Table 2 Evidence from studies involving the Gitelman’s Syndrome individuals in risk of nephropathy and T2DM

Yuan et al [32] (2017)

Case-control

Chinese

20

AUC glucose (mmol·h/L) ± SD = 17.4 ± 5.1; AUC insulin (μU·h/mL ± SD = 221.5 ± 128.1; ISSI±SD = 81,389 ± 34,680; QUICKI±SD = 0.6 ± 0.1;

GS/DN

This study reported abnormalities in glucose metabolism and insulin secretion in GS patients. It was also observed that the areas under the serum glucose curves were higher in the GS patients than those in the healthy controls (p = 0.02).

Tseng et al [35] (2012)

Follow-up

Taiwanese

NA

Female n = 47; Male n = 70; Duration of diabetes ± SD(years) = 23 ± 3; FBS ± SD = 131–225; S-Cr (mg/dl) ± SD = 2.2 ± 1.0

GS/DN

This study reported that a large proportion of GS-patients had triple SLC12A3 mutations. Also, these individuals showed an increased risk for the development of chronic kidney disease and T2DM.

Ren et al [33] (2013)

Case-control

Chinese

12

AUC glucose (mEq · h/L) = 16.1(IQR 12.5–25.4); AUC insulin (μU · h/mL) = 81.0 (IQR 58.9–138).

GS/DN

This study found that GS patients showed a higher glucose level compared with control group (p < 0.05).Also, Ren and colleagues observed that GS patients showed a delay of insulin secretion peak which was observed 120 min after a glucose load.

Balavoine et al [49] (2011)

Follow-up

French

5

Age (years) ± SD = 35 ± 15; BMI(kg/m2) ± SD = 24.3 ± 6.7; T2DM = 20% (3/15); S Cr (mg/l) ± SD = 8.2 ± 1.1.

GS/DN

In this study was found an increased susceptibility to glucose intolerance in GS heterozygous patients. Additionally, Balavoine and colleagues confirmed the presence of mutations of the SLC12A3 gene in 80% of cases.