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Objective: To determine the relationship between arterial function (stiffness and wave reflection) and glomerular hemodynamics., Methods: In 49 healthy normotensive individuals, glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured by urinary clearances of 99mTC-DTPA and 131I-hippuran, respectively. Filtration fraction was computed as GFR/ERPF. Arterial stiffness was estimated by carotid-femoral pulse wave velocity (PWV). Wave reflection was evaluated by carotid augmentation index (AIx), reflection magnitude and the round-trip travel time of the pressure wave., Results: PWV and round-trip travel time were not independently correlated with any renal hemodynamic parameter or urinary albumin-creatinine ratio (UACR). AIx and reflection magnitude were directly correlated with filtration fraction (r = 0.35 and 0.37, respectively) and UACR (r = 0.43 and 0.53, respectively). When the population was divided into quartiles of reflection magnitude, filtration fraction and UACR progressively increased from the lowest to the highest quartile and after adjustment for age, mean arterial pressure, heart rate but also sex for UACR (P linear trend = 0.031 and 0.001, respectively)., Conclusion: It is suggested that in normal individuals, the amplitude of wave reflection but not arterial stiffness is associated with signs evocative of increased glomerular pressure (filtration fraction and UACR), independently of systemic blood pressure.

The influence of a 3-month antihypertensive treatment on cardiac structure and renal function was assessed in patients with uncomplicated essential hypertension randomly allocated to treatment by the nonselective beta-blocker tertatolol or the angiotensin-converting enzyme inhibitor enalapril. Both tertatolol and enalapril treatments were associated with a similar decrease in mean arterial pressure (-26 +/- 6 and -15 +/- 2 mm Hg, respectively, both p < 0.05 in comparison with baseline values) and left ventricular mass (echocardiography: -48 +/- 17 vs. -18 +/- 6 g) but no change in glomerular filtration rate (DTPA clearance). Renal vascular resistance decreased similarly in both groups. Urinary albumin excretion was not significantly modified in either group. These results indicate that a consistent reduction in arterial pressure by either treatment was associated with a proportional change in left ventricular geometry and no alteration in renal function.

A case is reported of a 50-year-old man who took a massive overdose of diltiazem (5,400 mg), together with 1,350 mg potassium clorazepate and 390 mg nordazepate, five months after having experienced a myocardial infarction (MI). On admission, systolic blood pressure was 80 mmHg, with an irregular heart rate of 60 b.min-1. There was superficial polypnea (40 c.min-1) with hypoxia (PaO2: 63.5 mmHg). The ECG revealed, besides the MI scar, complete sinus arrest. Endotracheal intubation and mechanical ventilation were rapidly required. The patient then had gastric lavage, and was given activated charcoal. Treatment with 1.5 mg atropine and 2 g intravenous calcium chloride were unable to amend the cardiac dysrhythmia. A continuous isoproterenol infusion restored a sinus rhythm, but this was not maintained because of the risk of side-effects. Cardiovascular collapse was treated with dobutamine (10 micrograms.kg-1.min-1). As the peripheral and pulmonary vascular resistances were greatly diminished (464 dyn.s.cm-5 and 86 dyn.s.cm-5 respectively), alpha and beta mimetics were used: 1 microgram.kg-1.min-1 noradrenaline and 15 micrograms.kg-1.min-1 dobutamine. After 7 h of this treatment, spontaneous sinus rhythm returned abruptly. Noradrenaline and dobutamine were replaced thereafter with adrenaline (0.25 microgram.kg-1.min-1), which was stopped 24 h later. There was a marked respiratory and haemodynamic improvement, the patient leaving the intensive care unit on the fourth day and returning home one week after the overdose. The relationships between cellular calcium movements and the adrenergic system are discussed, as well as the possible mechanism of cardiac failure.

Purpose: Proteinuria is usually considered a manifestation of glomerular disease. We sought to describe the characteristics of patients with nephrotic-range proteinuria resulting from renovascular disease and to compare them with those of patients who had glomerulonephritis.Subjects and Methods: We identified 14 patients with nephrotic-range proteinuria and renovascular disease and compared them with 14 patients who had nephrotic-range proteinuria and biopsy-proven glomerulonephritis, matched for sex, age, and glomerular filtration rate.Results: Patients with renovascular disease were more likely to have known atherosclerotic vascular disease [13 of 14 (93%) vs 3 of 14 (21%), P < 0.0001) and were usually smokers [12 of 14 (85%) vs 3 of 14 (21%), P < 0.0001]. They also had a greater mean (+/- SD) difference between the lengths of their kidneys (29 +/- 10 vs 5 +/- 5 mm, P < 0.001); greater systolic blood pressure (203 +/- 22 vs 174 +/- 25 mm Hg, P < 0.005), plasma renin activity (17 +/- 19 vs 2 +/- 2 ng/mL/h, P = 0.005), and plasma aldosterone concentration (40 +/- 23 vs 11 +/- 10 ng/dL, P = 0.0001); and lower serum potassium levels (3.3 +/- 0.5 vs 3.8 +/- 0.5, P <0.05). Effective renal plasma flow was lower (139 +/- 68 vs 307 +/- 185 mL/min/1.73 m3) and filtration fraction was markedly greater (0.28 +/- 0.04 vs 0.15 +/- 0.07, P = 0.0001) in the patients with renovascular disease. After the oral administration of captopril, blood pressure, effective renal plasma flow, and glomerular filtration rate decreased only among patients with renovascular disease. Of the 14 patients with renovascular disease, 13 had evidence of renal artery thrombosis seen at angiography; 2 patients required dialysis, and 3 others died during follow-up.Conclusion: Our findings suggest that the patients with nephrotic-range proteinuria resulting from renovascular disease have distinct characteristics and a poor prognosis. [ABSTRACT FROM AUTHOR]