Creatinine plays a key role in the function and maturation of fetal kidneys throughout pregnancy. It is important to identify other markers that may help in the diagnosis of renal dysfunction. Our aim was to determine the profile of and the correlation between biochemical markers to be used to assess renal function and maturation of the fetus in the amniotic fluid during pregnancy and to determine the distribution of normal values for creatinine, N-acetyl-ß-D-glucosaminidase (NAG), ß2-microglobulin, glucose, urea, sodium, potassium, phosphorus, calcium, uric acid, albumin, and osmolality in three gestational age groups. This was a cross-section study that assessed 115 samples of amniotic fluid during three different periods of pregnancy, i.e., 13 to 20, 27 to 34, and 36 to 42 weeks. Concentrations of creatinine, NAG, urea, potassium and uric acid increased during pregnancy (P<0.05). ß2-Microglobulin, glucose, sodium, phosphorus, calcium, and albumin concentration and osmolality decreased (P<0.05), whereas ß2-microglobulin, glucose and uric acid presented significant correlations with gestational age and creatinine, respectively (r>0.6, P<0.05). Urea, potassium and phosphorus showed mild correlations with both (r>0.5, P<0.05). NAG, sodium, albumin and osmolality did not show significant correlations (r<0.5, P<0.05). These tests confirmed the important role of creatinine in terms of correlation with gestational age. ß2-Microglobulin, glucose and uric acid were significant as markers of function and maturation of fetal kidneys, whereas NAG did not demonstrate a useful role for the assessment of renal maturation.

Background/Aim: Diabetes and mesangial stretch caused by hypertension increase mesangial matrix deposition which is induced by local production of transforming growth factor beta 1 (TGF-β1). Both conditions are associated with cortical GLUT1 overexpression. We evaluated the effect of genetically determined hypertension and its association with diabetes on urinary TGF-β1 and cortical GLUT1 and GLUT2 expression. Methods: We studied Wistar-Kyoto rats (controls, C) and spontaneously hypertensive rats (SHR), weighing ∼210 g, 30 days after the injection of streptozotocin (diabetic, D) or citrate buffer (10 C, 9 SHR, 12 C-D and 15 SHR-D). Twenty-four-hour urine was collected for glucose, albumin, and TGF-β1 determinations. Catheters were implanted into the femoral artery to measure the arterial blood pressure in conscious animals 1 day later. Then GLUT1 and GLUT2 protein levels (Western blotting) in renal cortex and medulla were evaluated. Results: The cortical GLUT1 levels were 5, 2, and 7 times higher in SHR, C-D, and SHR-D groups versus C group (p < 0.05); the GLUT2 contents were 1.5, 1.8, and 2.3 times higher in SHR, C-D and SHR-D groups versus C group (p < 0.05). The urinary TGF-β1 level was elevated by diabetes and diabetes and hypertension, but not by hypertension alone: 1.39 ± 0.2, 2.34 ± 0.6, 18.2 ± 3.2, and 28.8 ± 7.6 ng/24 h, respectively, in C, SHR, C-D, and SHR-D groups (p < 0.05). Conclusions: Diabetes, hypertension, and especially their association increase the renal cortical GLUT1 and GLUT2 levels. The magnitude of GLUT1 overexpression caused by hypertension is higher than that induced by diabetes alone. The impact on urinary TGF-β1 occurs when diabetes and hypertension are associated, suggesting an effect that is triggered in the presence of GLUT1 overexpression and hyperglycemia.

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