Related Experiment Video

Updated: Jul 14, 2026

A High-throughput Method for Measurement of Glomerular Filtration Rate in Conscious Mice
07:07

A High-throughput Method for Measurement of Glomerular Filtration Rate in Conscious Mice

Published on: May 10, 2013

Diabetes-induced hyperfiltration in adenosine A(1)-receptor deficient mice lacking the tubuloglomerular feedback

J Sällström1, P-O Carlsson, B B Fredholm

  • 1Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.

Acta Physiologica (Oxford, England)
|June 22, 2007
PubMed
Abstract

Insights

Diabetic kidney disease involves glomerular hyperfiltration, potentially linked to tubuloglomerular feedback (TGF). This study in adenosine A(1)-receptor knockout mice shows TGF is not the primary driver of this early diabetic nephropathy complication.

Area of Science:

  • Nephrology
  • Endocrinology
  • Physiology

Background:

  • Glomerular hyperfiltration is an early indicator of diabetic nephropathy.
  • The tubuloglomerular feedback (TGF) mechanism is hypothesized to cause hyperfiltration via altered macula densa signaling.

Purpose of the Study:

  • To investigate the role of the TGF mechanism in diabetes-induced glomerular hyperfiltration.
  • To assess if blocking TGF by deleting the adenosine A(1)-receptor (A1AR) affects hyperfiltration in diabetic mice.

Main Methods:

  • Diabetes was induced using alloxan in wild-type and A1AR knockout mice.
  • Glomerular filtration rate (GFR) was measured by inulin clearance.
  • Urinary electrolytes and histological changes were evaluated.

Main Results:

  • Diabetic A1AR knockout mice exhibited similar glomerular hyperfiltration as diabetic wild-type mice.
  • Hyperglycemia was confirmed in alloxan-treated animals.
  • No significant differences in glomerular volume or interstitial fibrosis were observed between genotypes.

Conclusions:

  • The TGF mechanism, mediated by A1AR, is not the primary cause of diabetes-induced glomerular hyperfiltration.
  • Glomerular hyperfiltration in this model is independent of the TGF pathway and not related to changes in glomerular filtration area.

More Related Videos

Assessment of Kidney Function in Mouse Models of Glomerular Disease09:16

Assessment of Kidney Function in Mouse Models of Glomerular Disease

Published on: June 30, 2018

A Murine Model of Hemodialysis Access-Related Hand Dysfunction08:39

A Murine Model of Hemodialysis Access-Related Hand Dysfunction

Published on: May 31, 2022

Related Concept Videos

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...
Diabetes Insipidus II: Pathophysiology01:22

Diabetes Insipidus II: Pathophysiology

Normally, water balance is maintained through three interconnected mechanisms: the hypothalamic thirst center, the synthesis and release of antidiuretic hormone (ADH, or vasopressin), and the kidneys' responsiveness to this hormone. ADH is synthesized in the hypothalamus, released from the posterior pituitary, and acts on the distal nephron, allowing water reabsorption and concentrated urine production.Diabetes Insipidus and Its TypesIn diabetes insipidus (DI), this regulatory system is...
Diabetes Insipidus I: Introduction01:29

Diabetes Insipidus I: Introduction

Definition Diabetes insipidus is a disorder marked by the production of large amounts of dilute urine because of impaired vasopressin production, release, or kidney response. The lack of effective vasopressin action limits water reabsorption in the renal collecting ducts, which leads to excessive urinary water loss and intense thirst.Clinical PresentationIndividuals with diabetes insipidus report persistent thirst and very high urine output. In severe cases, fluid intake can reach up to 20...
Glomerular Filtration Rate and its Regulation01:28

Glomerular Filtration Rate and its Regulation

The Glomerular Filtration Rate (GFR) is a measure of kidney function, reflecting the volume of filtrate formed per minute in the kidneys. On average, GFR is approximately 125 mL/min in males and 105 mL/min in females. Maintaining a relatively constant GFR is essential for the kidneys to effectively regulate body fluid homeostasis and maintain extracellular stability.
GFR regulation involves two primary intrinsic controls: the myogenic and tubuloglomerular feedback mechanisms.
The myogenic...
Antihypertensive Drugs: Action of Diuretics01:16

Antihypertensive Drugs: Action of Diuretics

Diuretics are antihypertensive drugs used to treat hypertension resulting from sodium and water retention. Sodium, vital for fluid balance and nerve or muscle function, is regulated by the kidneys through millions of nephrons. Blood enters nephrons via afferent arterioles, which branch into capillaries called glomeruli. These filter blood plasma, allowing water and solutes, like sodium ions, to pass through capillary walls into Bowman's capsule. The filtrate then flows through various tubules...
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...