Effect of antihypertensive treatment on kidney function in diabetic nephropathy.

Parving, Hans‐Henrik; Andersen, Andreas; Smidt, Ulla M; Hommel, Eva; Mathiesen, Elisabeth Reinhardt; Svendsen, P.

doi:10.1136/bmj.294.6585.1443

Cited by 518 publications

(190 citation statements)

References 34 publications

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“…First, patients must be followed for severel years until reliable and meaningful data may be obtained [391 to evaluate whether a treatment is truly beneficial for the patients or not. Second, Parving et al showed that effective antihypertensive treatment with metoprolol, hydralazin and furosemide could slow the progression of nephropathy [5,40]. The rate of decline in GFR with those drugs (0.37ml.min-a.month -1 [401, 0.22ml.min -1 9 month -t [5], 0.49ml-min-l-month -1 [3]) appears to be comparable to the rate with enalapril (0.40 ml.…”

Section: Discussionmentioning

confidence: 99%

“…Hypertension is often associated with diabetic nephropathy [2], and effective antihypertensive treatment has proven to be effective in slowing the progression rate of nephropathy [3][4][5]. Recent studies in patients with diabetic nephropathy suggest that the use of angiotensin converting enzyme (ACE) inhibitors may possess specific advantages in decreasing proteinuria and slowing progression of nephropathy [6][7][8][9].…”

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confidence: 99%

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Comparison of the renal effects of angiotensin converting enzyme inhibitor and calcium antagonist in hypertensive Type 2 (non-insulin-dependent) diabetic patients with microalbuminuria: a randomised controlled trial

1989

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Summary. Seven of eight hypertensive Type 2 (non-insulindependent) diabetic patients with microalbuminuria completed a randomised crossover trial to compare the renal effects of angiotensin converting enzyme inhibitor (enalapril) and calcium antagonist (nicardipine). Four-week fixed oral maintenance dosages of enalapril (10-20 rag/day) and nicardipine (60-120 rag/day) significantly (p<0.05) lowered the systolic and diastolic blood pressures without altering renal blood flow, glomerular filtration rate and filtration fraction. Both drugs significantly reduced (p< 0.05) urinary albumin excretion rate and fractional clearance of albumin to similar extents. Total renal vascular resistance decreased significantly by nicardipine (p<0.05) and non-significantly by enalapril. Plasma osmotic pressure, plasma aldosterone concentration, total serum protein concentration, serum electrolytes and HbAlc remained unchanged by these drugs, whereas plasma renin activity was significantly higher (/7<0.05) in the enalapril than in the control and nicardipine phases. These results suggest that both drugs have similar renal function preserving effects with a concomitant hypotensive action in hypertensive Type 2 diabetic patients with microalbuminuria, and that the angiotensin converting enzyme inhibitor may not have advantageous renal effects when compared to the calcium antagonist and vice versa. Both drugs might be useful for treatment of high blood pressure in hypertensive diabetic patients, if long-term studies of these drugs can be shown to benefit the patients over other conventional antihypertensive therapies.

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Section: Discussionmentioning

confidence: 99%

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Comparison of the renal effects of angiotensin converting enzyme inhibitor and calcium antagonist in hypertensive Type 2 (non-insulin-dependent) diabetic patients with microalbuminuria: a randomised controlled trial

1989

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“…Systemic blood pressure is important in the PGC and the progression of diabetic nephropathy [8,27]. The aim of our study was to find if glomerular hypertension exists and causes albuminuria in patients with early diabetic nephropathy before systemic blood pressure clearly increases.…”

Section: Discussionmentioning

confidence: 99%

Glomerular hypertension as one cause of albuminuria in Type II diabetic patients

et al. 1999

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Glomerular capillary hypertension may cause albuminuria and nephropathy in diabetes mellitus, according to animal studies [1±5]. This hypothesis has been supported by the results of many clinical studies showing that antihypertensive drugs, especially angiotensin-converting enzyme (ACE) inhibitors, can reduce albuminuria and slow the progression of diabetic nephropathy [6±8]. Direct measurement of glomerular capillary hydraulic pressure (PGC) by the micropuncture method in diabetic rats given an ACE inhibitor showed that in this animal model, glomerular hypertension is one cause of albuminuria and diabetic nephropathy [9,10]. In humans, PGC cannot, however, be measured directly, so changes in glomerular haemodynamics in diabetic patients have not been reported. Recently, a method for the clinical assessment of glomerular haemodynamics was published [11±13]. Here, using this method, we investi- Diabetologia (1999) Abstract Aims/hypothesis. Results from animal models of glomerular hypertension have suggested that this disorder is one cause of albuminuria in diabetic nephropathy. We evaluated this hypothesis clinically. Methods. The subjects were 20 patients with Type II (non-insulin-dependent) diabetes mellitus but without uraemia or hypertension: 8 had normoalbuminuria and 12 had albuminuria ( ³ 20 mg/min). In the 2-week study, patients were on a diet with ordinary amounts of sodium for 1 week and on a sodium-restricted diet for 1 week. Urinary excretion of sodium and albumin and the systemic blood pressure were measured daily. Intrarenal haemodynamics, in terms of the glomerular pressure and resistance of afferent and efferent arterioles, were calculated from renal clearance, the plasma total protein concentration, and the pressure-natriuresis relation. In 8 of the 12 patients with albuminuria, an angiotensin-converting enzyme inhibitor, cilazapril, was given orally (2 mg/ day) and the 2-week study was repeated.Results. In patients with albuminuria, resistance of efferent arterioles and the glomerular pressure were higher than in patients with normoalbuminuria (glomerular pressure, 53 ± 5 vs 43 ± 5 mmHg, means ± SD, p < 0.001). Urinary excretion of albumin correlated (n = 20, r = 0.675, p < 0.001) with the glomerular pressure but not with systemic pressure. The increased glomerular pressure and the albuminuria were decreased by cilazapril but systemic pressure was not. Conclusion/interpretation. These findings are consistent with the hypothesis that glomerular hypertension is present in Type II diabetic patients with early nephropathy and can cause albuminuria. [Diabetologia (1999

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“…Furthermore, long-term correction of hyperglycaemia with intensified insulin administration fails to stop the progression of renal damage in diabetic patients [4]. In contrast, treatment of hypertension can retard the decline in glomerular filtration rate in diabetic nephropathy [5]. Recent work has indicated that the risk of diabetic nephropathy in Type 1 diabetes is increased with parental history of hypertension, especially if associated with poor glycaemic control [6].…”

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confidence: 99%

Leucocyte Na+/H+ antiport activity in Type 1 (insulin-dependent) diabetic patients with nephropathy

Simmons²,

Frighi³

et al. 1990

Diabetologia

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Effect of antihypertensive treatment on kidney function in diabetic nephropathy.

Cited by 518 publications

References 34 publications

Comparison of the renal effects of angiotensin converting enzyme inhibitor and calcium antagonist in hypertensive Type 2 (non-insulin-dependent) diabetic patients with microalbuminuria: a randomised controlled trial

Comparison of the renal effects of angiotensin converting enzyme inhibitor and calcium antagonist in hypertensive Type 2 (non-insulin-dependent) diabetic patients with microalbuminuria: a randomised controlled trial

Glomerular hypertension as one cause of albuminuria in Type II diabetic patients

Leucocyte Na+/H+ antiport activity in Type 1 (insulin-dependent) diabetic patients with nephropathy

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