We investigated electrocardiographic changes occurring after hemodialysis in 20 male patients with chronic renal failure, changes in the configuration of T wave, ST segment and R wave consistent with ischemia were found in 30, 45 and 75%, respectively. Contrary to prior speculation the R wave height did not vary with the volume changes of body fluid occurring in dialysis. It is concluded that ischemic-appearing changes of uncertain significance are common in the postdialysis population.
The kallikrein-kininogen-kinin system has been postulated to play a role in the regulation of blood pressure and modulation of renal salt and water transport. The activity of this system has usually been determined by measurements of urinary kallikrein excretion. However, urinary kallikrein rarely correlates with simultaneously measured urinary kinins. To further evaluate the factors influencing urinary kinin excretion, we evaluated the role of urinary kininogen in this system. Urines were analyzed from normal subjects and individuals with untreated essential hypertension and end-stage renal disease. Intact urinary kininogen was significantly correlated with urinary kinins in normal subjects (r = 0.65, P = 0.003) and essential hypertensives (r = 0.52, P = 0.026). In both essential hypertension and end-stage renal disease, urinary kinins were significantly decreased (8.00 +/- 1.93, 0.90 +/- 0.18, P less than 0.05, respectively) compared to controls (23.73 +/- 5.20). In essential hypertensives, the reduction in urinary kinins was paralleled by a reduction in intact kininogen with a normal excretion of kallikrein. In end-stage renal disease, the reduction in kinins was paralleled by a reduction in kallikrein with a normal excretion of intact kininogen. This data suggests that kininogen may be an important determinant of urinary kinin excretion in various disease states.
The kallikrein-kininogen-kinin system (KKK) has been implicated in the renal sodium excretion response to changes in dietary sodium. However, both increases and decreases in the activity of this system have been observed when urinary sodium excretion is augmented by a variety of maneuvers. To further evaluate the potential physiologic role of this system, we measured three components of the KKK system in urine. Total kallikrein, intact kininogen, and kinin were measured twice in normal individuals during balance on both a high (250 mEq/day) or low (10 mEq/day) sodium intake. A consistent and significant reduction in the activity of all three components of the KKK system was noted during the high salt intake. Furthermore, during the high sodium intake, further acute reductions in components of this system were observed when an acute saline but not water load was administered. The consistent response of the various components of the KKK system to both acute and chronic sodium loading suggests that the system is physiologically linked to the regulation of sodium balance. However, the directional changes argue against a primary natriuretic effect of this system.
10 long-term hemodialysis patients had immediate and redistribution thallium-201 myocardial imaging performed after a course of hemodialysis. Subjects had EKGs done on the same day before and after dialysis. 3 of the 10 subjects had resting thallium-201 myocardial imaging obtained on non-dialysis days. 60% of the electrocardiograms showed changes with dialysis. All 13 thallium studies were abnormal, showing multiple transient filling defects at rest. Most subjects had permanent filling defects as well. It is concluded that hemodialysis patients have a high frequency of abnormal thallium-201 myòcardial images at rest. The cause of these abnormal studies is uncertain.
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