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Biomedical subjects

G Conte

Publications and source records attributed to G Conte.

At least 127 records · Page 7Linked to original sources
PubMed1987

Renal handling of urea in subjects with persistent azotemia and normal renal function.

Fourteen subjects with persistent azotemia and normal glomerular filtration rate were studied by renal clearances and hormonal determinations to establish the nephron site of altered urea transport and the mechanism(s) responsible for their azotemia. During constant alimentary protein, urea nitrogen appearance was normal and urea clearance was much lower than in 10 age-matched control subjects (23.3 +/- 2.1 ml/min and 49.6 +/- 2.6 ml/min per 1.73 m2, P less than 0.001). Inulin and para-aminohippurate clearances, blood volume and plasma concentration of antidiuretic hormone were within normal limits. During maximal antidiuresis, in spite of greater urea filtered load, the urinary excretion of urea was less, and both the maximum urinary osmolality and the free-water reabsorption relative to osmolar clearance per unit of GFR were greater than in control subjects. After sustained water diuresis, the plasma urea concentration markedly decreased to near normal levels in azotemic subjects. The basal urinary excretion of prostaglandins E2 was significantly reduced in azotemic subjects and was directly correlated with fractional urea clearance (r = 0.857, P less than 0.001). An additional group of control subjects (N = 8) showed a marked reduction of fractional clearance of urea after inhibition of prostaglandin synthesis (P less than 0.01). These data suggest that azotemia is due to increased tubular reabsorption of urea in the distal part of nephron, presumably because of increased back diffusion in the papillary collecting duct, accounting for the enhanced maximum urinary osmolality and free-water reabsorption. Renal prostaglandin E2 may participate in the pathogenesis of azotemia by altering recycling of urea in the medulla.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Effects of PGE2 infusion on renal function in normal man before and after angiotensin II inhibition by captopril.

Increasing doses of prostaglandin E2 (PGE2) (5, 10, 20, 40, 60 ng/kg/min) were infused in 7 normal volunteers before and after angiotensin II synthesis inhibition by captopril (100 mg by mouth). PGE2 infusion alone did not alter blood pressure, while it increased the urinary excretion of both epinephrine and norepinephrine, enhanced p-aminohyppuric clearance (CPAH), inulin clearance (CIn), sodium and water excretion and decreased urinary osmolality. No changes of CIn, CPAH and catecholamines were observed after captopril alone, whilst there was a significant increase in urine output and sodium excretion and a decrease in urinary osmolality. In the presence of captopril, the infusion of PGE2 caused a significant fall in blood pressure and CIn, enhanced epinephrine excretion and sodium excretion, while it did not significantly reduce CPAH. Our findings suggest that an intact renin-angiotensin system is necessary to maintain GFR during PGE2 infusion.

Adult↗
PubMed1987

The causal role of salt depletion in acute renal failure due to captopril in hypertensive patients with a single functioning kidney and renal artery stenosis.

Captopril (C) causes ARF in hypertensive patients with renal artery stenosis (RAS) with a single functioning kidney (SK). Retrospective studies in two patients showed that episodes of C-induced ARF were preceded by a rise in urinary Na+ excretion and a rapid decrease in body weight. These observations prompted us to investigate whether extracellular fluid volume depletion secondary to C-induced natriuresis can be responsible for ARF. Prospective studies were performed in four patients with RAS-SK treated with C. These studies have shown that: ARF is associated with negative Na+ balance and is corrected by salt replacement, even without interrupting C; ARF is preceded by a rise in urinary prostaglandin (PG) E2 and 6-keto-F1 alpha; ARF is prevented by either saline infusion or aspirin administration; ARF does not occur when the dose of C is not sufficient to raise PGs and urinary N + excretion. We conclude therefore that C-induced ARF in patients with RAS-SK can be secondary to salt depletion dependent on a raised secretion of PGs.

Acute Kidney Injury↗
PubMed1986

Early life events and affective disorder revisited.

The incidence of traumatic events during the first ten years of life was investigated in two groups of patients suffering from major affective disorder, as well as in mixed psychiatric patients and in healthy subjects. While there were no significant differences between the two groups of affective patients or between the two control groups, the incidence of subjects who underwent such trauma was significantly higher in depressives, compared with controls. These differences are small and are further reduced if events secondary to psychiatric disturbances of family members are excluded.

Adolescent↗
PubMed1986

Polyuric prerenal failure after reduction from high to normal dietary intake of sodium.

In a patient with renal amyloidosis secondary to chronic urinary tract infection with nephrotic syndrome, polyuric acute renal failure developed after reduction from a high to a normal dietary intake of sodium and was reversed by salt replacement therapy. As documented by functional and morphological studies, the patient had a marked defect of tubular sodium reabsorption at the proximal site and along the ascending limb of Henle's loop, a distal tubular unresponsiveness to aldosterone, and severe tubulointerstitial damage in the medulla. We propose that the sodium dietary reduction in conjunction with severe tubular dysfunction and hypovolemia due to nephrotic syndrome is responsible for this unused form of polyuric acute prerenal failure.

Acute Kidney Injury↗