Renal functional reserve in IDDM patients.
The aim of this study was to determine whether renal functional reserve (RFR) is altered in insulin-dependent diabetic (IDDM) patients according to the stage of diabetic nephropathy. RFR was examined in 33 IDDM patients in similar glycaemic and metabolic control and compared to 12 healthy control subjects, during eight 1 h clearance periods prior to, during and after a 3-h stimulation by amino acid infusion (4.5 mg x kg(-1) x min[-1]). RFR was calculated as the difference between stimulated and baseline glomerular filtration rates (GFR). In 14 early normotensive diabetic patients with normal urinary albumin excretion, mean baseline GFR (133 +/- 3 ml x min(-1) x 1.73 m[-2]) was higher whereas RFR (10 +/- 4 ml x min(-1) x 1.73 m[-2]) was lower (p < 0.05) than in control subjects (113 +/- 4 and 28 +/- 2 ml x min(-1) x 1.73 m(-2), respectively). In 10 normotensive patients who had lived with IDDM for 16 years and who had microalbuminuria, baseline GFR and RFR (109 +/- 7 and 24 +/- 6 ml x min(-1) x 1.73 m(-2), respectively) were similar to those in control subjects. In 9 patients who had suffered IDDM for 23 years and had developed macroalbuminuria and hypertension, baseline GFR (78 +/- 8 ml x min(-1) x 1.73 m[-2]) was lower than in control subjects (p < 0.05) and RFR (8 +/- 4 ml x min(-1) x 1.73 m[-2]) was not significant. In addition, renal vascular resistance decreased significantly during infusion (p < 0.05) in microalbuminuric normotensive patients as well as in control subjects (by 9 +/- 4 and 11 +/- 4 mmHg x l(-1) x min(-1) x 1.73 m(-2), respectively) but not in normoalbuminuric normotensive or macroalbuminuric hypertensive patients. These results indicate that microalbuminuric normotensive patients retain a normal RFR, whereas RFR is reduced or suppressed at two opposite stages of the disease: in normoalbuminuric normotensive patients with a high GFR and in macroalbuminuric hypertensive patients with a decreased GFR. This dissimilar impairment reveals permanent glomerular hyperfiltration in both early IDDM without nephropathy and IDDM with overt diabetic nephropathy, but not in IDDM with incipient nephropathy.
Sackmann
H
H
Service d'Endocrinologie-Diabétologie, Rangueil University Hospital, Toulouse, France.
Tran-Van
T
T
Tack
I
I
Hanaire-Broutin
H
H
Tauber
J P
JP
Ader
J L
JL
D000328:Adult; D000419:Albuminuria; D000450:Aldosterone / Q000097:blood; D000596:Amino Acids / Q000493:pharmacokinetics; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D002096:C-Peptide / Q000097:blood; D003404:Creatinine / Q000378:metabolism; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000503:physiopathology; D003928:Diabetic Nephropathies / Q000503:physiopathology*; D004044:Dietary Proteins; D005260:Female; D005919:Glomerular Filtration Rate; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D007668:Kidney / Q000503:physiopathology*; D008297:Male; D012016:Reference Values; D012079:Renal Circulation; D012083:Renin / Q000097:blood; D014655:Vascular Resistance
D000450:Aldosterone; D000596:Amino Acids; D001786:Blood Glucose; D002096:C-Peptide; D003404:Creatinine; D004044:Dietary Proteins; D006442:Glycated Hemoglobin; D012083:Renin