Congenital Nephron Deficit and Chronic Kidney Disease

Mahmoud Kallash, Tyrus Stewart, Randall Craver, Vesa Matti Vehaskari


Background: Congenitally low nephron number, often associated with low birth weight, has been shown to be a risk factor for hypertension and cardiovascular disease in humans. Epidemiological studies have also linked it to development of chronic kidney disease (CKD) but this has been difficult to verify experimentally. Previously, we showed that rats with congenitally low nephron number did not develop CKD by 11 months of follow-up. In this study, we tested the hypothesis that animals with congenital nephron deficit have a higher risk for development of kidney disease when exposed to postnatal insults.

Methods: Pregnant Sprague-Dawley rats were exposed to low protein (LP) versus control diet to induce decreased nephron numbers. Offspring from each group were either stressed by unilateral nephrectomy (UN) and high salt diet (HS), or exposed to standard salt diet and sham surgery.

Results: Forty-two percent of stressed animals in both C and LP groups died of renal failure compared to no mortality in non-stressed animals (P = 0.0001). By 6 months of age, non-stressed LP animals did not develop significant renal disease. However, stressed LP animals had significant decrease in kidney function (P = 0.033), high albumin excretion (P = 0.012), and extensive renal histologic damage. The changes tended to be more severe in males.

Conclusions: Congenital low nephron number in our model does not result in CKD by 6 months of life. However, they have increased risk for development of CKD when exposed to postnatal insults, and the risk depends on the severity of deficit.

World J Nephrol Urol. 2013;2(2):47-54


Congenital nephron deficit; High salt diet; Kidney disease; Low birth weight

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