Role of NH3 and NH4+ transporters in renal acid-base transport.
ABSTRACT Renal ammonia excretion is the predominant component of renal net acid excretion. The majority of ammonia excretion is produced in the kidney and then undergoes regulated transport in a number of renal epithelial segments. Recent findings have substantially altered our understanding of renal ammonia transport. In particular, the classic model of passive, diffusive NH3 movement coupled with NH4+ "trapping" is being replaced by a model in which specific proteins mediate regulated transport of NH3 and NH4+ across plasma membranes. In the proximal tubule, the apical Na+/H+ exchanger, NHE-3, is a major mechanism of preferential NH4+ secretion. In the thick ascending limb of Henle's loop, the apical Na+-K+-2Cl- cotransporter, NKCC2, is a major contributor to ammonia reabsorption and the basolateral Na+/H+ exchanger, NHE-4, appears to be important for basolateral NH4+ exit. The collecting duct is a major site for renal ammonia secretion, involving parallel H+ secretion and NH3 secretion. The Rhesus glycoproteins, Rh B Glycoprotein (Rhbg) and Rh C Glycoprotein (Rhcg), are recently recognized ammonia transporters in the distal tubule and collecting duct. Rhcg is present in both the apical and basolateral plasma membrane, is expressed in parallel with renal ammonia excretion, and mediates a critical role in renal ammonia excretion and collecting duct ammonia transport. Rhbg is expressed specifically in the basolateral plasma membrane, and its role in renal acid-base homeostasis is controversial. In the inner medullary collecting duct (IMCD), basolateral Na+-K+-ATPase enables active basolateral NH4+ uptake. In addition to these proteins, several other proteins also contribute to renal NH3/NH4+ transport. The role and mechanisms of these proteins are discussed in depth in this review.
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ABSTRACT: Overdiagnosis of renal tubular acidosis (RTA) has been recently detected in Mexican children, perhaps due to diagnostic errors as well as in a lack of knowledge regarding the pathophysiology and molecular biochemistry involved in this illness. The objective of the present study is to facilitate the knowledge and diagnosis of RTA, a clinical condition infrequently seen worldwide. RTA is an alteration of the acid-base equilibrium due to a bicarbonate wasting in the proximal renal tubules (proximal RTA, pRTA or type 2 RTA) or due to a distal nephron hydrogen ion excretion defect (distal RTA, dRTA or type 1 RTA). Hyperkalemic, or type 4 RTA, is due to alterations in aldosterone metabolism.Boletín médico del Hospital Infantil de México. 06/2013; 70(3):178-194.
Article: Renal Tubular Acidosis.The Journal of pediatrics 12/2013; · 4.02 Impact Factor
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ABSTRACT: The review deals with modern ideas on the processes that determine the urine protein composition of healthy people. In the past decade, the development of highly sensitive mass-spectrometric methods of protein detection stimulated studies of the protein composition of various human body fluids, including urine. Nowadays, the methods of separating complex protein mixtures and identification of individual components of these mixtures provide an opportunity to detect a significant amount of proteins and peptides of different origins in human urine. Physiological variation of the urine protein composition determined by the methods of proteomics remains a poorly studied but very important problem. Under physiological conditions, there are many factors that influence the filtering of plasma proteins in the glomeruli and reabsorption in the proximal tubules of the nephron. These are hypoxia, oxidative stress, changes in the acid-base balance and blood pressure, the effects of the parathyroid hormone, angiotensin-II, and other substances that control water and electrolyte metabolism. It is demonstrated that, because of the close structural and functional relationships between reabsorption processes in the proximal tubules of the nephron, reabsorption and modulation of sodium, water, chloride, phosphate, and bicarbonate depend on changes in various parts of the process of protein reabsorption.Human Physiology 03/2013; 39(2).