Renal tubules regulate blood pressure and humoral homeostasis. Mediators that play a significant role in regulating the transport of solutes and water include angiotensin Ⅱ （AngⅡ） and nitric oxide （NO）. AngⅡca...Renal tubules regulate blood pressure and humoral homeostasis. Mediators that play a significant role in regulating the transport of solutes and water include angiotensin Ⅱ （AngⅡ） and nitric oxide （NO）. AngⅡcan signifcantly raise blood pressure via effects on the heart, vasculature, and renal tubules. AngⅡ generally stimulates sodium reabsorption by triggering sodium and fuid retention in almost all segments of renal tu-bules. Stimulation of renal proximal tubule （PT） trans-port is thought to be essential for AngⅡ-mediated hy-pertension. However, AngⅡ has a biphasic effect on in vitro PT transport in mice, rats, and rabbits： stimulation at low concentrations and inhibition at high concentra-tions. On the other hand, NO is generally thought to inhibit renal tubular transport. In PTs, NO seems to be involved in the inhibitory effect of AngⅡ. A recent study reports a surprising fnding： AngⅡ has a mono-phasic stimulatory effect on human PT transport. De-tailed analysis of signalling mechanisms indicates that in contrast to other species, the human NO/guanosine 3’,5’-cyclic monophosphate/extracellular signal-regulat-ed kinase pathway seems to mediate this effect of Ang Ⅱ on PT transport. In this review we will discuss recent progress in understanding the effects of AngⅡ and NO on renal tubular transport.展开更多
Background Distal renal tubular acidosis(dRTA)is a kidney tubulopathy that causes a state of normal anion gap metabolic acidosis due to impairment of urine acidification.This review aims to summarize the etiology,path...Background Distal renal tubular acidosis(dRTA)is a kidney tubulopathy that causes a state of normal anion gap metabolic acidosis due to impairment of urine acidification.This review aims to summarize the etiology,pathophysiology,clinical findings,diagnosis and therapeutic approach of dRTA,with emphasis on genetic causes of dRTA.Data sources Literature reviews and original research articles from databases,including PubMed and Google Scholar.Manual searching was performed to identify additional studies about dRTA.Results dRTA is characterized as the dysfunction of the distal urinary acidification,leading to metabolic acidosis.In pediatric patients,the most frequent etiology of dRTA is the genetic alteration of genes responsible for the codification of distal tubule channels,whereas,in adult patients,dRTA is more commonly secondary to autoimmune diseases,use of medications and uropathies.Patients with dRTA exhibit failure to thrive and important laboratory alterations,which are used to define the diagnosis.The oral alkali and potassium supplementation can correct the biochemical defects,improve clinical manifestations and avoid nephrolithiasis and nephrocalcinosis.Conclusions dRTA is a multifactorial disease leading to several clinical manifestations.Clinical and laboratory alterations can be corrected by alkali replacement therapy.展开更多
文摘Renal tubules regulate blood pressure and humoral homeostasis. Mediators that play a significant role in regulating the transport of solutes and water include angiotensin Ⅱ （AngⅡ） and nitric oxide （NO）. AngⅡcan signifcantly raise blood pressure via effects on the heart, vasculature, and renal tubules. AngⅡ generally stimulates sodium reabsorption by triggering sodium and fuid retention in almost all segments of renal tu-bules. Stimulation of renal proximal tubule （PT） trans-port is thought to be essential for AngⅡ-mediated hy-pertension. However, AngⅡ has a biphasic effect on in vitro PT transport in mice, rats, and rabbits： stimulation at low concentrations and inhibition at high concentra-tions. On the other hand, NO is generally thought to inhibit renal tubular transport. In PTs, NO seems to be involved in the inhibitory effect of AngⅡ. A recent study reports a surprising fnding： AngⅡ has a mono-phasic stimulatory effect on human PT transport. De-tailed analysis of signalling mechanisms indicates that in contrast to other species, the human NO/guanosine 3’,5’-cyclic monophosphate/extracellular signal-regulat-ed kinase pathway seems to mediate this effect of Ang Ⅱ on PT transport. In this review we will discuss recent progress in understanding the effects of AngⅡ and NO on renal tubular transport.
文摘Background Distal renal tubular acidosis(dRTA)is a kidney tubulopathy that causes a state of normal anion gap metabolic acidosis due to impairment of urine acidification.This review aims to summarize the etiology,pathophysiology,clinical findings,diagnosis and therapeutic approach of dRTA,with emphasis on genetic causes of dRTA.Data sources Literature reviews and original research articles from databases,including PubMed and Google Scholar.Manual searching was performed to identify additional studies about dRTA.Results dRTA is characterized as the dysfunction of the distal urinary acidification,leading to metabolic acidosis.In pediatric patients,the most frequent etiology of dRTA is the genetic alteration of genes responsible for the codification of distal tubule channels,whereas,in adult patients,dRTA is more commonly secondary to autoimmune diseases,use of medications and uropathies.Patients with dRTA exhibit failure to thrive and important laboratory alterations,which are used to define the diagnosis.The oral alkali and potassium supplementation can correct the biochemical defects,improve clinical manifestations and avoid nephrolithiasis and nephrocalcinosis.Conclusions dRTA is a multifactorial disease leading to several clinical manifestations.Clinical and laboratory alterations can be corrected by alkali replacement therapy.
