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Related Concept Videos

Diabetic Nephropathy01:28

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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...
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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...
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Pyelonephritis is a bacterial infection that primarily affects the renal parenchyma and collecting system, including the renal pelvis, tubules, and interstitial tissue of one or both kidneys. It can be classified as either acute—a sudden, severe infection—or chronic, which refers to long-term or recurrent kidney infections.The primary cause of acute pyelonephritis (APN) is bacterial infection, with Escherichia coli accounting for approximately 70-80% of cases. Other bacteria, such as Proteus,...
Nephrons01:10

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Chronic Kidney Disease I: Introduction01:25

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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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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...

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Acute phosphate nephropathy.

Glen S Markowitz1, Mark A Perazella

  • 1Department of Pathology, Columbia University Medical Center, New York, New York 10032, USA. gsm17@columbia.edu

Kidney International
|August 14, 2009
PubMed
Summary
This summary is machine-generated.

Acute phosphate nephropathy (APhN) is kidney damage from oral sodium phosphate (OSP) purgatives. Avoiding OSP in high-risk patients and ensuring hydration are key prevention strategies.

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Direct Detection of the Acetate-forming Activity of the Enzyme Acetate Kinase
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05:51

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Published on: December 19, 2011

Area of Science:

  • Nephrology
  • Gastroenterology
  • Pathology

Background:

  • Acute phosphate nephropathy (APhN) is a serious kidney condition linked to oral sodium phosphate (OSP) bowel purgatives.
  • It can lead to both acute and chronic renal failure, with biopsy findings showing tubular injury and calcium phosphate deposits.

Purpose of the Study:

  • To review the clinical and pathological characteristics of APhN.
  • To identify risk factors and understand the pathomechanism of OSP-induced kidney injury.
  • To discuss prevention strategies for APhN.

Main Methods:

  • Review of biopsy-proven APhN cases.
  • Analysis of existing epidemiologic studies on OSP and acute kidney injury (AKI).
  • Synthesis of information on risk factors and pathomechanisms.

Main Results:

  • 37 biopsy-proven APhN cases reported.
  • Risk factors include older age, female gender, hypertension, CKD, and use of ACE inhibitors, ARBs, and diuretics.
  • Pathomechanism involves hypovolemia, high distal phosphate load, and calcium phosphate precipitation.

Conclusions:

  • OSP tablets remain available despite the withdrawal of OSP solutions.
  • Prevention is crucial, focusing on avoiding OSP in high-risk individuals.
  • Strategies include aggressive hydration and dose minimization.