[Clinical picture, diagnosis and therapy of renovascular hypertension].
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Biomedical subjects
Publications and source records attributed to U Kuhlmann.
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The nephrotic syndrome may be associated with several complications caused by severe proteinuria. The consequences of severe renal protein loss are disturbances of water and electrolyte metabolism, thromboses and thromboembolic complications, hyperlipidemia with accelerated atherosclerosis and, finally, some other complications due to the decreased oncotic pressure and the renal loss of transport globulins and immunoglobulins. Diagnosis and treatment of these complications are important in the management of patients with nephrotic syndrome. In the present study, the frequency and localization of thromboses and thromboembolic complications in 11 patients with nephrotic syndrome are described. In addition, factors which are known to be responsible for the hypercoagulable state in nephrotic syndrome were evaluated and correlated to the thromboembolic complications in these patients. An important finding was that in all patients with thromboses and thromboembolic complications, the serum albumin concentrations were below 2 g/100 ml, whereas, with one exception, serum albumin levels were above 2 g/100 ml in cases without thromboembolic complications. Our results indicate that serum albumin levels may be used as an indirect parameter to assess the risk of thromboembolic complications in patients with nephrotic syndrome.
The basic features of Goldenhar syndrome are preauricular appendices, epibulbar dermoids, vertebral and cardiac anomalies, and hypoplasia of the lungs. The syndrome appears to be caused by early damage during the first or second month of embryonic development. Prognosis is most often determined by the underlying heart disease. In the present study a 24-year-old female student is reported who exhibited a preauricular appendix on the right side, severe thoracic scoliosis, aplasia of the middle and lower lobes of the right lung, dextropositio cordis and an atrial septal defect with severe pulmonary hypertension. Cineangiocardiography revealed a mitral valve prolapse with slight mitral regurgitation and a dilated right ventricle with severe tricuspid regurgitation. Left and right ventricular function was slightly to moderately reduced. Selective coronary arteriography revealed a coronary fistula from an atrial branch of the left coronary artery to the right atrium. Symptomatic therapy with digitalis, anticoagulation and repeated venesection was initiated because of the severe hemodynamic findings. However, the patient developed syncope at increasingly frequent intervals and died 3 months after the initial examination.
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Percutaneous transluminal dilatation was performed in 5 patients with unilateral atherosclerotic renovascular disease and one patient with occlusion of a renal artery. Hemodynamic activity of the stenosis was documented by determination of pre- and poststenotic blood pressure values and by measurement of renal plasma flow. Flowing transluminal dilatation all patients showed a significant drop in blood pressure and antihypertensive treatment could be reduced or even discontinued. Only one patient became hypertensive again 3 months after the dilatation procedure. In this patient both the reduction of renal plasma flow and the delayed nephrographic effect on the stenotic side in the intravenous urogram were interpreted as symptoms of a recurrence of significant renal artery stenosis. In 2 of the six patients with impaired kidney function glomerula filtration are increased, as documented by a decrease in serum creatinine values. The results show that percutaneous transluminal dilatation may be a valuable method in the management of renovascular hypertension.
The oto-vertebral syndrome is a rare combination of malformations of the ears, spinal anomalies, and congenital heart disease. The syndrome appears to be caused by early embryonic exogenous damage during the 6th or 7th week of embryonic development. The case is reported of a 28-year-old man with bilateral aplasia of the external ear, bilateral aplasia of the ear canal, hypoplasia of the mandibula, severe thoracic scoliosis, and ventricular septal defect with pulmonary hypertension. He was admitted with dyspnea on exertion, syncope, and severe cyanosis. Cardiac catheterization revealed severe pulmonary hypertension with moderate right-to-left and slightly left-to-right shunt (Eisenmenger syndrome). Right and left ventricular function, as evaluated by angiocardiography, was slightly reduced. Because of the severe hemodynamic alterations, symptomatic therapy with digitalis, repeated venesection, and anticoagulation was initiated.
Percutaneous transluminal dilatation of a left sided renal artery stenosis was performed in a 61 year old patient with hypertension. Biochemical and hemodynamic activity of the renal artery stenosis was demonstrated by measurement of renal venous renin-activity and determination of renal plasma flow and of pre- and poststenotic blood pressure values. Shortly after the dilatation procedure hypertension disappeared and renal plasma flow increased. The described procedure might be an alternative method to renal vascular surgery.
Percutaneous transluminal dilatation of a left-sided renal-artery stenosis was done in a 61-year-old patient with hypertension. Shortly after dilatation blood-pressure fell to normal and renal plasma flow increased. Dilatation might be an alternative to renal vascular surgery in severe renal hypertension.
Acute oliguric renal failure due to acute interstitial nephritis developed in a patient after treatment with phenylbutazone. The histological, immuno-histological and serological features in this case are compatible with the involvement of a delayed hypersensitivity reaction in the pathogenesis of this drug-induced interstitial nephritis. Other side effects of phenylbutazone on the kidney and the water and electrolyte metabolism are discussed.
In three patients with diabetes and hyporeninemic hypoaldosteronism changes in renin activity, plasma aldosterone and cortisol were examined under various conditions: orthostasis and intravenous furosemide, infusion of synthetic beta1-24 ACTH on two consecutive days and diurnal variations in basal hormone fluctuations. Each patient showed unmeasurably low renin activity unresponsive to orthostasis and intravenous furosemide while plasma aldosterone was below normal range. Under ACTH-infusion only marked increases in aldosterone were observed in one patient whereas cortisol responded normally in all diabetics tested. Analysis of diurnal night day fluctuations (20.00-8.00) in plasma aldosterone and cortisol revealed a close and statistically significant relationship between both hormones in each of the three patients (p less then 0.05-less than 0.001). Variations in plasma aldosterone thus were mediated through changes in endogenous pituitary ACTH. Compared with normal controls however, diurnal aldosterone curves were set at a lower level. Our results demonstrate that a reduced sensitivity of the adrenal gland to ACTH is not responsible for the observed subnormal plasma aldosterone levels in these patients. Therefore, the lack of circulating angiotensin II seems to be the causative reason of hypoaldosteronism. The exact mechanism of undetectable renin activity in these patients remains unknown.
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Plasma renin activity (PRA) was determined in both renal veins of 37 patients with angiographically proven renal artery stenosis. Renal venous PRA was determined in 17 patients without furosemide stimulation and in 20 patients before and 15 and 30 min after intravenous injection of 40 mg furosemide. 21 of 37 patients showed abnormally high peripheral PRA. In the 17 patients in whom renal venous PRA was measured without stimulation, 11 showed a PRA ratio (PRA stenotic side/PRA unaffected side) greater than or equal to 1.5. The 20 patients in whom stimulation with furosemide was performed were divided into 2 groups each containing 10 patients: The first group was characterized by an increase in PRA ratio after furosemide stimulation, while in the second group this PRA ratio decreased. In the first group mean duration of hypertension was 4.5 years compared to 7.5 years in the second group. In 17 of 37 patients renal artery stenosis was corrected by surgery. After operation 12 patients became normotensive and in 2 patients hypertension improved. There was no effect of renovascular surgery on blood pressure in only 3 patients. None of these patients showed an increasing ratio in response to furosemide. Our results suggest that the validity of renal venous PRA measurements is enhanced when the procedure is performed before and after administration of furosemide.
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A 39-year-old man with pulmonary disease due to Mycobacterium xenopi is described. He had received prednisone and azathioprine for 5 years and prednisone in combination with cyclosporin A for 1 year in an effort to prevent rejection of his renal transplant. Shortly after the renal allograft was removed because of chronic rejection, the patient developed dyspnea and a decrease in vitality. He had no history of preexisting lung disease. A chest roentgenogram showed multiple nodular infiltrates in both lungs. M. xenopi was cultured from three sputum samples. The organism was susceptible to isoniazid, streptomycin, ethambutol, rifampin, pyrazinamide, and ethionamide. The patient was treated successfully with isoniazid, ethambutol, and rifampin for 3 months and with isoniazid in combination with rifampin for an additional 9 months, while he was maintained on continuous ambulatory peritoneal dialysis (CAPD). The literature on mycobacterial disease, especially in renal transplant recipients and patients on CAPD, is reviewed.
Fungal infection is a rare cause of peritonitis in patients on chronic peritoneal dialysis. In this population, fungi are found in less than 2 percent of all cases of primary episodes of peritonitis (1). More often, a primary bacterial peritonitis treated with antibiotic therapy leads to secondary fungal infection (2). Candida species cause 74.5% of the episodes of fungal peritonitis (2). The fungi invade the peritoneal cavity from the skin peri- or intraluminally through the catheter (3). Filamentous fungi are rare (4,5). Treatment of fungal peritonitis commonly consists of removal of catheter and antifungal drugs (3). Here we describe two cases of fungal peritonitis caused by mycelial fungi, where the source of the microorganism could be special containers used for biological waste, which are popular in Germany