Biomedical subjects
L Oldrizzi
Publications and source records attributed to L Oldrizzi.
The role of systemic hypertension in the progression of nondiabetic renal disease.
BACKGROUND: A role for hypertension in the progression of renal disease has been convincingly shown in experimental animals only. In human studies, the relation between hypertension and progression is difficult to demonstrate due to several confounding factors: age, gender, race; the difficult choice of blood pressure (BP) parameters that correlate with progression; the abnormal circadian BP pattern; and the many non-hemodynamic factors of progression. An important role for hypertension in progressive nondiabetic renal disease has been suggested by observational studies and clinical trials originally intended to evaluate the effect of dietary protein restriction on progression. In addition, several studies, summarized by a recent meta-analysis, have shown that pharmacological agents which lower both BP and proteinuria, mainly the angiotensin-converting enzyme inhibitors (ACEI), significantly slow the rate of progression in these diseases. METHODS: In this article we review the effect of lowering BP on the progression of nondiabetic chronic renal disease, the patient characteristics that are associated with a greater or lesser benefit of blood pressure reduction, and the choice of antihypertensive regimens associated with better outcomes in patients with renal disease. RESULTS: Lower levels of achieved BP are associated with a slower decline in renal function, both in patients with and without proteinuria. ACEI are effective BP lowering agents and are associated with better preservation of renal function as opposed to antihypertensive regimens without ACEI. This protective effect of ACEI is in addition to their BP and urine protein lowering effects. The protective effect of ACEI on renal function is more pronounced in patients with proteinuria. CONCLUSION: In patients with nondiabetic renal disease and proteinuria, the risk of progression can be minimized by lowering both BP and proteinuria. ACEI have an additional beneficial effect.
Evaluation of a patient with hypertension and mild renal failure in whom facial and digital abnormalities are noted.
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6th Verona Seminar on Nephrology, Verona, Italy, September 19-21, 1996.
The Veronese biennial meeting aimes to provide an up-to-date overview on topics of recent interest and progress. In 1996 the Scientific Committee devised a programme which spent the spectrum from basic science to very practical clinical problems.
Low-dosage ibopamine treatment in progressive renal failure: a long-term multicentre trial.
A multicentre trial (11 nephrology centres) was carried out to test the effects of ibopamine, an orally active dopamine-like drug, on the progression of chronic renal failure. For a 2-year period 189 chronic renal failure patients (serum creatinine level 1.5-4.0 mg/dl) were observed. They were homogeneous for basic nephropathy, degree of residual renal function, blood pressure, and proteinuria. The patients were randomly divided into two groups: 96 took ibopamine at a dosage of 100 mg/day (group A) and 93 served as controls (group B). All were on a low-protein diet (mean 0.8 g/kg body weight). By the end of the observation period, the rate of decrease of the renal function indexes in time proved significantly slower (1.8 times) in group A than in group B. The survival curves for renal function (pre-established end points were creatinine level increases equal to or > 20% and equal to or > 40% of the basal values) proved significantly better (p < 0.02 and p < 0.002 respectively) in group A than in group B. The mean plasma creatinine values rose by 17% in group A and by 36% in group B. The creatinine clearance decreased by 5% in treated patients and by 14% in the controls. Statistical analysis ruled out any possible centre effect. The trial suggests that low-dosage ibopamine administration may be used as a valid and safe pharmacological adjunct for retarding the progression of renal failure in patients with mild or moderate chronic renal impairment.
Renal reserve in patients with solitary kidneys.
The first part of this article focuses on the risk of functional deterioration in subjects with solitary kidneys; the long-term clinical outcome of various subgroups of patients is reviewed. Thereafter, the pathophysiology of the renal functional reserve in subjects with a 50% reduction in renal parenchyma and the results coming from studies eliciting the renal reserve in these subjects are summarized. Finally, the clinical significance of the renal functional reserve and its usefulness in clinical practice are critically discussed.
Nutrition and the kidney: how to manage patients with renal failure.
Nutrition is believed to play a key role in the management of chronic and acute renal failure. Considerable evidence suggests that unrestricted protein diets accelerate the progression of chronic renal failure. As a result, recommendations have evolved limiting the quantity and quality of nitrogen intake with the goal of slowing the progression to dialysis dependency. Acute renal failure offers different challenges in view of its common association with hypermetabolic states. With respect to nitrogen substrate administration, the use of mixed formulations of essential plus nonessential amino acids seems to be as effective as essential amino acids alone.
Renal endpoints in non-diabetic patients.
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The place of hypertension among the risk factors for renal function in chronic renal failure.
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Diet and chronic renal failure.
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Renal response to colloid volume expansion in patients with solitary kidneys or mesangial glomerulonephritis.
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Therapy of systemic hypertension in chronic renal failure.
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Dynamic evaluation of renal function in subjects with solitary kidneys.
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Is there a "point of no return" in progressive renal disease?
The pathogenesis of progressive renal damage is most probably multifactorial. Whatever the mechanisms involved in renal disease progression, the existence of a "point of no return" has been hypothesized, that is, a stage of structural and functional damage beyond which progression of renal disease occurs independently of dietary measures and/or pharmacological treatment. In experimental animals, dietary protein and phosphate restriction is not fully successful in ameliorating the progression of functional deterioration if administered when renal injury is severe and long standing. Similarly, late treatment with various pharmacological agents (mainly antihypertensive drugs) is less effective than early administration of the same substances. A serum creatinine of 176 mumol/L seems a critical point discriminating the results of either dietary protein and phosphate restriction or antihypertensive treatment in patients with chronic renal disease. The protective effects of both dietary and nondietary intervention seem to be most effective when at least 50% of the residual renal mass is still functioning. The extent to which glomerular sclerosis, vascular hyalinosis, and interstitial fibrosis have already developed can probably blunt or avert the expected results of treatment. Some clinical tests may identify those patients who would benefit from measures such as the reduction in glomerular hemodynamic stress, the long-term inhibition of the renin-angiotensin system, and the aggressive treatment of systemic hypertension. The continuous search for a rational preventive treatment before the disease process has reached the "point of no return" will undoubtedly constitute a formidable task for the modern nephrologist.
Effect of dietary proteins and lipids in patients with membranous nephropathy and nephrotic syndrome.
Twenty-four patients with idiopathic membranous nephropathy, long-lasting nephrotic syndrome and serum creatinine less than 2 mg/dl ate sequentially, in a randomized cross-over design, a normal protein diet containing 1.1 +/- 0.3 g/kg/day of proteins and a low protein diet containing 0.7 +/- 0.1 g/kg/day of protein, each diet for a period of 3 months. Both diets were low in fat (less than 30% of total calories) and cholesterol (less than 200 mg/day) content and rich in polyunsaturated fatty acids and in linoleic acid (10% of energy). Random assignment to one of the two 3 month diet periods was done after a RUN-IN period of at least one month on the hypolipidic normal protein diet. Glomerular filtration rate (inulin clearance), 24 hour urinary protein loss and serum albumin concentration did not significantly differ at the end of the two diet periods, indicating that long-term restriction of protein intake does not modify GFR or urinary protein loss in nephrotic patients. Serum total and LDL-cholesterol and daily proteinuria were significantly lower at the end of both diet periods than at the beginning and at the end of the RUN-IN period. We suggest that these changes were a consequence of the manipulation of dietary fat intake.
The solitary kidney: a risky situation for progressive renal damage?
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Effect of dietary manipulation on the lipid abnormalities in patients with chronic renal failure.
Disorders of lipid metabolism could play an important role in mediating the progression of chronic renal disease toward uremia. The hypothesis of the nephrotoxicity of lipids has been considered in a large population of patients on long-term dietary protein restriction. In our experience, there is no evidence that lipid disorders may accelerate the progression of renal disease. Hypercholesterolemia and/or hypertriglyceridemia are probably only some of the many factors affecting the prognosis of renal disease. Dietary protein restriction seems to be effective in maintaining normal or only slightly elevated serum lipids in patients with early renal failure, even after years of dietary treatment, despite the natural progression of renal functional deterioration. Moreover, this dietary regimen has a favorable effect on lipid composition of erythrocyte membrane when compared with those of patients on a free diet.
Factors influencing dietary compliance in patients with chronic renal failure on unsupplemented low-protein diet.
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