scholarly journals Glurenorm in diabetic nephropathy: effects on renal function and vascular endothelium

1996 ◽  
Vol 42 (2) ◽  
Author(s):  
M. V. Shestakova ◽  
M. Sh. Shamkhalova ◽  
T. T. Ukhanova ◽  
M. G. Ryndina ◽  
I. I. Dedov

Study of the effects of glurenorm, an oral sugar- reducing drug, on renal function and vascular endothelium in patients with noninsulin-dependent diabetes mellitus at different stages of diabetic involvement of the kidneys, including those with chronic renal insufficiency, revealed that glurenorm in therapeutic doses had no nephrotoxic effect; moreover, it maintained the filtration function of the kidneys even in patients with the initial stage of chronic renal insufficiency (with blood serum creatinine of up to 200 mmol/liter. Therapy with glurenorm for 3 and 6 months caused a reliable reduction of the production of thromboxane A, a vasoconstrictor, this probably improving the intrarenal hemodynamics, and exerting an antiproteinuric effect in patients with manifest diabetic nephropathy. At the same time, glurenorm therapy did not appreciably influence the production of factors released by vascular endothelium (prostacyclin and endothelin-1). Hence, a detailed study of renal function and vascular endothelium in patients with type II diabetes demonstrated that administration of glurenorm to patients with manifest renal involvement was not only safe, but even favorably affected the intrarenal hemodynamics and had an antiproteinuric effect.

1997 ◽  
Vol 43 (6) ◽  
pp. 17-20
Author(s):  
Yu. I. Grinshtein ◽  
S. V. Ivliev ◽  
N. B. Osetrova ◽  
S. S. Ilyenkov

The conjunctival bloodflow was examined in patients with diabetic nephropathy with different status of renal function and changes in the microcirculatory bed assessed after endovascular laser therapy. Twenty-five donors and twenty-one patients with medium-severe and grave type I diabetes complicated by diabetic nephropathy were followed up. Microcirculatory disorders in the eyeball conjunctiva progressed as renal function deteriorated, which was evident from a reliable increase of the total conjunctival index in parallel with the progress of chronic- renal insufficiency. A course of endovascular laser therapy reliably improved the microcirculation: the arterio-venular coefficient increased and the total conjunctival index decreased in patients with latent and conservatively curable stages of chronic renal insufficiency due to normalization of vascular tone, boosting of the bloodflow, and decrease of red cell sludging.


1986 ◽  
Vol 70 (5) ◽  
pp. 501-505 ◽  
Author(s):  
C. D. Mistry ◽  
C. J. Lote ◽  
R. Gokal ◽  
W. J. C. Currie ◽  
M. Vandenburg ◽  
...  

1. The renal effects of therapeutic doses of sulindac were studied in nine patients with stable renal insufficiency, mean creatinine clearance 37.0 ± 2.2 ml min−1 1.73 m−2 (range 24.7–54.6 ml min−1 1.73 m−2). 2. Nine days' treatment with sulindac produced a small, but significant, reduction in the mean creatinine clearance (37.0 ± 2.2 to 34.7 ± 2.2 ml min−1 1.73 m−2; P < 0.02) and 99mTc diethylenetriaminepenta-acetate (DTPA) clearance (35.5 ± 3.4 to 31.4 ± 3.6 ml min−1 1.73 m−2; P < 0.02) without altering body weight, effective renal plasma flow [131I]hippuran clearance), plasma renin activity (PRA), 24 h urinary volume or electrolyte excretion. 3. After discontinuation of sulindac, creatinine clearance returned to pretreatment values. 4. In five female patients, pretreatment urinary excretion of the 6-ketoprostaglandin F1α (6-keto-PGF1α), a stable breakdown product of prostacyclin (PGI2), was significantly reduced (P < 0.02) when compared with four healthy controls, whereas prostaglandin E2 (PGE2) was unchanged. Administration of sulindac did not significantly alter the excretion rate of PGE2 or 6-ketoPGF1α in this group of patients. 5. In chronic renal disease with moderate renal impairment, reduced renal prostacyclin synthesis may be an important predisposing factor to the renal toxicity associated with the use of nonsteroidal anti-inflammatory drugs (NSAID). Short term use of sulindac in therapeutic doses does not appear to influence the excretion of prostaglandins and produces only a minor reversible change in renal function; used cautiously it may have advantages over other NSAID in these patients.-


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