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Related Concept Videos

Urinary Tract Calculi II: Pathophysiology and Clinical Manifestations01:26

Urinary Tract Calculi II: Pathophysiology and Clinical Manifestations

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Renal calculi, commonly termed kidney stones, are crystalline solid masses that form in the kidneys but can occur at any point within the urinary system, encompassing the kidneys, ureters, bladder, and urethra.The pathophysiology of renal stones involves several key factors: supersaturation of the urine with stone-forming constituents, changes in urine pH, a decrease in urine volume, and the presence of substances that promote or inhibit stone formation.Supersaturation of Urine: This is the...
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Renal Corpuscle01:20

Renal Corpuscle

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The glomerulus and Bowman's capsule are two essential components of the nephron, which is the functional unit of the kidney. These microscopic structures play a critical role in the process of blood filtration to produce urine.
Glomerulus: Structure and Function
The glomerulus is a tiny, intricate network of capillaries located at the beginning of the nephron. It's enveloped by the Bowman's capsule and receives its blood supply from an afferent arteriole, which divides into numerous...
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Urinary Tract Calculi I: Introduction01:28

Urinary Tract Calculi I: Introduction

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Renal calculi, or kidney stones, are solid deposits of minerals and salts formed inside the kidneys. In medical terminology, "calculus" refers to the stone itself, while "lithiasis" describes the process of stone formation. Depending on their location within the urinary system, these stones may be classified as either urolithiasis, when situated within the urinary tract, or nephrolithiasis, when located within the kidneys. Each term signifies the specific impact of the stone.Predisposition...
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Nephrons01:10

Nephrons

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The kidneys are intricate organs with millions of working units known as nephrons. Each nephron features two major structures: the renal corpuscle, which facilitates blood plasma filtration, and the renal tubule, which handles the glomerular filtrate. Blood supply is directly linked to the nephrons. The renal corpuscle consists of the glomerulus, a capillary network, and the Bowman's capsule, a double-walled epithelial structure that encases the glomerulus. The filtering of blood plasma...
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Chronic Kidney Disease II: Clinical Manifestations01:24

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Chronic Kidney Disease (CKD) progressively impairs multiple body systems due to the accumulation of uremic toxins, which disrupt cellular functions across various organs.Neurologic symptomsNeurologic symptoms often arise early in CKD, as uremic toxin buildup drives changes in cognitive and motor functions. Patients frequently experience fatigue, headache, confusion, difficulty concentrating, and, in severe cases, seizures. Peripheral neuropathy commonly manifests as burning sensations in the...
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Nephrotic Syndrome I : Introduction01:24

Nephrotic Syndrome I : Introduction

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Nephrotic Syndrome is a chronic kidney disorder defined by clinical findings such as severe proteinuria, hypoalbuminemia, hyperlipidemia, and edema. These symptoms result from damage to the glomeruli, the kidney’s filtering units, increasing their permeability to proteins.Definition and Meaning:Proteinuria, defined as the loss of more than 3.5 grams of protein per day in adults, is a crucial feature of nephrotic syndrome. This condition is often accompanied by edema, the accumulation of...
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Estimation of Urinary Nanocrystals in Humans using Calcium Fluorophore Labeling and Nanoparticle Tracking Analysis
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[Bilateral nephrocalcinosis: primary hyperoxaluria involved].

T Deprez1, M Sempels2

  • 1Étudiant Master 3 Médecine, ULiège, Belgique.

Revue Medicale De Liege
|August 4, 2022
PubMed
Summary
This summary is machine-generated.

Primary hyperoxaluria type 1 causes oxalate overproduction due to a deficiency in alanine-glyoxylate transaminase (AGT). This rare genetic disorder can lead to kidney failure, but new treatments like lumasiran offer hope.

Keywords:
LumasiranNephrocalcinosisOxalosisUrolithiasisPrimary hyperoxaluria type 1

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Area of Science:

  • Biochemistry
  • Genetics
  • Nephrology

Background:

  • Primary hyperoxaluria type 1 (PH1) is a rare, autosomal recessive metabolic disorder.
  • It results from a deficiency in the liver enzyme alanine-glyoxylate transaminase (AGT), leading to oxalate overproduction.
  • Accumulated oxalate causes oxalosis, systemic deposition of calcium oxalate crystals, primarily affecting the kidneys.

Observation:

  • The disease often presents with urinary issues, and without timely intervention, can progress to end-stage renal failure.
  • Historically, combined liver-kidney transplantation was the only etiological treatment, restoring AGT function and replacing damaged kidneys.
  • Recent research has focused on novel therapeutic strategies, including pharmacological interventions.

Findings:

  • Lumasiran, a new drug, has shown promising results in managing PH1.
  • This clinical case explores various therapeutic management options for PH1.
  • The study highlights the evolving treatment landscape for this rare genetic condition.

Implications:

  • Advances in treatment, such as lumasiran, may offer alternatives to transplantation for PH1 patients.
  • Early diagnosis and intervention are crucial to prevent severe renal complications.
  • Further research into PH1 management is essential to improve patient outcomes and quality of life.