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J F Wetzels

Publications and source records attributed to J F Wetzels.

123 records · Page 7Linked to original sources
PubMed1987

Cyclosporin treatment with conversion after three months versus conventional immunosuppression in renal allograft recipients.

In a prospective randomised trial, 72 recipients of cadaver renal allografts received cyclosporin for 3 months followed by azathioprine and prednisone (cyclosporin group), and 71 received azathioprine and prednisone from the day of transplantation (conventional group). Graft survival was better in the cyclosporin group at 3 months and 1 year (93% and 80%) than in the conventional group (83% and 70%). This was not a significant difference. The incidence of acute rejection episodes in the first 3 months was significantly lower in the cyclosporin group (35% versus 77%, p less than 0.00001), as was the number of grafts lost because of immunological failure (1 versus 10, p less than 0.02). After conversion, renal function improved. Only 5 patients had acute rejection after conversion. These episodes were easily reversible in all cases and did not lead to graft loss. The numbers of grafts lost after conversion were similar in the two groups. Conversion of cyclosporin to azathioprine 3 months after renal transplantation is a safe procedure that obviates the long-term toxic effects of cyclosporin.

Acute Disease↗
PubMed1987

The natriuretic effect of the dihydropyridine calcium antagonist felodipine: a placebo-controlled study involving intravenous angiotensin II in normotensive volunteers.

Changes in systemic and renal hemodynamics and in the renin-angiotensin system caused by infusion of the calcium antagonist felodipine were investigated in a placebo-controlled study with 12 normotensive volunteers before and during a graded infusion of angiotensin II (AII). In spite of a fall in blood pressure through vasodilatation, felodipine had a natriuretic effect. There was only a transient rise in effective renal plasma flow (ERPF), whereas glomerular filtration rate (GFR) did not change. Urinary sodium excretion remained elevated when ERPF had normalized. Urinary potassium excretion did not change. AII-induced reductions in ERPF, GFR, and sodium excretion were abolished by felodipine. Felodipine also partly antagonized the rise in plasma aldosterone levels caused by AII. We conclude that the natriuretic effect of dihydropyridine calcium antagonists is probably not caused by a single mechanism, but may be dependent on changes in renal hemodynamics together with a diminished sodium reabsorption at multiple tubular sites. Interference with AII-mediated renal mechanisms and an impairment of the action of aldosterone may contribute to this natriuretic effect as well.

Adult↗
PubMed1986

Prednisone-induced fluctuations of proteinuria in patients with a nephrotic syndrome.

We studied the effect of prednisone on urinary protein excretion in 19 patients with a nephrotic syndrome, who were treated with prednisone (125-150 mg) on alternate days. We found a typical, fluctuating pattern of proteinuria resulting from an increased protein excretion rate on prednisone days and a decreased protein excretion rate on nonprednisone days. The urinary protein excretion on prednisone days was 9.9 +/- 3.3 g/24 h, as compared to 5.7 +/- 3.8 g/24 h on nonprednisone days (mean +/- SD). In the whole group of patients the percentual change in proteinuria was significantly correlated with the endogenous creatinine clearance. However, systematic differences between creatinine excretion rates on prednisone and nonprednisone days were not found in individual patients. In 6 patients, renal hemodynamics were studied more precisely, using a single injection technique. Only a slight and nonsignificant decrease in glomerular filtration rate was found on nonprednisone days (delta = -9.6 +/- 16.3%; mean +/- SD). Filtration fraction remained unchanged. It is therefore suggested that the effects of prednisone on proteinuria are not simply mediated by overall changes in renal hemodynamics.

Adolescent↗
PubMed1986

Influence of cadaver donor age on renal graft survival.

It has been suggested that kidneys from young and old donors do less well after transplantation. We have studied this problem in a retrospective analysis of all cadaveric transplants performed in our center during the last 10 years. All patients were followed for at least six months. Recipients younger than 16 years were excluded from this analysis. Thirty-six patients received a kidney from a donor younger than 11 years (group A), 374 received a kidney from a donor aged between 11 and 51 years (group B) and 21 a kidney from a donor aged older than 51 years (group C). In the young donor age group graft survival was significantly worse than in the two other groups with a one year graft survival of 45.6%, 75.0% and 75.9% for group A, B and C respectively. There were significantly more technical failures in group A, but if these were excluded a significant difference in graft survival remained present. At three months there were no significant differences in hypertension, proteinuria, or serum creatinine between the three groups. These results suggest that young but not old donor kidneys have a worse graft survival. This decreased graft survival is only partly caused by technical problems. Therefore young grafts also seem to be more susceptible to the host's immune response.

Adolescent↗
PubMedDate not supplied

Drug-induced nephrotoxicity. Aetiology, clinical features and management.

There is a growing number of hospitalised patients who develop a drug-induced renal problem because increasing numbers of potent drugs have been added to the therapeutic arsenal in recent years. The 3 clinical syndromes that can be recognised in drug-induced nephropathy are acute renal failure, chronic interstitial nephritis and the nephrotic syndrome. The first can be caused by prerenal problems, acute interstitial nephritis, acute tubular necrosis and intratubular obstruction. The most important drugs that cause prerenal failure are NSAIDs, captopril and cyclosporin. NSAIDs inhibit the synthesis of prostaglandins, and consequently vasoconstriction of the afferent arteriole leads to lowering of the glomerular filtration rate (GFR); captopril blocks the formation of angiotensin II (which also leads to a lower GFR), and should be used with caution in patients with stenotic renal arteries; cyclosporin causes vasoconstriction of the afferent arteriole, which is probably mediated by the sympathetic system. Combinations of these drugs result in increased nephrotoxicity. The drugs most likely to cause acute interstitial nephritis are antibiotics and NSAIDs. Normally, signs of an allergic reaction are also present. Acute interstitial nephritis is usually self-limiting, but in some studies it is claimed that steroids may promote recovery. Four important causal agents of acute tubular necrosis are aminoglycosides, amphotericin B, radiocontrast agents and cyclosporin. Approximately half of the cases of drug-induced renal failure are related to the use of aminoglycosides: generally, 10 days after start of treatment a nonoliguric renal failure develops, with recovery after withdrawal of the drug in almost all cases. The aminoglycosides are particularly nephrotoxic when combined with other nephrotoxic drugs. 80% of amphotericin B-treated patients develop renal insufficiency, a percentage that increases as the cumulative dose exceeds 5g. It is because of its unique antifungal properties that there are still some indications for the use of this highly nephrotoxic drug; the high percentage of nephrotoxicity can probably be prevented in part by sodium loading. The nephrotoxicity of radiocontrast agents is largely dependent on renal function: from 0.6% in patients with normal renal function to 100% in patients with a serum creatinine above 400 mumol/L. Diabetes mellitus does not add greatly to the risk of radiocontrast nephrotoxicity. The nephrotoxicity of cyclosporin is dose-dependent and reversible, although there are some reports of irreversibility after long term use. Cyclosporin can also result in nephrotoxicity in combination therapy.(ABSTRACT TRUNCATED AT 400 WORDS)

Acute Kidney Injury↗