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Biomedical subjects

C Campo

Publications and source records attributed to C Campo.

At least 55 records · Page 3Linked to original sources
PubMed1994

Randomly allocated study of the effects of standard therapy versus ACE inhibition on micro-albuminuria in essential hypertension.

OBJECTIVE: To compare the effects of standard therapy (diuretic, beta-blocker or both) with those of angiotensin converting enzyme (ACE) inhibition with quinapril on renal function and urinary albumin excretion in patients with essential hypertension. METHODS: A 1-year, placebo-controlled, randomly allocated study was conducted in a group of 40 patients with essential hypertension. Before beginning the active treatment phase, all patients were given a matched placebo for quinapril for at least 14 days. At baseline and after 1, 3, 6 and 12 months of treatment, blood pressure, heart rate, body weight, renal plasma flow, glomerular filtration rate, plasma renin activity, plasma aldosterone and urinary albumin excretion were measured. RESULTS: Both the standard therapy and quinapril produced similar decreases in blood pressure, but only quinapril produced a significant decrease in micro-albuminuria, from 68.5 +/- 16.7 to 47.2 +/- 14.9 mg/24 h (P < 0.05). The renal plasma flow remained constant in both study groups while the glomerular filtration rate and filtration fraction decreased significantly (P < 0.05) in the quinapril group. CONCLUSIONS: The results of this study indicate that long-term therapy for essential hypertension with ACE inhibition has a more favorable effect on micro-albuminuria than standard therapy for an equal level of blood pressure control.

Adrenergic beta-Antagonists↗
PubMed1993

Chronic renal insufficiency after an episode of macroscopic hematuria in IgA nephropathy.

Several cases of acute renal failure associated with episodes of macroscopic hematuria (EMH) in IgA nephropathy (IgAN) have been reported; in every case renal function returned to normal. We report 2 cases with previous normal renal function that developed acute renal failure during EMH of 17 and 30 days duration, respectively. Renal biopsies showed mesangial proliferation with IgA deposits, crescents in 10-15% of glomeruli and a marked tubular necrosis with red blood cell casts obstructing the lumen in 30-45% of tubules. Although renal function improved after EMH cessation, it did not recover previous normal values. Thus, EMH can produce permanent loss of renal function in patients with IgAN.

Creatinine↗
PubMed1993

The kidney and arterial hypertension.

It has been known for some time that a relationship exists between the kidney and blood pressure. The renal origin of arterial hypertension has been demonstrated in different animal models resembling human hypertension, with data from humans seeming to confirm this hypothesis. On the other hand, the renal vasculature also suffers the consequences of arterial hypertension, and renal insufficiency can develop as a result of elevated blood pressure levels. Antihypertensive therapy can prevent the development of renal damage secondary to hypertension. For example, calcium antagonists possess specific renal effects that not only facilitate their antihypertensive capacity but also protect the kidney from the development of renal failure.

Animals↗
PubMed1992

Nephrotic syndrome and focal glomerulosclerosis in adult polycystic kidney disease.

We report a 35-year-old man with adult polycystic kidney disease (APKD) that developed nephroptic syndrome accompanied by a rapid worsening of renal function. Histologic examination showed marked tubulointerstitial chronic abnormalities and focal glomerulosclerosis (FGS) lesions in 24% of the glomeruli. With captopril, an renal function continued to deteriorate. No other cases of nephrotic-range proteinuria were detected among 65 APKD patients with renal insufficiency. Histologic examination of an other 12 kidneys removed from patients with APKD showed striking interstitial lesions, most of the glomeruli being normal. However, those patients with higher amounts of proteinuria had more glomeruli (14-32%) with FGS lesions.

Adult↗
PubMed1991

Tubular dysfunction in nephrotic syndrome: incidence and prognostic implications.

Although some cases of tubular dysfunction (TD) associated with nephrotic syndrome have been described, the incidence and the characteristics of this complication remain unknown. We investigated the presence of TD (renal glycosuria, aminoaciduria, metabolic acidosis with normal anion gap, hypouricaemia, and throughout hypophosphataemia) in 36 patients with nephrotic syndrome. Ten patients (group 1) showed glycosuria at some time during the course of their illness, ranging from 2.5 to 11.2 g/24 h. In addition, seven of them had metabolic acidosis with normal anion gap, five aminoaciduria, and two hypouricaemia. Membranous glomerulonephritis was the most frequent aetiology in group 1 patients (7 of 10). Proteinuria and serum creatinine (SCr) were significantly higher in group 1 patients than in the 26 remaining patients without TD (group 2): 10.2 +/- 3.7 versus 6.7 +/- 2.9 g/24 h (P less than 0.01) and 3.2 +/- 1.9 versus 1.6 +/- 0.9 mg/dl (P less than 0.05) respectively. The appearance of TD coincided with a clear worsening of renal function in most of group 1 patients. In addition, at the end of follow-up, SCr had increased from 3.2 +/- 1.9 to 5.6 +/- 3.3 mg/dl (P less than 0.05) in this group. In contrast, SCr did not show significant changes in group 2 (1.6 +/- 0.9 versus 2.1 +/- 2.2 mg/dl). In conclusion, a significant proportion (27.7%) of patients with nephrotic syndrome present TD data at some moment of their course; the appearance of this complication appears to be a sign of poor prognosis.

Adolescent↗
PubMed1991

Tolerance to nitrendipine in patients with arterial hypertension accompanying chronic renal failure.

To test the tolerance to nitrendipine in arterial hypertension secondary to chronic renal parenchymatous disease, a group of 10 patients so diagnosed and adequately controlled with a diuretic alone or with a beta-blocker were switched to nitrendipine at a dose to insure similarly adequate control of blood pressure. Patients were followed for 1 year at monthly intervals during which blood pressure measurement and the determination of a biochemical profile were performed. During the follow-up, nitrendipine adequately controlled blood pressure and a significant fall was observed in hematocrit (p less than 0.05) and serum uric acid (p less than 0.01) values. Meanwhile, the glomerular filtration rate, determined by the creatinine clearance, did not exhibit significant changes nor did the 24-h urinary excretion of proteins. The tolerance of the drug was adequate, with two patients presenting minimal ankle edema. These results seem to indicate that nitrendipine can be safely used in patients with arterial hypertension secondary to chronic renal parenchymatous disease.

Adult↗