Protection of kidney function and decrease in albuminuria by captopril in insulin dependent diabetics with nephropathy.

Parving, Hans‐Henrik; Hommel, Eva; Smidt, Ulla M

doi:10.1136/bmj.297.6656.1086

Cited by 301 publications

(109 citation statements)

References 42 publications

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“…2,6 We previously evaluated the most appropriate competing-risks methodology for analyzing this kind of data 11 and, on the basis of that evaluation, used Fine and Gray models for the current analysis, as has been proposed by others. 13 The limitations of the study include our inability to control for important predictors of end-stage renal disease and death without end-stage renal disease, such as glycemic, blood pressure and lipid control, and related changes in medical practice, such as the introduction of angiotensinconverting enzyme inhibitors, 30 that occurred during the course of the study period. However, these factors would not have affected the difference in age of diabetes onset between First Nations and non-First Nations people.…”

Section: Strengths and Limitationsmentioning

confidence: 99%

Differential mortality and the excess burden of end-stage renal disease among First Nations people with diabetes mellitus: a competing-risks analysis

Jiang

Osgood

Lim

et al. 2013

CMAJ

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Section: Strengths and Limitationsmentioning

confidence: 99%

Differential mortality and the excess burden of end-stage renal disease among First Nations people with diabetes mellitus: a competing-risks analysis

Jiang

Osgood

Lim

et al. 2013

CMAJ

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“…The patients comprise the entire treatment group in a non-randomized controlled trial of matched hypertensive IDDM patients with nephropathy treated with captopril and frusemide or bendrofluazide [16]. All patients fulfilled the following inclusion criteria: age under 50, persistent albuminuria (> 300 mg/day), a serum creatinine concentration less than 120 p.mol/1, no oedema, diagnosis of hypertension, but not receiving antihypertensive treatment (including diuretics), development of diabetes before the age of 31, and not blind.…”

Section: Patientsmentioning

confidence: 99%

“…[Diabetologia (1994) Abbreviations: IDDM, Insulin-dependent diabetes mellitus blood pressure and development and progression of diabetic glomerulopathy [4][5][6][7][8][9][10]. Several studies [11][12][13][14][15][16][17] have demonstrated that the rate of decline in glomerular filtration rate can be reduced by antihypertensive treatment. However the beneficial effect of antihypertensive treatment on the progression of the diabetic nephropathy is highly variable.…”

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confidence: 99%

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Reduction in albuminuria predicts a beneficial effect on diminishing the progression of human diabetic nephropathy during antihypertensive treatment

et al. 1994

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Summmr/ Diabetic nephropathy is the main cause of increased mortality and morbidity in IDDM patients. The effect of antihypertensive treatment on the progression of the nephropathy is highly variable. The aim of this study was to evaluate putative predictors of the progression in diabetic nephropathy during long-term antihypertensive treatment. Eighteen hypertensive IDDM patients with diabetic nephropathy, who had not been treated previously, were followed during 3 years of treatment with captopril and frusemide or bendrofluazide. Glomerular filtration rate, arterial blood pressure, albuminuria and adjusted albuminuria were used as putative predictors of rate of decline in glomerular filtration. Fall rate in glomerular filtration rate was 4.6 (4.0) ml. min-1 .year 1 (mean (SD)) during treatment. Relative change in albuminuria (ratio of first year of treatment/baseline) and albuminuria during first year of treatment were significantly correlated to fall rate in glomerular filtration rate during 3 years of treatment (r --0.73, p < 0.001) and (r = 0.60, p < 0.01), respectively. Arterial blood pressure and glomerular filtration rate measured at baseline, during first year of treatment or relative changes in these variables did not correlate with fall rate in glomerular filtration rate during 3 years of treatment. Haemoglobin AI:, serum-cholesterol, protein intake and sodium excretion remained unchanged during treatment, and were not correlated with loss of kidney function. Reduction in albuminuria during captopril treatment predicts an attenuated rate of decline in glomerular filtration rate in early diabetic nephropathy (glomerular filtration rate > 70 ml. rain -1-1.73 m-Z). The finding suggests a clinical application in monitoring the efficacy of antihypertensive treatment in early diabetic nephropathy. [Diabetologia (1994) 37: 511-516] Key words Diabetic nephropathy, albuminuria, antihypertensive treatment, glomerular filtration rate.Diabetic nephropathy develops in 30-40 % of IDDM patients [1,2], and nephropathy is the main cause of increased morbidity and mortality in these patients [1]. Diabetic nephropathy is a clinical syndrome characterized by persistent albuminuria, a relentless decline in glomerular filtration rate, and raised arterial blood pressure [3]. Human and animal studies have demonstrated a correlation between elevation in arterial Received: 21 September 1993 and in revised form: 3 December 1993Corresponding author: Dr. R Rossing~ Steno Diabetes Center, Niels Steensens Vej 2, DK-2820 Gentofte, DenmarkAbbreviations: IDDM, Insulin-dependent diabetes mellitus blood pressure and development and progression of diabetic glomerulopathy [4][5][6][7][8][9][10]. Several studies [11][12][13][14][15][16][17] have demonstrated that the rate of decline in glomerular filtration rate can be reduced by antihypertensive treatment. However the beneficial effect of antihypertensive treatment on the progression of the diabetic nephropathy is highly variable. From a clinical point of view, identification of predic...

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“…In the 1980s, several small, short-term studies in patients who had diabetic nephropathy with and without hyper-tension (10,11) showed a slower rate of decline of renal function when treatment with an ACEI, captopril, was given. In the study that was conducted by Lewis et al (12) in patients with established diabetic nephropathy, treatment with captopril reduced by 50% the risk for doubling serum creatinine, although BP control was similar in both groups.…”

Section: Nephroprotection By Blockade Of the Rasmentioning

confidence: 99%

Dual Blockade of the Renin-Angiotensin System in the Progression of Renal Disease

Fernández-Juárez¹,

Barrio²,

Vinuesa³

et al. 2006

Journal of the American Society of Nephrology

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There is clear evidence that pharmacologic blockade of the renin-angiotensin system (RAS) with angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB) reduces proteinuria and slows the progression of renal disease in diabetic and nondiabetic nephropathies, a beneficial effect that is not related to BP control. Some patients exhibit a significant beneficial response, whereas others do not. The absence of response may be explained by the incomplete blockade of the RAS obtained with ACEI. In the search of new alternatives that could improve the antiproteinuric and nephroprotective effects of RAS blockers, the association of ACEI and ARB might prove useful. ARB produces a complete blockade of the RAS. Several studies have shown a more marked antiproteinuric effect of the dual blockade of the RAS versus ACEI or ARB alone. A recent study also demonstrated that this more marked antiproteinuric effect is associated with less progression of renal disease in primary nondiabetic nephropathies despite a similar effect on BP. Until now, there has not been any reference to a beneficial effect on progression of the dual blockade in type 2 diabetic nephropathy, which is the most frequent cause of ESRD. A multicenter, prospective, open, active-controlled, and parallel-group trial was designed to compare the effects of an ACE inhibitor versus an ARB or its combination on renal disease progression, proteinuria, and cardiovascular events in type 2 diabetic nephropathy. S ingle-nephron hyperfiltration hypothesis, put forward by Brenner more than 20 yr ago, helped to explain the inexorable decline in renal function that is observed in chronic renal disease once the initial insult has disappeared. Angiotensin II is responsible for the increase in glomerular hydraulic capillary pressure by means of increasing systemic BP along with vasoconstriction of the efferent arteriole, thereby increasing filtration pressure in glomerular capillary walls. In experimental rat models with renal disease, a decrease of similar magnitude in systemic BP can be achieved either with angiotensin-converting enzyme inhibitors (ACEI) or with a combination of diuretics, reserpine and hydralazine, although only in those who are treated with ACEI is a reduction in glomerular capillary pressure and in progression of renal disease observed (1). J Am Soc NephrolBesides these hemodynamic changes, many other experimental models of renal damage that result in severe proteinuria (e.g., nephrosis by adriamycin or immune-complex glomerulonephritis [2,3]) have implicated angiotensin as a mediator in most of the inflammatory mechanisms that are involved in the progression of chronic renal disease. In proteinuric nephropathies, protein trafficking through proximal tubular cells, besides damaging this tubular segment, stimulates the production of NF-B, in part induced by angiotensin (4). NF-B is present in all cellular types and plays a crucial role in inflammation and apoptosis. In experimental models of nephritis, activation of NF-B results i...

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Protection of kidney function and decrease in albuminuria by captopril in insulin dependent diabetics with nephropathy.

Cited by 301 publications

References 42 publications

Differential mortality and the excess burden of end-stage renal disease among First Nations people with diabetes mellitus: a competing-risks analysis

Differential mortality and the excess burden of end-stage renal disease among First Nations people with diabetes mellitus: a competing-risks analysis

Reduction in albuminuria predicts a beneficial effect on diminishing the progression of human diabetic nephropathy during antihypertensive treatment

Dual Blockade of the Renin-Angiotensin System in the Progression of Renal Disease

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