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Fetal Exposure to Maternal Type 1 Diabetes Associated with Renal Dysfunction at Adult Age

Posted: Tuesday, November 09, 2010

Reduced functional reserve may reflect a reduced number of nephrons undergoing individual hyperfiltration. If so, offspring of Type 1 diabetic mothers may be predisposed to glomerular and vascular diseases.

In animal studies, hyperglycemia during fetal development reduces nephron numbers. Researchers tested whether this observation translates into renal dysfunction in humans by studying renal functional reserve in adult offspring exposed in utero to maternal Type 1 diabetes.

Nineteen nondiabetic offspring of Type 1 diabetic mothers were compared with 18 offspring of Type 1 diabetic fathers (control subjects). Glomerular filtration rate (51cr-EDTA clearance), effective renal plasma flow (123I-hippurate clearance), mean arterial pressure, and renal vascular resistances were measured at baseline and during amino acid infusion, which mobilizes renal functional reserve.

Offspring of Type 1 diabetic mothers were similar to control subjects for age (median 27, range 18–41, years), sex, BMI (23.1 ± 3.7 kg/m2), and birth weight (3,288 ± 550 vs. 3,440 ± 489 g). During amino acid infusion, glomerular filtration rate and effective renal plasma flow increased less in offspring of Type 1 diabetic mothers than in control subjects: from 103 ± 14 to 111 ± 17 ml/min (8 ± 13%) vs. from 108 ± 17 to 128 ± 23 ml/min (19 ± 7%, P = 0.009) and from 509 ± 58 to 536 ± 80 ml/min (5 ± 9%) vs. from 536 ± 114 to 620 ± 140 ml/min (16 ± 11%, P = 0.0035). Mean arterial pressure and renal vascular resistances declined less than in control subjects: 2 ± 5 vs. −2 ± 3% (P = 0.019) and 3 ± 9 vs. −14 ± 8% (P = 0.001).

Researchers found that fetal exposure to maternal Type 1 diabetes was associated with a reduced renal reserve in offspring of humans at adult age. Results in humans are consistent with what has been observed in rats regarding the impact of moderate hyperglycemia during fetal development on adult kidney dysfunction. They suggest a reduced number of nephrons in offspring of Type 1 diabetic mothers even though the precise quantification was not performed, as noninvasive methods are not currently available in humans.

In conclusion, this study supports that moderate hyperglycemia (or its related metabolic alterations) during fetal development may alter kidney function in human adults. As pregnancy is now common in Type 1 diabetic women, attention should be paid to the renal and vascular status of their offspring during adulthood.

Source: http://www.diabetesincontrol.com/index.php?option=com_content&view=article&id=10031&catid=1&Itemid=17, Diabetes Aug. 2010, doi: 10.2337/db10-0419

 
 
 
 
 
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