[Definitive end-stage chronic kidney failure after cisplatin treatment]. / Insuffisance rénale chronique terminale définitive après traitement par le cisplatine.

Renal failure secondary to CDDP is due to acute tubular necrosis and is usually reversible. We report 4 cases of definitive renal failure secondary to administration of cisplatin (CDDP). Three women and one man, mean age 40 +/- 8 years (24 to 64 years), at onset of dialysis are reported. They had received 1 to 4 courses of CDDP for an endometrial carcinoma (n = 2), a breast carcinoma or a thymoma. The mean total dose of CDDP was 447 +/- 169 mg (160 to 900 mg). There was no additional nephrotoxic drug. Before treatment serum creatinine concentration was normal (77 +/- 7 mumol per liter) in all patients. In 2 cases dehydration (due to vomiting and use of mannitol) occurred during CDDP treatment. One patient was treated 30 days after a nephrectomy. At the onset of dialysis, renal ultrasound was normal. In 3 cases dialysis was necessary within 15 days following chemotherapy. In one case renal function deteriorated progressively to end stage renal failure 12 months after CDDP treatment. Dialysis was performed in 3 cases by hemodialysis and in one patient by peritoneal dialysis. All patients remained more than 6 months on dialysis. Three patients died from their cancer. One patient, being considered cured from his thymoma, is currently being evaluated for a kidney transplantation. Our observations outline the potential severity of CDDP nephrotoxicity. Systemic hydration with serial serum creatinine measurements are mandatory during and after CDDP administration these patients.

[Renal effects of intravenous tertatolol in essential arterial hypertension]. / Effets rénaux du tertatolol intraveineux dans l'hypertension artérielle essentielle.

The acute renal effects of intravenous tertatolol were studied in eight patients with moderate essential hypertension: the study included a 100 mmol/day sodium intake during 3 days. Then, tertatolol was infused after a water load during 2 consecutive periods of 30 min (priming dose followed by constant infusion) in order to obtain plasma concentrations of tertatolol at 2 different levels: 10 ng/ml, then 40 ng/ml successively; the measurements were obtained at 15, 30, 45 and 60 min. The renal plasma flow (RPF) and the glomerular filtration rate (GFR) were calculated from the 131I-Hippuran clearance and the 125I-Iothalamate clearance respectively; a bladder catheter allowed a precise urine collection. The results indicate that intravenous tertatolol, at low dose, induced a marked and early renal vasodilatation; higher dose of tertatolol attenuated the vasodilator response, probably because of a decrease in cardiac output (suggested by the decrease in heart rate); thus, the systemic effects would hide the direct renal hemodynamic effects of tertatolol. Natriuresis and kaliuresis were unchanged by intravenous tertatolol.

[Renal effects of captopril in hypertension with renal artery stenosis. Comparison between Tc-99m-DTPA scintigraphy and clearance method]. / Effets rénaux du captopril dans l'hypertension avec sténose d'artère rénale. Comparaison entre scintigraphie au Tc-99m-DTPA et méthode des clairances.

In eleven hypertensive patients with renal artery stenosis, the acute renal effects of captopril were investigated using two methods: 1) the Tc99m-DTPA renography with determination of an index of renal perfusion (IP), an index of glomerular filtration (IF) and the ratio of these indices (F/P); 2) the renal hemodynamics obtained by the clearance method using a continuous infusion of I131-hippuran and I125-iothalamate for calculation of renal blood flow (RBF), glomerular filtration rate (GFR) and filtration fraction (FF). The studies were performed before and after captopril treatment. Patients were classified according to the acute response to captopril as responders (R; n = 6) and non responders (NR; n = 5). Results are as follows: (B: basal, C = captopril). (table; see text) These data confirm that captopril produced a significant decrease in F/P and FF in R whereas these indices did not change in NR; it was found that IF and GFR decreased in R whereas IF increased and GFR did not change in NR; a significant correlation was observed between delta IF and delta GFR in R (r = 0.834, p less than 0.05). These results indicate that 1) data obtained before and after captopril by renography and by clearance methods are in good correlation either in Ror in NR patients; 2) Captopril test including renography or renal hemodynamic measurements is useful for selection of R patients.

Effects of perindopril on renal haemodynamics and natriuresis in essential hypertension.

Renal haemodynamics and natriuresis were studied before and 6 h after oral intake of perindopril (8 mg) in eight hypertensive patients without renal failure. The patients were then treated with perindopril (8 mg per day) and renal haemodynamics were measured on the fifth day, 6 h after the morning intake. Sodium intake was controlled during the study (100 mmol sodium per day). Renal blood flow and the glomerular filtration rate were measured by the clearance method using 131I-hippuran and 125I-iothalamate, respectively. Mean blood pressure decreased from 135 to 110 after 6 h, and was 118 mmHg on the fifth day (P less than 0.001, respectively). Renal vascular resistance decreased significantly after acute drug intake from 0.19 to 0.15 arbitrary units (P less than 0.001) and on the fifth day to 0.16 arbitrary units (P less than 0.001). Renal blood flow rose from 708 to 723 after 6 h, and to 750 ml/min per 1.73 m2 on the fifth day but the change was no significant. There was no alteration in the glomerular filtration rate so that the filtration fraction decreased from 0.27 to 0.26 (after 6 h), and to 0.25 on the fifth day (P less than 0.02). Natriuresis increased after the first intake between the first and tenth hours. On the fifth day, maximum natriuresis was observed between the fourth and sixth hours. Perindopril caused strong renal vasodilation after the first intake and during the following days, with no change in the glomerular filtration rate. There was a significant decrease in the filtration fraction, indicating efferent, as well as afferent, arteriolar vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute and chronic effects of a new calcium inhibitor, nicardipine, on renal hemodynamics in hypertension.

Renal hemodynamics and natriuresis were studied in 10 hypertensive patients without renal failure, 2 and 4 h after oral intake of 30 mg nicardipine; then, nicardipine was given at a dose of 30 mg three times a day and the hemodynamic study was repeated on the 6th day (2 h after the morning dose). The first dose of nicardipine produced an increase in renal blood flow (from 888 +/- 45 to 999 +/- 59 ml/min 1.73 m2, p less than 0.01) and a decrease in renal vascular resistances (from 0.16 +/- 0.01 to 0.12 +/- 0.01 arbitrary unit, p less than 0.05). Glomerular filtration rate did not change and the decrease in filtration fraction was not significant. Sodium excretion increased markedly during the first 2 h (from 0.17 +/- 0.04 to 0.29 +/- 0.06 mmol/min, p less than 0.05). On the 6th day renal vascular resistances and filtration fraction remained lowered whereas glomerular filtration rate was unchanged. Nicardipine did not produce any significant alteration in plasma renin activity and plasma aldosterone after acute or chronic administration. These results confirm the potent renal vasodilatory effect of nicardipine; glomerular filtration rate was not significantly altered whereas renal blood flow and filtration fraction returned to normal levels. An early and transient natriuretic effect was observed after the first dose of nicardipine, and body weight showed a significant decrease during the study indicating that no sodium retention was induced by nicardipine.

[Comparative effects of nifedipine and indapamide in the treatment of arterial hypertension]. / Effets comparés de la nifédipine et de l'indapamide dans le traitement de l'hypertension artérielle.

A controlled multicentre trial was organised to compare the effects of 20 mg Nifedipine tablets (N) and 2,5 mg Indapamide tablets (I) during a 4 months' treatment period after a placebo period, in 59 patients with moderate essential hypertension (n = 59). The results of blood pressure measurements of 18 patients treated by nifedipine (1 tablet twice daily) and 22 patients treated by indapamide (1 tablet every morning) were compared. The systolic blood pressure, after 10 minutes recumbency, fell from 165 +/- 10 mmHg to 148 +/- 13 mmHg (p less than 0.01), and the diastolic pressure from 104 +/- 6 mmHg to 86 +/- 7 mmHg (p less than 0.01) in the patients treated with nifedipine. In the indapamide group, the SBP fell from 164 +/- 13 mmHg to 152 +/- 15 mmHg (p less than 0.01) and the DBP from 100 +/- 4 mmHg to 87 +/- 6 mmHg (p less than 0.01). There were no significant changes of heart rate with either drug; plasma creatinine, potassium and uric acid concentrations were also unchanged. There was a higher incidence of headaches and tiredness in the nifedipine group, whilst patients treated with indapamide complained more often of muscular cramps. Flushing was observed in nearly a quarter of the patients in both groups. These results confirm that both nifedipine and indapamide induce significant and persistant falls in systolic and diastolic blood pressure. Although the fall was greater with nifedipine than with indapamide, the difference was not statistically significant. The tolerance was satisfactory in both groups of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

[Acute and chronic effects of a new calcium blocker, nicardipine, on renal hemodynamics in arterial hypertension]. / Effets aigus et chroniques d'un nouvel inhibiteur calcique, la nicardipine, sur l'hémodynamique rénale dans l'hypertension artérielle.

Renal hemodynamics and natriuresis were studied in 9 hypertensive patients without renal failure, 2 hours and 4 hours after oral intake of Nicardipine 30 mg; sodium intake was kept constant during the study (100 mmol per day). Then, Nicardipine was given at a dose of 30 mg three times a day and the hemodynamic study was repeated on the 6th day (2 hours after the morning dose). Renal blood flow (RBF) and glomerular filtration rate (GFR) were measured by the clearance methods using 131I-hippuran and 125I-iothalamate respectively. Results are as follows: (Table: see text). These results confirm the potent renal vasodilatory effect of Nicardipine; GFR was not significantly altered while RBF and FF returned to normal levels. An early and transient natriuretic effect was observed after the first dose of Nicardipine and body weight showed a significant decrease during the study indicating that no sodium retention was induced by Nicardipine.

[Anuria caused by tight stenosis of the renal arteries. 2 cases]. / Anurie par sténose serrée des artères rénales. Deux observations.

Two patients developed anuria associated with tight stenosis, though not complete obstruction, of the renal arteries. This rare and little known accident is found in atheromatous patients with severe arterial hypertension of renovascular origin. It usually occurs when blood pressure falls under the influence of a precipitating factor. Diagnosis rests on angiography. Diuresis is resumed immediately after surgical revascularization. The operation must be performed in every case, even after a long delay, since the kidneys remain viable for a long time due to the development of an extensive collateral circulation. Such anurias are particularly severe in patients with poor underlying condition and when vascular lesions are diffuse.

Comparative study of muzolimine and acebutolol in the treatment of moderate hypertension.

In a controlled double-blind study the effect of muzolimine (20 mg o.d.) and acebutolol (400 mg o.d.) were investigated in outpatients suffering from moderate essential hypertension. After a three week placebo run-in period, 49 patients were recruited and followed by a cooperative group of general practitioners over a period of 3 months. Blood pressure decreased to the same extent in both groups. With regard to clinical and biological tolerance, no differences appeared between the two drugs.

[Malignant arterial hypertension, symptomatic and prognostic aspects. Retrospective study of 140 cases]. / Hypertension artérielle maligne, aspect sémiologique et pronostique. Etude rétrospective de 140 observations.

140 cases of malignant hypertension were diagnosed in our clinic from January 1966 to December 1982. On admission the mean blood pressure was 183 +/- 17 mm Hg, and all patients had grade III to IV retinopathy according to the Keith and Wagener classification; 84% of the patients had renal failure (10% of acute origin). 43% of the patients presented with clinical signs of left heart failure. Hypertension was associated with various renal diseases in 48%, was essential in 41%, and renovascular lesions were found in 9% of the cases. Headaches, asthenia and visual disorders were the 3 main symptoms of malignant hypertension, as classically described. Severe cerebral damage (including all the neurological manifestations present on admission) was found in 27% of the patients. Among the 122 patients available to follow-up, half died during the study period. The survival rate, calculated on a 5-year basis, has doubled compared with a similar patient population 17 years ago, increasing from 35% (period 1966 to 1970) to 72% (period 1977-1982). This remarkable achievement in survival rate is due to more intensive research and therapeutic progress (including, more recently, extrarenal epuration) reaching an increasingly large hypertensive population.

Pre- and posttransplant glomerulonephritis in a case of sarcoidosis.

A 39-year-old woman with documented sarcoidosis and membranous glomerulonephritis (GN) with renal failure received a kidney from her identical twin. A few months after transplantation a proliferative GN appeared with hematuria, proteinuria and progressive renal failure over 2 years. Indeed the occurrence of GN in patients with sarcoidosis raises the question of whether the relationship between these two conditions is causal or fortuitous. This report suggests that GN is secondary to sarcoidosis.

[Cardiovascular effects of prostacyclin]. / Effets cardio-vasculaires de la prostacycline.

Numerous studies have recently been devoted to the effects of prostaglandins on blood vessels. Prostacyclin (PGI2) produces relaxation of vascular smooth muscles, thereby contributing, with other vasoactive substances, to the regulation of general and local haemodynamics. Moreover, it would appear that the effects of some risk factors in atherosclerosis are mediated, at least partly, by changes in prostaglandin production. The potent vasodilator action of prostacyclin has been confirmed in man and has been investigated in some pathological conditions, such as lower limb arteriopathy, malignant arterial hypertension and coronary artery disease. The vascular effects of many therapeutic drugs are now known to be associated with their action on the biosynthesis of prostaglandins. Further studies are required to determine the role of prostaglandins, especially prostacyclin, in the pathophysiology, prevention and treatment of vascular diseases.