This study examines the overall and relative contributions of a variety of family environment measures to a child's alcohol, marijuana and other drug use, delinquent activity, and dysfunctional methods of coping with problems. The family environment variables tapped aspects of parental behaviors and attitudes, parenting styles, and family harmony and cohesion. Data were collected as part of a prospective, longitudinal study that examined the acquisition and maintenance of a variety of behaviors. Data were gleaned at two points in time, spanning 3-year intervals, from subjects ranging in age from early to late adolescence. In general, alcohol use among the younger subjects was more strongly determined by the use and attitudes of the same sex parent. In contrast, among older subjects, father's alcohol use was important to the offspring's use. While models predicting illicit drug use and the extent of problems related to alcohol and marijuana use fared least well, it was generally found that hostility and lack of warmth on the part of the parents contributed most to these outcomes in subjects. Finally, hostility displayed by both parents helped to determine the incidence of delinquency among sons and the use of dysfunctional coping methods among sons and daughters.
Summary
Little is known about the effects of thalassaemia on the kidney. Characterization of underlying renal function abnormalities in thalassaemia is timely because the newer iron chelator, deferasirox, can be nephrotoxic. We aimed to determine the prevalence and correlates of renal abnormalities in thalassaemia patients, treated before deferasirox was widely available, using 24-h collections of urine. We calculated creatinine clearance and urine calcium-to-creatinine ratio and measured urinary β2-microglobulin, albumin, and protein. We used multivariate modelling to identify clinical, therapeutic, and laboratory predictors of renal dysfunction. One-third of thalassaemia patients who were not regularly transfused had abnormally high creatinine clearance. Regular transfusions were associated with a decrease in clearance (P = 0·004). Almost one-third of patients with thalassaemia had hypercalciuria, and regular transfusions were associated with an increase in the frequency and degree of hypercalciuria (P < 0·0001). Albuminuria was found in over half of patients, but was not consistently associated with transfusion therapy. In summary, renal hyperfiltration, hypercalciuria, and albuminuria are common in thalassaemia. Higher transfusion intensity is associated with lower creatinine clearance but more frequent hypercalciuria. The transfusion effect needs to be better understood. Awareness of underlying renal dysfunction in thalassaemia can inform decisions now about the use and monitoring of iron chelation.
Renal handling of homologous labeled rat growth hormone (125I-rGH) was studied in the intact rat and in a filtering and nonfiltering isolated perfused rat kidney preparation. Plasma disappearance rate, renal accumulation, renal clearance (C), glomerular sieving coefficient (GSC), absorption rates, and fate of absorbed hormones were determined. 125I-rGH is extensively filtered (GSC approximately 0.6) and subsequently absorbed by the tubular epithelium (C/GRF less than 1%). The absorption process of 125I-rGH has a high capacity and is inhibited by iodoacetate. Absorbed 125I-rGH is catabolized and a detectable product of catabolism (125I-monoiodotyrosine) is returned to the circulation. A nonfiltering kidney preparation with adequate renal perfusate flow was developed to study the contribution of the peritubular side to the renal handling of small proteins. Experiments in the nonfiltering kidney show that renal accumulation, extraction, and catabolism of 125I-rGH from the peritubular side is minimal when compared to that occurring from the luminal side. The ratio of the renal extraction rate of 125I-rGH in the isolated kidney and the mean plasma disappearance rate of 125I-rGH in the intact rat was 0.67, demonstrating that the kidneys account for the major fraction of the total plasma turnover of GH in the rat.
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