A subdepressor low dose of ramipril lowers urinary protein excretion without increasing plasma potassium

Keilani, Taha; Danesh, Farhad R.; Schlueter, William; Molteni, Agostino; Batlle, Daniel

doi:10.1016/s0272-6386(99)70181-2

Cited by 28 publications

(15 citation statements)

References 32 publications

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“…Serum aldosterone levels were shown to increase as renal function progressively declines [13]. This observation is of interest, since it should be taken into consideration while treating patients with renal failure by ACE inhibitors [14]. In contrast to aldosterone concentrations, when we compared TTKG in DIH patients with that of control 2 patients, we found that TTKG in DIH was significantly lower than in control 2 normokalemic azotemic patients (2.58 ± 0.36 vs. 5.5 ± 0.9, p < 0.01).…”

Section: Discussionmentioning

confidence: 99%

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Trans-Tubular Potassium Gradient in Patients with Drug-Induced Hyperkalemia

Mayan

Kantor²,

Farfel³

2001

Nephron

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Background: Trans-tubular potassium gradient (TTKG) is considered to reflect mainly aldosterone bioactivity with regard to its kaliuretic response. We determined both TTKG and aldosterone serum concentrations in patients with severe drug-induced hyperkalemia (DIH). Methods: Ten hyperkalemic patients with serum potassium of more than 5.5 mEq/l, and serum creatinine of less than 2.5 mg/dl (221 µmol/l) were studied prospectively. Two control groups of 10 patients each were used. Control 1 group with normal renal function, and control 2 group with normokalemia and renal failure of the same magnitude as that of the hyperkalemic patients. Serum osmolarity, electrolytes, creatinine, aldosterone and urine electrolytes and osmolarity were measured and TTKG calculated. Results: DIH patients had lower TTKG values than control 1 patients (2.58 ± 0.36 vs. 6.68 ± 0.55, p < 0.001), and also lower than that of the control 2 patients (2.58 ± 0.36 vs. 5.51 ± 0.87, p < 0.01). Serum aldosterone concentration in the DIH group was higher than that of the control 1 group [24.30 ± 5.0 vs. 7.4 ± 2.1 pg/ml (674 ± 139 vs. 205 ± 58 pmol/l), p < 0.006] but not different from that of the control 2 group [24.3 ± 5.0 vs. 15.3 ± 3.8 pg/ml (674 ± 139 vs. 424 ± 106 pmol/l), respectively, p = 0.18]. Although there was some overlap in TTKG between DIH and control groups, 6 of 10 DIH patients had TTKG of less than 2.5, while none of the control patients had such a low value. Conclusion: DIH is characterized by lower TTKG values than those observed in patients with normal or mild-to-moderate renal failure. Other factors in addition to aldosterone seem to be involved.

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Section: Discussionmentioning

confidence: 99%

“…In renal failure specific drugs may affect differently serum aldosterone and TTKG. For instance, it was shown in patients with mild-to-moderate renal failure that ACE inhibitors cause hyperkalemia without a change in serum aldosterone [14]. …”

Section: Discussionmentioning

confidence: 99%

Trans-Tubular Potassium Gradient in Patients with Drug-Induced Hyperkalemia

Mayan

Kantor²,

Farfel³

2001

Nephron

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“…1,2 In this respect, isolated reports have shown episodes of life-threatening hyperkalemia 3 In addition, few retrospective studies, and even fewer prospective studies, have shown increased serum K ϩ in azotemic patients taking ACE inhibitors (ACEIs). 4,5 The hyperkalemia is thought to result from aldosterone inhibition secondary to decreased angiotensin (Ang) II production. 1 However, the final balance is also affected by serum K ϩ and by Na ϩ and water delivery to distal secretory sites.…”

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confidence: 99%

Hyperkalemia, Renal Failure, and Converting-Enzyme Inhibition

García

Baigorria²,

Juncos³

2001

Hypertension

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Abstract-Hyperkalemia is widely viewed as a common complication of ACE inhibition in azotemic patients. These renal failure patients are the patients who benefit most from ACE inhibition. Because we could not confirm this notion after a retrospective evaluation of 236 azotemic patients, we studied 2 models of renal mass reduction. In the first, we did a 5/6 nephrectomy (Nx) on rats and studied them 2 weeks after surgery (before chronic renal changes had developed). A second group was studied 16 weeks after Nx, once chronic renal failure was established. Rats in both models were treated with quinapril in drinking water. After baseline evaluation, we challenged them either by a high-K ϩ diet or by blocking aldosterone receptors. We found that although quinapril blocked the K ϩ -induced increase in aldosterone, serum K ϩ levels and K ϩ balance were maintained before and during high K ϩ intake or during simultaneous spironolactone administration. We conclude that in hemodynamically stable rats with reduced renal mass and renal dysfunction, the administration of an ACE inhibitor does not cause severe hyperkalemia.

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“…[23][24][25][26] In a recent study of 13 patients with mild chronic renal insufficiency (GFR; 51 ± 5.5 ml/minute), Keilani et al found a low dose (1.25 mg) of ramipril to be just as effective in reducing proteinuria as a higher (10 mg) dose, even though the low dose did not significantly reduce BP. 27 In contrast, in a recent study of patients with chronic heart failure, a small, but statistically significant, difference in the combined endpoint of mortality and morbidity was reached, favouring high-dose (33.2 mg) lisinopril over a lower (4.5 mg) dose. 28 Since almost all ACE-I or their active metabolites are excreted by the kidneys, doses should be reduced in renal failure.…”

Section: Discussionmentioning

confidence: 82%

High serum enalaprilat in chronic renal failure

Elung-Jensen

Heisterberg

Kamper

et al. 2001

J Renin Angiotensin Aldosterone Syst

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BackgroundMost angiotensin-converting enzyme (ACE) inhibitors and their metabolites are excreted renally and doses should hence be reduced in renal insufficiency. We studied whether the dosage of enalapril in daily clinical practice is associated with drug accumulation of enalaprilat in chronic renal failure. MethodsFifty nine out-patients with plasma creatinine >150 µmol/L and chronic antihypertensive treatment with enalapril were investigated, in a cross-sectional design. ResultsMedian glomerular filtration rate (GFR) was 23 (range 6-60) ml/minute/1.73 m 2 . The daily dose of enalapril was 10 (2.5-20) mg and the trough serum concentration of enalaprilat was 31.8 (<2.5-584.7) ng/ml. Ninety percent of the patients had higher serum concentrations of enalaprilat than has been reported in subjects with normal kidney function, and a marked elevation of serum enalaprilat was observed in patients with GFR <30 ml/minute. All but three patients had serum ACE activity below the reference range. The ACE genotype did not influence the results. Additional pharmacokinetic studies were done in nine patients in whom GFR was 23 (10-42) ml/minute/1.73 m 2 . The median clearance of enalaprilat was 28 (16-68) ml/minute and correlated linearly with GFR (r=0.86, p=0.003). Intra-subject day-to-day variation in trough concentrations was 19.7%.

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A subdepressor low dose of ramipril lowers urinary protein excretion without increasing plasma potassium

Cited by 28 publications

References 32 publications

Trans-Tubular Potassium Gradient in Patients with Drug-Induced Hyperkalemia

Trans-Tubular Potassium Gradient in Patients with Drug-Induced Hyperkalemia

Hyperkalemia, Renal Failure, and Converting-Enzyme Inhibition

High serum enalaprilat in chronic renal failure

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