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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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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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5/6 Nephrectomy Using Sharp Bipolectomy Via Midline Laparotomy in Rats
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Acute phosphate nephropathy.

Frank P Hurst1, Kevin C Abbott

  • 1Nephrology Service, Walter Reed Army Medical Center, Washington, DC 20307, USA. frank.hurst@us.army.mil

Current Opinion in Nephrology and Hypertension
|July 29, 2009
PubMed
Summary
This summary is machine-generated.

Acute phosphate nephropathy (APN) linked to oral sodium phosphate (OSP) bowel purgatives presents diagnostic challenges. Further research is crucial to understand APN pathophysiology and identify at-risk populations.

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Published on: December 19, 2011

Area of Science:

  • Nephrology
  • Gastroenterology
  • Clinical Pathology

Background:

  • Acute phosphate nephropathy (APN) is a recognized complication following oral sodium phosphate (OSP) bowel purgative use.
  • Biopsy-confirmed APN cases exhibit bland urinary sediment, mild proteinuria, and elevated creatinine levels.
  • Prospective diagnosis of APN is challenging due to the invasive nature of renal biopsy, which is infrequently performed for such clinical presentations.

Purpose of the Study:

  • To review the identification and characteristics of acute phosphate nephropathy (APN) in patients exposed to oral sodium phosphate (OSP) bowel purgatives.
  • To evaluate the challenges in prospective diagnosis of APN.
  • To discuss the implications of APN on OSP product usage and regulatory actions.

Main Methods:

  • Review of observational studies assessing acute kidney injury (AKI) after OSP exposure using creatinine changes as a surrogate for APN.
  • Analysis of existing literature on biopsy-confirmed APN cases.
  • Examination of regulatory actions and market withdrawals related to OSP products.

Main Results:

  • Observational studies using creatinine changes as a surrogate for APN have yielded conflicting results regarding the incidence of AKI after OSP exposure.
  • Previous studies have been unable to definitively quantify the overall risk of APN associated with OSP compared to alternative bowel preparation agents.
  • The association between APN and OSP has led to regulatory warnings and cessation of production for certain OSP products.

Conclusions:

  • The current diagnostic approach for APN is limited, necessitating further research.
  • More studies are required to elucidate the pathophysiology of APN.
  • Identifying specific patient subsets at higher risk for developing APN is essential for preventative strategies.