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Heart sounds, the acoustic vibrations produced by the mechanical processes of the cardiac cycle, are modulated by respiratory activity. We have used computational techniques of cluster analysis and classification to study the effects of the respiratory phase and the respiratory resistive load on the temporal and morphological properties of the first (S1) and second heart sounds (S2), acquired from 12 healthy volunteers. Heart sounds exhibited strong morphological variability during normal respiration and nearly no variability during apnea. The variability was shown to be periodic, with its estimated period in good agreement with the measured split morphology was observed for S1 and S2 during inspiration. At high-breathing load, these changes became more prominent and occurred earlier in the respiratory cycle. Unsupervised cluster analysis was able to automatically identify the distinct morphologies associated with different respiratory phases and load. Classification of the respiration phase (inspiration or expiration) from the morphology of S1 achieved an average accuracy of 87 [+ or -] 7%, and classification of the breathing load was accurate in 82 [+ or -] 7%. These results suggest that quantitative heart sound analysis can shed light on the relation between respiration and cardiovascular mechanics and may be applied to continuous cardiopulmonary monitoring. phonocardiography; cardiopulmonary interaction; cluster analysis; classification; noninvasive monitoring

Epidemiologic studies now strongly support the hypothesis, proposed over two decades ago, that developmental programming of the kidney impacts an individual's risk for hypertension and renal disease in later life. Low birth weight is the strongest current clinical surrogate marker for an adverse intrauterine environment and, based on animal and human studies, is associated with a low nephron number. Other clinical correlates of low nephron number include female gender, short adult stature, small kidney size, and prematurity. Low nephron number in Caucasian and Australian Aboriginal sub-jects has been shown to be associated with higher blood pressures, and, conversely, hypertension is less prevalent in individuals with higher nephron numbers. In addition to nephron number, other pro-grammed factors associated with the increased risk of hypertension include salt sensitivity, altered expression of renal sodium transporters, altered vascular reactivity, and sympathetic nervous system overactivity. Glomerular volume is universally found to vary inversely with nephron number, suggesting a degree of compensatory hypertrophy and hyperfunction in the setting of a low nephron number. This adaptation may become overwhelmed in the setting of superimposed renal insults, e.g. diabetes mellitus or rapid catch-up growth, leading to the vicious cycle of on-going hyperfiltration, proteinuria, nephron loss and progressive renal functional decline. Many millions of babies are born with low birth weight every year, and hypertension and renal disease prevalences are increasing around the globe. At present, little can be done clinically to augment nephron number; therefore adequate prenatal care and careful postnatal nutrition are crucial to optimize an individual's nephron number during development and potentially to stem the tide of the growing cardiovascular and renal disease epidemics worldwide. [ABSTRACT FROM AUTHOR]

Two coding sequence variants in the APOL1 gene (G1 and G2) explain much of the increased risk for FSGS, HIV-associated nephropathy, and hypertension-attributed ESRD among people of recent African ancestry. The ApoL1 protein is expressed in a wide variety of cell tissues. It has been assumed that the majority of circulating ApoL1 is produced by the liver, but this has not been shown. Using mass spectrometry, we genotyped and quantified the circulating ApoL1 in two liver transplant recipients whose native APOL1 genotype differed from the genotype of the deceased donors, allowing us to differentiate liver- from nonliver-produced ApoL1. Our findings confirm that the liver is indeed the main source of circulating ApoL1. However, the liver is not the sole source of circulating ApoL1, because we found that residual amounts of native ApoL1 continued to circulate in the blood, even after the liver transplant., (Copyright © 2017 by the American Society of Nephrology.)