Biomedical subjects
Publications and source records attributed to P Cacoub.
The authors report the case of an AIDS patient presenting with both Streptococcus pneumoniae pneumoniae and pneumocystosis. What was remarkable in that case was the appearance, in an otherwise favourable course, of a large excavation in the territory of the pneumonia. The responsibility of Pneumocystis carinii in this excavation is discussed.
Concomitant renal and ocular lesions have been described in a few systemic diseases. The association of acute interstitial nephritis (AIN) and anterior uveitis without determined cause was first described in children. Recently, the same clinical association has been reported in adults. We report 3 cases of this association and present a review of the literature. Including our 3 patients, 7 cases of this association have been reported in adults. All patients were females aged 27-74 years. Initial symptoms were either ocular, or pseudoviral (fever, myalgia and fatigue). Histological renal studies revealed acute interstitial nephritis with tubular lesions. Immunofluorescence and electron microscopy were not contributive. Ocular prognosis was always good. In 5 patients, the evolution of renal function was excellent with complete resolution of acute renal failure within a few weeks. Chronic renal failure developed in two of the four patients who did not receive systemic steroid therapy (with evolution towards terminal renal failure in one patient). Three of the patients received 60 mg per day of prednisone and none of them developed chronic renal failure. Despite the small number of patients reported and the possibility of spontaneous regression, these data suggest a beneficial effect of systemic steroid therapy to prevent or reduce interstitial inflammation and subsequent fibrosis.
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Renal function has been evaluated in 21 patients treated with cyclosporin A (CyA) for 9 months for idiopathic uveitis. Serum creatinine, which was 82 mumol.l-1 before treatment, was significantly elevated after 1 month (111 mumol.l-1). After 9 months of treatment, and despite a decrease in CyA dosage, the mean plasma creatinine remained elevated at 132 mumol.l-1. Hypertension developed in 6 patients, five of them being concomitantly treated with corticosteroids. In 8 patients serum creatinine 3 months after CyA had been stopped had decreased from 148 to 93 mumol.l-1. Two of those patients remained hypertensive 3 months after CyA treatment had ceased. In patients with idiopathic uveitis CyA induces a reversible increase in serum creatinine. However the reversibility of such a biochemical marker does not preclude a histopathological lesion. Chronic renal damage may be responsible for the persistence of hypertension after cessation of CyA treatment.
Plasma atrial natriuretic peptide (ANP) concentrations were measured by radioimmunoassay 1 to 12 days after operation in six patients with artificial hearts. The mean levels were significantly higher in artificial heart recipients (58.2 pg.ml-1) than in controls (12.6 pg.ml-1). The mechanism underlying the raised values is not clear, although it is suggested that elevated atrial pressure may have been the stimulus for higher ANP release. In 3 patients plasma ANP concentrations were also measured 1 to 5 days after orthotopic transplantation. In all of them ANP concentrations had increased by 20 to 74% despite lower right atrial pressure. An increase in atrial tissue mass may have contributed to the raised plasma ANP after orthotopic transplantation. It also suggests that the functioning sympathetic nervous system is not a necessary condition for ANP release.
Animals and humans undergoing treatment with ciclosporin (CS) show a reversible increase in renal vascular resistance and a decrease in glomerular filtration rate. The causes of these abnormalities have not yet been established. We evaluated the effects of a 1-week treatment with CS on creatinine clearance, renal arachidonic acid metabolites, plasma renin activity (PRA), plasma aldosterone levels, urinary excretion and plasma levels of catecholamines in 7 patients with idiopathic uveitis. We show that CS treatment induces a significant (p less than 0.05) decrease in creatinine clearance (from 132 +/- 0.5 to 108 +/- 8 ml/min); urinary 6-keto-PGF1 excretion (from 17.8 +/- 4.9 to 10.9 +/- 3.3 ng/mmol creatinine), urinary thromboxane B2 excretion (from 7.0 +/- 1.0 to 3.6 +/- 0.9 ng/mmol creatinine), upright PRA (from 4.2 +/- 0.9 to 2.3 +/- 0.8) and supine PRA (from 2.0 +/- 0.5 to 1.1 +/- 0.3). We found no change in plasma aldosterone levels and plasma levels and urinary excretion of catecholamines. We suggest that the reversible renal vasoconstriction observed in patients treated with CS may be induced by inhibition of renal prostacyclin synthesis. In this setting inhibition of PRA and angiotensin II formation may impair autoregulation of effective filtration pressure and therefore glomerular filtration rate.
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Foscarnet (FC) is a new antiviral agent which has been recently proposed for the treatment of severe cytomegalovirus (CMV) infections in immunocompromised patients. When used intravenously (i.v.), main adverse effects of FC are a fall in hemoglobin, and an increase in liver enzymes and serum calcium. Although increased serum creatinine have been noted in several patients, deterioration of renal function is often accounted for by the concomitant use of other nephrotoxic drugs, the severity of underlying disease or the presence of graft rejection. Consequently FC is often considered as a non or poorly nephrotoxic drug. We report 4 cases of acute renal failure (ARF) which can be exclusively attributed to FC. FC was used for CMV chorioretinitis in 3 AIDS patients and in one non-immunocompromised patient. ARF was diagnosed between the 6th and 15th day of treatment, with oligoanuria in two patients (one of whom required two hemodialysis periods). ARF was most likely secondary to acute toxic tubulopathy. Three patients did not receive any other nephrotoxic drug. The fourth patient received concomitantly sulfadiazine but renal function returned to baseline value after FC completion although sulfadiazine was continued. In conclusion, our 4 observations suggest that FC may be responsible for acute tubulopathy. We suggest that in these patients renal function should be carefully monitored and dehydration promptly corrected to limit the risk of nephrotoxicity.
The case histories of the 49 patients who died in a series of 165 patients admitted to the Medical Unit between 1958 and 1984 with polyarteritis nodosa (PAN) were reviewed. The causes of death of the 29 men and 20 women, mean age 51.44 +/- 7.4 years, were classified into 6 groups. Infection accounted for 26.5% (13/49) of deaths, the initial site of infection being pulmonary, complicated by septicaemia in 6 cases. Cardiovascular events were responsible for death in 24.4% (11/49): terminal cardiac failure (4 cases), myocardial infarction (1 case), ventricular tachycardia (1 case), stroke (1 case), pulmonary embolism (2 cases), fulminant hemoptysis (1 case). Gastrointestinal complications were the cause of death in 16.3% (8/49): ischemic necrosis (5 cases), acute pancreatitis (2 cases), oesophageal ulceration (1 case). Renal failure was observed in 10.2% (5/49), all occurring before 1972: acute renal failure (3 cases), chronic renal failure (2 cases). Cancer was the cause of death in 10.2% (5/49): primary bronchial carcinoma (2 cases), laryngeal carcinoma (1 case), carcinoma of the vulva (1 case), bone metastases (1 case). Finally, 14.2% (7/49) could not be classified in the preceding groups. Sudden death occurred in 3 patients, shock in 1 patient, multivisceral PAN in 2 patients and anaphylactic shock in 1 patient. Three of the 12 patients who had post-mortem studies had signs of progressive vasculitis. The results are compared with other reports in the literature and the pathogenic mechanisms are discussed. The infections and cardiovascular deaths occurred early or late and were not related to the state of the activity of the vasculitis. Immunosuppressive treatment seems to play an important role in their pathogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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Animals and humans undergoing a treatment with cyclosporin (CsA) show a reversible increase in renal vascular resistance and decrease in glomerular filtration rate. The causes of these abnormalities have not yet been established. In animals potential mechanisms for CsA induced renal functional impairment are an increase in urinary thromboxane A2 excretion, plasma renin activity and renal sympathetic nervous system activity and an enhancement of vasopressin stimulated Ca++ mobilisation and cell contraction in vascular smooth muscle cells. In human, the problem is far less clear. CsA induces an inhibition in PRA and urinary prostaglandins excretion. Furthermore CsA does not modify urinary and plasma levels of catecholamines. Whatever the mechanism underlying the vasoconstriction induced by CsA, the inhibition of PGI2 synthesis and angiotensin II formation may participate in the decrease in renal blood flow and glomerular filtration rate which is observed in patients receiving CsA.
The effects of calcium channel blockade with nifedipine (N) on cis-diammine dichloroplatinum II (CDDP)-induced nephrotoxicity were tested in male Sprague-Dawley rats. Renal function was evaluated before and five days after CDDP administration (5 mg/kg). The rats were treated with various doses of N (0.1; 0.3; 0.6 mg/kg/day) 2 days before CDDP administration and throughout the study. The severity of CDDP-induced acute renal failure was markedly modified in N-treated animals according to the daily dosage of N. At 0.3 and 0.6 mg/kg BW/day, N enhanced CDDP nephrotoxicity. Serum creatinine was 637 +/- 45 and 611 +/- 71 mumoles/liter, respectively, 5 days after CDDP administration (vs. 313 +/- 24 mumoles in animals treated with CDDP alone; p less than 0.05). In these animals the plasma potassium level was significantly elevated at day 7 when compared with CDDP-treated and control rats. In contrast, at the dose of 0.1 mg/kg BW/day N attenuated CDDP nephrotoxicity with a serum creatinine of 214 +/- 35 mumoles at the end of the study. The pathologic changes were also more severe in the groups receiving 0.3 and 0.6 mg/kg of nifedipine. We postulate that at the higher doses (0.3 and 0.6 mg/kg) the systemic hemodynamic effects of nifedipine may override the potentially beneficial intrarenal effect which may account for the favorable results recorded with a dosage of 0.1 mg/kg.
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