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BACKGROUND: Overscreening occurs when people without symptoms undergo tests for diseases and the results will not improve their health. In this commentary, we examine three examples of how campaigns to screen and treat specific vascular, metabolic, and oncologic diseases in asymptomatic individuals have produced substantial overdiagnosis and may well have contributed to more harm than good. These conditions were chosen because they may not be as well known as other cases such as screening for breast or prostate cancer. MAIN TEXT: Screening for carotid artery stenosis can be a lucrative business using portable equipment and mobile vans. While this fatty buildup of plaque in the arteries of the neck is one risk factor for ischemic stroke, current evidence does not suggest that performing carotid dopplers to screen for CAS reduces the incidence of stroke or provide long-term benefits. After a positive screening, the follow-up procedures can lead to heart attacks, bleeding, strokes, and even death. Similarly, many organizations have launched campaigns for "prediabetes awareness." Screening for prediabetes with a blood sugar test does not decrease mortality or cardiovascular events. Identifying people with prediabetes could lead to psychological stress and starting medication that may have significant side effects. Finally, palpating people's necks or examining them with ultrasounds for thyroid cancer is common in many countries but ineffective in reducing mortality. Deadly forms of thyroid cancer are rare, and the overall 5-year survival rate is excellent. Interventions from treatment for more prevalent, less aggressive forms of thyroid cancer can lead to surgical complications, radiation side effects, or require lifelong thyroid replacement therapy. CONCLUSIONS: Screening for carotid artery stenosis, prediabetes, and thyroid cancer in an asymptomatic population can result in unnecessary, harmful, and costly care. Systemic challenges to lowering overscreening include lack of clinician awareness, examination of conflicts of interests, perverse financial incentives, and communication with the general public.
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In rat terminal inner medullary collecting duct (tIMCD), the Na,K-ATPase mediates NH uptake, which increases secretion of net H(+) equivalents. K(+) and NH compete for a common binding site on the Na,K-ATPase. Therefore, NH uptake should increase during hypokalemia because interstitial K(+) concentration is reduced. We asked whether upregulation of the Na,K-ATPase during hypokalemia also increases basolateral NH uptake. To induce hypokalemia, rats ate a diet with a low K(+) content. In tIMCD tubules from rats given 3 days of dietary K(+) restriction, Na,K-ATPase beta(1)-subunit (NK-beta(1)) protein expression increased although NK-alpha(1) protein expression and Na,K-ATPase activity were unchanged relative to K(+)-replete controls. However, after 7 days of K(+) restriction, both NK-alpha(1) and NK-beta(1) subunit protein expression and Na,K-ATPase activity increased. The magnitude of Na,K-ATPase-mediated NH uptake across the basolateral membrane (J) was determined in tIMCD tubules perfused in vitro from rats after 3 days of a normal or a K(+)-restricted diet. J was the same in tubules from rats on either diet when measured at the same extracellular K(+) concentration. However, in either treatment group, increasing K(+) concentration from 10 to 30 mM reduced J >60%. In conclusion, with 3 days of K(+) restriction, NH uptake by Na,K-ATPase is increased in the tIMCD primarily from the reduced interstitial K(+) concentration.