Renal tubular acidosis

Santos, Fernando; Gil‐Peña, Helena; Alvarez-Alvarez, Silvia

doi:10.1097/mop.0000000000000460

Cited by 29 publications

(21 citation statements)

References 16 publications

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“…Type 1 RTA results from failure of normal collecting ductmediated urine acidification-bicarbonate reabsorption and type 2 RTA results from impaired proximal tubule (PT) reabsorption of filtered bicarbonate. [7][8][9] In contrast, type 4 RTA, defined as the combination of hyperkalemia with hyperchloremic, nonanion gap metabolic acidosis that is not due to reduced glomerular filtration, 10,11 is not due to a failure of bicarbonate transport, but instead is thought to primarily arise from abnormal ammonia excretion, 10,12 although "aldosterone-resistance" and alterations in distal proton secretion have also been postulated.…”

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confidence: 99%

Mechanism of Hyperkalemia-Induced Metabolic Acidosis

Harris

Grimm

Lee

et al. 2018

JASN

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Hyperkalemia in association with metabolic acidosis that are out of proportion to changes in glomerular filtration rate defines type 4 renal tubular acidosis (RTA), the most common RTA observed, but the molecular mechanisms underlying the associated metabolic acidosis are incompletely understood. We sought to determine whether hyperkalemia directly causes metabolic acidosis and, if so, the mechanisms through which this occurs. We studied a genetic model of hyperkalemia that results from early distal convoluted tubule (DCT)-specific overexpression of constitutively active Ste20/SPS1-related proline-alanine-rich kinase (DCT-CA-SPAK). DCT-CA-SPAK mice developed hyperkalemia in association with metabolic acidosis and suppressed ammonia excretion; however, titratable acid excretion and urine pH were unchanged compared with those in wild-type mice. Abnormal ammonia excretion in DCT-CA-SPAK mice associated with decreased proximal tubule expression of the ammonia-generating enzymes phosphate-dependent glutaminase and phosphoenolpyruvate carboxykinase and overexpression of the ammonia-recycling enzyme glutamine synthetase. These mice also had decreased expression of the ammonia transporter family member Rhcg and decreased apical polarization of H-ATPase in the inner stripe of the outer medullary collecting duct. Correcting the hyperkalemia by treatment with hydrochlorothiazide corrected the metabolic acidosis, increased ammonia excretion, and normalized ammoniagenic enzyme and Rhcg expression in DCT-CA-SPAK mice. In wild-type mice, induction of hyperkalemia by administration of the epithelial sodium channel blocker benzamil caused hyperkalemia and suppressed ammonia excretion. Hyperkalemia decreases proximal tubule ammonia generation and collecting duct ammonia transport, leading to impaired ammonia excretion that causes metabolic acidosis.

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Mechanism of Hyperkalemia-Induced Metabolic Acidosis

Harris

Grimm

Lee

et al. 2018

JASN

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“…The group of diseases characterized as renal tubular acidosis (RTA) refers to a condition in which there is normal serum anion gap or hyperchloremic metabolic acidosis in the presence of well-preserved glomerular function. This is caused by the inability of the renal tubule to reabsorb bicarbonate or to secrete hydrogen ions [ 5 ]. In most sources, primary RTA is divided into a proximal (type II), distal (type I), and a hyperkalemic form associated with hyperaldosteronism or aldosterone resistance (Type IV).…”

Section: Discussionmentioning

confidence: 99%

A Rare Case of Transient Proximal Renal Tubular Acidosis in Pregnancy

Narcisse

Agarwal

Kumar

2017

Case Reports in Nephrology

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Renal tubular acidosis (RTA) is a disorder that has improper function of renal acid-base regulation and is rarely encountered during pregnancy. Currently, there is no clear evidence on management and outcomes in patients with this condition. We report a case of a previously healthy 23-year-old female at 30 weeks of gestation who presented with proximal RTA and had spontaneous resolution of the condition shortly after delivery.

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“…Inherited proximal RTA is a rare disorder that may be inherited as an autosomal recessive or dominant trait [44]. The more common autosomal recessive form has been associated with mutations in the basolateral sodium bicarbonate cotransporter NBCe1, encoded by the SLC4A4 gene.…”

Section: Regulation Of Urinary Acidificationmentioning

confidence: 99%

Understanding the Pathophysiology of Nephrocalcinosis

Priante¹,

Ceol²,

Terrin³

et al. 2017

Updates and Advances in Nephrolithiasis - Pathophysiology, Genetics, and Treatment Modalities

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Many in vitro and in vivo studies on the mechanisms underlying calcium nephrolithiasis have provided evidence of a frequently associated condition, i.e., a microscopic renal crystal deposition that can occur within the tubular lumen (intratubular nephrocalcinosis) or in the interstitium (interstitial nephrocalcinosis). Medullary nephrocalcinosis is the typical pattern seen in 98% of cases of human nephrocalcinosis, with calcification clustering around each renal pyramid. It is common in patients with metabolic conditions that predispose them to renal calcium stones. Cortical nephrocalcinosis is rare and usually results from severe destructive disease of the cortex. It has been described in chronic glomerulonephritis, but often in association with another factor, such as an increased calcium ingestion, acute cortical necrosis, chronic pyelonephritis or trauma. The most accredited hypothesis to explain the onset of interstitial nephrocalcinosis is purely physicochemical, relating to spontaneous Ca 2 PO 4 crystallization in the interstitium due to oversaturation of Ca 2 PO 4 salts in this milieu. The theory that nephrocalcinosis is a process driven by osteogenic cells was first proposed by our group. We review nephrocalcinosis in terms of its definition, genetic associations, and putative mechanisms, pointing out how much evidence in the literature suggests that it may have some features in common with, and pathogenic links to vascular calcification.

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Renal tubular acidosis

Abstract: We briefly update the current information on RTA, put forward the need of additional studies in children to validate urinary indexes used in the diagnosis of RTA and offer a perspective on diagnostic genetic tests.

Cited by 29 publications

References 16 publications

Mechanism of Hyperkalemia-Induced Metabolic Acidosis

Mechanism of Hyperkalemia-Induced Metabolic Acidosis

A Rare Case of Transient Proximal Renal Tubular Acidosis in Pregnancy

Understanding the Pathophysiology of Nephrocalcinosis

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