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Endogenous ANP in postischemic acute renal allograft failure
O Vinot1, J Bialek, S Canaan-Kühl
1Division of Nephrology, Stanford University School of Medicine, California 94305-5114, USA.
The American Journal of Physiology
|July 11, 1995
Summary
In renal transplant recipients, elevated atrial natriuretic peptide (ANP) did not improve kidney function despite normal ANP receptors. This suggests constricted blood vessels in the kidney are unresponsive to ANP in acute renal failure.
Area of Science:
- Nephrology
- Transplantation Immunology
- Cardiovascular Physiology
Background:
- Atrial natriuretic peptide (ANP) plays a role in regulating renal function.
- Post-transplant acute kidney injury is a significant clinical challenge.
Purpose of the Study:
- To investigate the role of ANP in renal transplant recipients with prompt versus delayed allograft function.
- To determine if ANP levels and glomerular receptor density correlate with kidney function after transplantation.
Main Methods:
- Measured circulating ANP and guanosine 3',5'-cyclic monophosphate (cGMP) levels in renal transplant recipients.
- Assessed glomerular ANP receptor density via autoradiography in allograft biopsies.
- Correlated these measurements with glomerular filtration rate (GFR) and renovascular resistance.
Main Results:
- Subjects with delayed allograft function showed higher renovascular resistance and lower GFR.
- Plasma ANP and glomerular ANP receptor density were similar in both groups initially and at day 3 post-transplant.
- Despite rising ANP levels, delayed function group had higher cGMP levels and fractional clearance, indicating impaired signaling.
Conclusions:
- Elevated ANP levels do not improve renal function or alleviate vasoconstriction in transplant recipients with postischemic acute renal failure.
- Glomerular ANP receptors are present, but the afferent arterioles appear unresponsive to ANP's vasorelaxant effects in this condition.