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Related Concept Videos

Chronic Kidney Disease II: Clinical Manifestations01:24

Chronic Kidney Disease II: Clinical Manifestations

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...
Diabetic Nephropathy01:28

Diabetic Nephropathy

Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...
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...
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...
Acute Kidney Injury I: Introduction01:22

Acute Kidney Injury I: Introduction

Introduction:Acute Kidney Injury (AKI) describes a swift decrease in kidney function occurring over hours to days, characterized by the kidneys' failure to remove waste products from the bloodstream. This leads to dangerous complications like metabolic acidosis, fluid overload, and electrolyte imbalances, such as hyperkalemia, which can cause life-threatening arrhythmias. AKI is common in both hospital and outpatient settings, often triggered by dehydration, sepsis, or exposure to nephrotoxic...
Chronic Kidney Disease I: Introduction01:25

Chronic Kidney Disease I: Introduction

Chronic Kidney Disease (CKD) arises when the kidneys progressively lose their ability to function, ultimately leading to end-stage renal disease. At this advanced stage, the kidneys can no longer filter waste or maintain essential body functions, requiring renal replacement therapy (RRT) through dialysis or a kidney transplant for survival.Early-stage chronic kidney disease and detection challengesIn CKD's early stages, symptoms often remain absent because healthy nephrons compensate for...

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Related Experiment Video

Updated: May 10, 2026

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat
08:50

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat

Published on: July 3, 2013

[Contrast-induced nephropathy].

A Humbert1, S Kissling, D Teta

  • 1Service de néphrologie et consultation d'hypertension, Département de médecine interne, CHUV, 1011 Lausanne. antoine.humbert@chuv.ch

Revue Medicale Suisse
|June 27, 2013
PubMed
Summary
This summary is machine-generated.

Contrast-induced nephropathy, a cause of hospital-acquired acute kidney injury, can be prevented with intravenous fluids. Sodium bicarbonate may be more effective than saline for preventing contrast-induced nephropathy.

Related Experiment Videos

Last Updated: May 10, 2026

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat
08:50

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat

Published on: July 3, 2013

Area of Science:

  • Nephrology
  • Radiology
  • Pharmacology

Context:

  • Contrast-induced nephropathy (CIN) is a significant cause of hospital-acquired acute kidney injury.
  • Patients with specific risk factors are particularly susceptible to CIN, which increases morbidity and mortality.
  • Effective prevention strategies for CIN are crucial in clinical practice.

Purpose:

  • To review the current evidence on the prevention of contrast-induced nephropathy.
  • To compare the efficacy of different intravenous fluid strategies for CIN prevention.
  • To evaluate the role of N-acetylcysteine in CIN prophylaxis.

Summary:

  • Volume expansion with intravenous fluids, specifically sodium chloride 0.9% or sodium bicarbonate 1.4%, is the primary method for preventing contrast-induced nephropathy.
  • Comparative randomized controlled trials suggest a potential benefit of sodium bicarbonate over saline in preventing CIN.
  • Current evidence indicates that N-acetylcysteine does not offer additional protective benefits when used with intravenous fluids for CIN prevention.

Impact:

  • Highlights the importance of appropriate fluid management in patients undergoing procedures with contrast media.
  • Suggests a preferred intravenous fluid (sodium bicarbonate) for CIN prevention based on available evidence.
  • Informs clinical decision-making regarding the use of N-acetylcysteine, advising against its routine use for CIN prophylaxis.