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Nephrons01:10

Nephrons

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 happens...
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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...
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Poliomyelitis

Poliomyelitis is caused by poliovirus, a small, non-enveloped, positive-sense RNA virus of the Picornaviridae family and Enterovirus genus. Transmission occurs primarily via the fecal-oral route, often through ingestion of contaminated water or food. The virus initially replicates in the oropharynx and intestinal mucosa, particularly in lymphoid tissues such as the tonsils, Peyer’s patches, and regional lymph nodes. Primary viremia follows, allowing dissemination throughout the body.In most...
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...
Nephrotic Syndrome I : Introduction01:24

Nephrotic Syndrome I : Introduction

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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...

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Measurement of BK-polyomavirus Non-Coding Control Region Driven Transcriptional Activity Via Flow Cytometry
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Published on: July 13, 2019

Polyomavirus nephropathy.

Emilio Ramos1, Cinthia Drachenberg

  • 1Department of Medicine, Division of Nephrology, University of Maryland School of Medicine, Maryland, USA.

Saudi Journal of Kidney Diseases and Transplantation : an Official Publication of the Saudi Center for Organ Transplantation, Saudi Arabia
|January 19, 2008
PubMed
Summary
This summary is machine-generated.

A latent urinary tract virus, Polyomavirus, reactivates in renal transplant patients due to immunosuppression. This Polyomavirus nephropathy causes significant kidney dysfunction and graft loss, necessitating further research for effective antiviral treatments.

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Area of Science:

  • Nephrology
  • Virology
  • Transplantation Immunology

Background:

  • Polyomavirus is a latent virus typically found in the urinary tract.
  • Potent immunosuppression in renal transplant recipients can lead to Polyomavirus reactivation.
  • Reactivation occurs within the allograft kidney, leading to significant complications.

Purpose of the Study:

  • To highlight the re-emergence and impact of Polyomavirus in renal transplant patients.
  • To underscore the link between Polyomavirus reactivation and renal allograft dysfunction.
  • To emphasize the need for further research into Polyomavirus pathogenicity and treatment.

Main Methods:

  • Observational analysis of renal transplant patients.
  • Histopathological examination for Polyomavirus nephropathy.
  • Clinical assessment of renal function and graft outcomes.

Main Results:

  • Polyomavirus reactivation was observed in renal allografts.
  • Overt renal dysfunction occurred in 40-70% of affected patients.
  • Histologically confirmed Polyomavirus nephropathy led to graft loss in a significant proportion of cases.

Conclusions:

  • Polyomavirus reactivation is a serious complication in renal transplant recipients.
  • Polyomavirus nephropathy significantly contributes to renal dysfunction and graft loss.
  • Further research is crucial to understand Polyomavirus pathogenicity and develop antiviral therapies.