inhibition of DNA synthesis by hydroxyurea (HU) or aphidicolin (AC), depletion of the ribonucleotide-reductase subunit Rnr2p, and DNA damage induced by methylmethane sulfonate (MMS) or UV light (UV). Deleting RAD53, which encodes a downstream effector kinase for both the DNA-replication and DNA-damage checkpoint pathways, completely abolished the filamentous growth caused by all the genotoxins tested. Deleting RAD9, which encodes a signal transducer of the DNA-damage checkpoint, specifically blocked the filamentous growth induced by MMS or UV but not that induced by HU or AC. Deleting MRC1, the counterpart of RAD9 in the DNA-replication checkpoint, impaired DNA synthesis and caused cell elongation even in the absence of external genotoxic insults. Together, the results indicate that the DNA-replication/damage checkpoints are critically required for the induction of filamentous growth by genotoxic stress. In addition, either of two mutations in the FHA1 domain of Rad53p, G65A, and N104A, nearly completely blocked the filamentous-growth response but had no significant deleterious effect on cell-cycle arrest. These results suggest that the FHA domain, known for its ability to bind phosphopeptides, has an important role in mediating genotoxic-stress–induced filamentous growth and that such growth is a specific, Rad53p-regulated cellular response in C. albicans