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Related Concept Videos

Renal Regulation of Acid-Base Balance01:29

Renal Regulation of Acid-Base Balance

Metabolic reactions in the body produce nonvolatile acids, such as sulfuric acid, which generate an acid load of approximately 1 mEq of H+ per kilogram of body weight daily. Excreting H+ in the urine is essential to balance this acid load.
In the kidneys, cells within the proximal convoluted tubules (PCT) and the collecting ducts secrete hydrogen ions (H+) into the tubular fluid. Specifically, in the PCT, Na+/H+ antiporters secrete H+ while reabsorbing Na+.
However, the intercalated cells in...
Renal Tubule and Collecting Duct01:24

Renal Tubule and Collecting Duct

The renal tubule is divided into three parts: the proximal convoluted tubule (PCT), the Loop of Henle (LOH), and the distal convoluted tubule (DCT).
Proximal Convoluted Tubule (PCT):
The PCT is the initial segment of the renal tubule, extending from the Bowman's capsule that encloses the glomerulus. Its convoluted structure and microvilli-lined cells increase the surface area for reabsorption. The PCT reabsorbs glucose, amino acids, sodium, and water from the filtrate, ensuring essential...
Acute Kidney Injury III: Clinical Manifestations01:29

Acute Kidney Injury III: Clinical Manifestations

Acute Kidney Injury (AKI) progresses through distinct clinical phases: the oliguric, diuretic, and recovery phases, each marked by unique manifestations and challenges.Oliguric Phase:The oliguric phase is the initial stage of AKI, typically lasting 10 to 14 days. This phase is marked by a significant reduction in urine output, usually less than 400 mL per day, indicating decreased kidney function. Fluid retention is a prominent feature, leading to symptoms such as edema, hypertension, and...
Renal Drug Excretion: Tubular Secretion01:28

Renal Drug Excretion: Tubular Secretion

Active tubular secretion is a robust, energy-demanding process that utilizes carrier systems to transport drugs into renal tubules. The active renal secretion systems include the organic anion transporter (OAT) for weak acids and the organic cation transporter (OCT) for weak bases. Structurally similar drugs can compete for the same transporter, potentially leading to drug accumulation and toxicity. However, this principle can be exploited therapeutically. One example is probenecid (Probalan),...
Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
Drug Elimination by Renal Route: Tubular Reabsorption01:22

Drug Elimination by Renal Route: Tubular Reabsorption

During the process of renal excretion, as the glomerular filtrate progresses to the distal convoluted tubule (DCT), drugs that are highly permeable, lipophilic, and nonionized undergo passive reabsorption from the tubular fluid into the surrounding peritubular capillaries. This reabsorption process restricts their elimination through the kidneys. However, the majority of drugs are either weak acids or weak bases, and their ionization level is dependent on pH. By altering the pH of urine, the...

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Updated: May 7, 2026

Isolation, Characterization, And High Throughput Extracellular Flux Analysis of Mouse Primary Renal Tubular Epithelial Cells
09:40

Isolation, Characterization, And High Throughput Extracellular Flux Analysis of Mouse Primary Renal Tubular Epithelial Cells

Published on: June 20, 2018

[Tubular renal acidosis].

A Seidowsky1, L Moulonguet-Doleris2, T Hanslik3

  • 1Université Versailles Saint-Quentin-en-Yvelines, 78000 Versailles, France; Service de médecine interne, hôpital Ambroise-Paré, AP-HP, 92104 Boulogne-Billancourt cedex, France; Service de néphrologie, hôpital Ambroise-Paré, AP-HP, 92104 Boulogne-Billancourt cedex, France.

La Revue De Medecine Interne
|September 28, 2013
PubMed
Summary
This summary is machine-generated.

Renal tubular acidosis (RTAs) are metabolic disorders affecting kidney tubules, leading to acid buildup. Treatment involves alkalinization to manage conditions like type I, II, and IV RTAs.

Keywords:
Acidose tubulaire distaleAcidose tubulaire proximaleDistal tubular renal acidosisNephrocalcinosisNéphrocalcinoseProximal tubular renal acidosisTrou anionique urinaireUrinary anionic gap

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Area of Science:

  • Nephrology
  • Internal Medicine
  • Pediatrics

Background:

  • Renal tubular acidosis (RTAs) encompass metabolic disorders characterized by metabolic acidosis and a normal plasma anion gap.
  • These conditions arise from impaired kidney tubule function, affecting acid-base balance.

Observation:

  • Three primary forms exist: proximal RTA (type II) due to bicarbonate reabsorption failure, and distal RTA (type I and IV) from impaired acid excretion.
  • Type IV RTA is frequently linked to hypoaldosteronism, while type I is associated with hypokalemia and type IV with hyperkalemia.

Findings:

  • RTA type II results from proximal tubule dysfunction in bicarbonate reabsorption.
  • Distal RTA (types I and IV) involves the inability to excrete daily acid loads, potentially causing hypokalemia (type I) or hyperkalemia (type IV).

Implications:

  • Complications include nephrocalcinosis and obstructive nephrolithiasis.
  • Alkalinization therapy is the fundamental treatment approach for all RTA types.
  • Understanding RTA subtypes is crucial for accurate diagnosis and targeted management.