Harvey Lester White (1896-1977) graduated from Washington University (St. Louis) School of Medicine and subsequently spent his entire professional career in the School's Department of Physiology. White's interest in the function of the kidney was evident early in his academic career when he pioneered research related to renal physiology. His first papers dealt with studies of renal tubular function (1923). He performed what appear to represent the first micropuncture studies in the kidney of Necturus maculosus (1926) and thus confirmed the observations of Wearn and Richards regarding glomerular filtration. Through these studies, he was the first to show that glucose reabsorption occurs in the proximal tubules of Necturus. It also appears that White et al. were the first to demonstrate that volume expansion increases bicarbonate excretion in dogs (1926). He studied the influence of posture on renal "activity" in man (1926). Intracapsular pressure determinations in Necturus kidney (1928) were done using micropuncture techniques. White and co-workers presented (1933) a comparison of clearances of creatinine and various sugars confirming the work of Jolliffe, Shannon and Smith (1932) who had proposed the clearances of non-metabolizable sugars to be a measure of glomerular filtration. Between 1932 and 1936, in an effort to better understand the process of glomerular filtration, he began a series of studies on streaming potentials, surface conductance, electro-endosmosis and other related topics. In 1937, White began work on yet another aspect of renal physiology--endocrine influences on renal function. He would immerse himself in these investigations throughout the remainder of his scientific career. We hope that this account will reveal at least a small dimension of the man and his contributions to renal physiology.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1159/000063758 | DOI Listing |
FASEB J
January 2025
Department of Urology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Renal fibrosis is a common pathological process in various chronic kidney diseases. The accumulation of senescent renal tubular epithelial cells (TECs) in renal tissues plays an important role in the development of renal fibrosis. Eliminating senescent TECs has been proven to effectively reduce renal fibrosis.
View Article and Find Full Text PDFFront Physiol
January 2025
College of Dental Medicine, Lincoln Memorial University, Harrogate, TN, United States.
Front Pediatr
January 2025
Department of Pediatric Nephrology, Children's Hospital of Hebei Province Affiliated to Hebei Medical University, Shijiazhuang, China.
Background: Primary coenzyme Q10 (CoQ10) deficiency is an autosomal recessive genetic disease caused by mitochondrial dysfunction. Variants in Coenzyme Q8B () can cause primary CoQ10 deficiency. -related glomerulopathy is a recently recognized glomerular disease that most often presents as steroid-resistant nephrotic syndrome (SRNS) in childhood.
View Article and Find Full Text PDFPediatr Nephrol
January 2025
NIHR Great Ormond Street Hospital Biomedical Research Centre, University College London Great Ormond Street Institute of Child Health, London, UK.
Acute kidney injury (AKI) in paediatric kidney transplant recipients is common. Infection including urinary tract infection (UTI) and rejection are the most common causes in children. Surgical complications often cause AKI early post-transplant, whereas BK polyomavirus nephropathy rarely occurs in the first month post-transplant.
View Article and Find Full Text PDFEMBO J
January 2025
Department of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT, 84112-5650, USA.
Na-K-Cl cotransporters functions as an anion importers, regulating trans-epithelial chloride secretion, cell volume, and renal salt reabsorption. Loop diuretics, including furosemide, bumetanide, and torsemide, antagonize both NKCC1 and NKCC2, and are first-line medicines for the treatment of edema and hypertension. NKCC1 activation by the molecular crowding sensing WNK kinases is critical if cells are to combat shrinkage during hypertonic stress; however, how phosphorylation accelerates NKCC1 ion transport remains unclear.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!