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Related Concept Videos

Renal Regulation of Acid-Base Balance01:29

Renal Regulation of Acid-Base Balance

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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...
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Renal Drug Excretion: Effect of Urine pH, Flow Rate, and Drug pKa01:22

Renal Drug Excretion: Effect of Urine pH, Flow Rate, and Drug pKa

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The pH of urine, the drug's pKa, and the urine flow rate are vital parameters for drug reabsorption and excretion. Urinary pH varies between 4.6 and 8.0 and is influenced by diet, drug intake, and the patient's pathophysiology. It affects a drug's ionization state and reabsorption. For instance, carbohydrate-rich food produces alkaline urine promoting drug excretion, while proteins and certain medications like ascorbic acid lead to acidic urine enhancing reabsorption.
The pKa of a...
167
Diagnosing Acidosis and Alkalosis01:24

Diagnosing Acidosis and Alkalosis

220
Diagnosing acid-base imbalances involves systematically analyzing arterial blood samples, focusing on three key measurements: pH, bicarbonate (HCO3−) concentration, and carbon dioxide partial pressure (PCO2). This analysis follows a four-step process that helps identify the imbalance's underlying cause and nature.
First, the pH level is assessed to determine whether the blood pH is normal (7.35–7.45), low (acidosis), or high (alkalosis).
Next, the PCO2  and...
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Antihypertensive Drugs: Potassium-Sparing Diuretics01:28

Antihypertensive Drugs: Potassium-Sparing Diuretics

545
Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...
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Dialysis01:27

Dialysis

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Renal failure occurs when the kidneys lose their ability to filter waste products from the blood effectively. It can be classified into two types: acute renal failure (ARF) and chronic renal failure (CRF).
Acute kidney injury develops suddenly and can be caused by pre-renal causes (e.g., hypovolemia, shock), intrinsic renal causes (e.g., acute tubular necrosis), or post-renal causes (e.g., urinary obstruction). In contrast, chronic renal failure progresses gradually over time and is often...
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Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

429
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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A basic solution for a complex problem: does treatment of metabolic acidosis slow CKD progression?

Kevin Bodker1, Natalie Freidin1, Nayan Arora2

  • 1Medical University of South Carolina.

Current Opinion in Nephrology and Hypertension
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Routine treatment of metabolic acidosis in chronic kidney disease (CKD) patients is not supported by current evidence. Recent studies challenge earlier findings, suggesting alkali therapy may not slow CKD progression.

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Area of Science:

  • Nephrology
  • Internal Medicine
  • Clinical Practice Guidelines

Background:

  • Metabolic acidosis is common in chronic kidney disease (CKD), with prevalence increasing as kidney function declines.
  • Alkali therapy to normalize serum bicarbonate and slow CKD progression is a long-standing practice, based on animal models and controversial clinical trials.

Conclusions:

  • The current literature does not support the routine treatment of metabolic acidosis in patients with CKD.
  • Authors concur with upcoming KDIGO guidelines to de-emphasize this common practice.
  • Further research may be needed to clarify the role of alkali therapy in specific CKD populations.