The Brenner Hypothesis–developed by Barry Brenner of the Brigham and Women’s Hospital, author of the well-known Brenner & Rector “The Kidney” textbook–states that individuals with a congenital reduction in nephron number have a much greater likelihood of developing adult hypertension and subsequent renal failure. This hypothesis is supported by the observation that there is a strong epidemiologic relationship between intrauterine growth retardation (IUGR)/low birth weight and adult hypertension. The mechanistic explanation for this phenomenon is that compensatory hyperfiltration by the remaining nephrons–similar to what happens in diabetic nephropathy–results in accelerated renal decline. While this theory is appealing at several levels, it does not explain everything: for instance, why most kidney transplant donors, who instantaneously lose 50% of their nephron mass, for the most part do well post-transplant without developing hypertension or renal disease.
The Brenner Hypothesis is part of a larger body of work which posits that many common adult diseases (including diabetes and hypertension) are caused by factors which are established during early growth and development, the “fetal origins of adult disease” hypothesis.
Originally posted by Nate Hellman
Define Hypothesis, what is Hypothesis? Define Hypothesis Testing, null Hypothesis,
Hypertension in renal disease is a compensatory response to kidney damage, linked to sympathetic nervous system hyperactivity, as authors like Converse, Campese and Ye state in many of their works.
This is what has led to the hypothesis of the clinical usefulness of renal denervation in CKD, Hypertension and CHF.
And this also may be an explanation to why Renal Transplant donors don't develop Arterial Hypertension.