Table 2.

Effect of environmental factors on kidney development and programming of renal dysfunction and blood pressure.

Factors	Phenotype	References
Maternal low-protein diet	LBW, decreased nephron number, and salt-sensitive hypertension	[16, 38, 55–58]
Maternal cigarette smoking	Hypertension	[59–63]
Alcohol use	Decreased nephron number	[64–67]
Steroids	Decreased nephron number and hypertension	[68–71]
Vitamin A deficiency	Rat-renal hypoplasia	[72]
Iron deficiency	Rat-decreased birth weight and hypertension Rat-decreased nephron number and hypertension	[73, 74]
High-salt diet	Rat-hypertension in an offspring, children-increased responsiveness of blood pressure to changes in dietary salt intake	[75, 76]
Glucocorticoid exposure	Decreased GFR and reduced number of nephrons hypertension	[56, 68, 77–79]
NSAIDs	Abnormal glomerular and tubular development	[80–82]
ACEi/ARBs	Renal tubular dysgenesis and hypotension	[83]
COX-2 exposure	Decreased nephron number and hypertension	[84, 85]
GRN363S	Obesity and increased insulin resistance	[86, 87]
GRER22/23K	Protect against insulin resistance	[88]
Testosterone	Decreased nephron number and proteinuria, hypertension	[82, 89]
Uteroplacental insufficiency	Renal hypoplasia	[36, 52, 90–92]

LBW: low birth weight, GFR: glomerular filtration rate, NSAIDS: nonsteroidal anti-inflammatory drugs, ACEi: angiotensin-converting enzyme inhibitors, ARBs: angiotensin receptor blockers, COX-2: cyclooxygenase-2, and GR: glucocorticoid receptor.