Sodium-lithium countertransport activity in red cells of patients with insulin dependent diabetes and nephropathy and their parents.
OBJECTIVE
To determine whether there are familial and genetic aspects of sodium-lithium countertransport activity in red cells in diabetic nephropathy.


METHODS
Case-control study.


METHODS
Teaching hospital diabetic clinic.


METHODS
40 Patients with insulin dependent diabetes, both of whose parents were alive: 20 with persistent proteinuria and 20 with normal albumin excretion matched for age, duration of diabetes, and body mass index. All 80 parents.


METHODS
Sodium-lithium countertransport activity in red cells and arterial blood pressure.


RESULTS
Sodium-lithium countertransport activity in red cells was higher in the patients with proteinuria than in the patients with normoalbuminuria (mean (95% confidence interval) 0.47 (0.39 to 0.54) v 0.33 (0.28 to 0.38) mmol/l red cells/h respectively, p = 0.0036; mean difference 0.14 (0.04 to 0.22)). The mean countertransport activity for the two parents of each patient was calculated, and from this the mean value for each group of parents was calculated; the value was higher in the parents of the patients with proteinuria than in the parents of the patients with normoalbuminuria (0.40 (0.32 to 0.48) v 0.30 (0.26 to 0.33) mmol/l red cells/h respectively, p = 0.016; 0.10 (0.02 to 0.19)). Twenty-eight of the parents of the patients with proteinuria compared with 12 of the parents of the patients with normoalbuminuria had a countertransport activity that was above the median value in all 80 parents (p less than 0.001). Mean arterial blood pressure in the parents of the patients with proteinuria was related to that of their offspring (r = 0.46; p less than 0.01). There was a positive correlation between the sodium-lithium countertransport activity in red cells in the parents and their offspring when all parents and patients were considered (r = 0.37; p less than 0.001).


CONCLUSIONS
Increased sodium-lithium countertransport activity in red cells in the parents of diabetic patients with nephropathy provides further evidence that familial, and possibly genetic, factors related to a predisposition to arterial hypertension have a role in the susceptibility of diabetic renal disease.
Walker
J D
JD
Unit for Metabolic Medicine, United Medical School, Guy's Hospital, London.
Tariq
T
T
Viberti
G
G
D000293:Adolescent; D000328:Adult; D000419:Albuminuria / Q000097:blood; D001693:Biological Transport, Active; D001794:Blood Pressure / Q000502:physiology; D016022:Case-Control Studies; D003922:Diabetes Mellitus, Type 1 / Q000150:complications / Q000235:genetics; D003928:Diabetic Nephropathies / Q000097:blood / Q000235:genetics*; D004912:Erythrocytes / Q000378:metabolism*; D005260:Female; D005919:Glomerular Filtration Rate / Q000502:physiology; D006801:Humans; D008094:Lithium / Q000097:blood*; D008297:Male; D011507:Proteinuria / Q000097:blood / Q000235:genetics; D012964:Sodium / Q000097:blood*
D008094:Lithium; D012964:Sodium