Biomedical subjects
Publications and source records attributed to J E Kintzel.
1. Carpal tunnel syndrome independent of uremic polyneuropathy has been described in 4 patients. 2. Operative findings are consistent with intraneural vascular compression related to the forearm A-V fistula. 3. Intraneural neurolysis results in immediate and almost total symptomatic relief.
Transient neutropenia developed in a 62-year-old, white male on maintenance hemodialysis being treated with cimetidine for an in tractable duodenal ulcer. The probable mechanism was peripheral destruction of the granulocyte series, unlike the marrow depression reported with metiamide, another histamine H2 receptor antagonist.
The present study was carried out to determine if antidiuretic hormone (ADH) altered the solute handling characteristics of the peritoneal membrane. Lightly anesthetized dogs primed with urea-(14)C (60 mol wt) and inulin (5200 mol wt) were volume expanded with hypotonic saline solution to suppress endogenous ADH as assessed by urine/plasma osmolality. With ADH suppressed, two to three control peritoneal dialysis exchanges were carried out. A constant infusion of ADH in a physiologic dose of 150 mU/hr in saline was begun and the urine/plasma osmolality followed until it was significantly greater than one. Two to three experimental dialysis exchanges were then carried out. Dialysance across the peritoneal membrane was calculated for inulin (D(I)) and urea (D(U)). In 16 such studies D(U) fell in all but three (the mean value for the fall was 2.8 +/-2.6 ml/min; P < 0.001). D(I) varied randomly and showed no significant change. In all 16 studies D(I)/D(U) rose (D(I)/D(U) = 0.054 +/- 0.054; P < 0.005). Seven dogs were studied with an identical protocol but saline was infused without ADH. D(U) and the dialysance ratio varied randomly. D(U) fell in one and did not change or rose in four and D(I)/D(U) rose in two and fell in three. The data are interpreted to show a fall in area but an increase in mean pore radius of the "peritoneal membrane" in response to physiologic amounts of intravenous ADH. The fall in area is consistent with a decreasing splanchnic blood flow.
To evaluate the effects of saline loading on distal sodium reabsorption in hypertensive man, studies were performed during both water deprivation and water diuresis in eight hypertensive subjects, and the results were compared to data obtained from similar studies in normal subjects. All hypertensive patients exhibited an enhanced excretion of filtered sodium (C(Na)/C(In)) at any level of distal delivery of sodium compared to normal controls. Free water reabsorption (T(c) (H2O)) during hypertonic saline loading was quantitatively abnormal in the hypertensives at high levels of osmolar clearance (C(Osm)), and also the curve of T(c) (H2O) vs. C(Osm) leveled off above a C(Osm) of 18 ml/min per 1.73 m(2) in the hypertensive group in contrast to the normal controls in whom T(c) (H2O) showed no evidence of achieving an upper limit. Sodium depletion exaggerated the abnormality in T(c) (H2O) in hypertensives, and resulted in a positive free water clearance (C(H2O)) during hydropenia. During hypotonic saline loading in water diuresis, changes in free water clearance per 100 ml of glomerular filtrate (C(H2O)/C(In)) were less at any given increment in urine flow per 100 ml of glomerular filtrate (V/C(In)) in the hypertensives compared to normal controls (P < 0.001). This abnormality in C(H2O)/C(In) in the hypertensives in conjunction with the defect in T(c) (H2O) observed during hydropenia indicates that sodium reabsorption in the loop of Henle was abnormal at any given rate of distal delivery of sodium in hypertension. Furthermore, these abnormalities in T(c) (H2O) and C(H2O) coincided temporally with the development of the exaggerated natriuresis. Although the distal defect in sodium transport, in large part, accounted for the augmented natriuresis in hypertension, evidence was present also for enhanced rejection of sodium in the proximal tubule during saline loading in the hypertensives. Additional studies utilizing acetazolamide which increases distal delivery of sodium without extracellular fluid volume expansion showed only minimal abnormalities in C(H2O) in the hypertensive group, indicating that the defect in sodium transport in the loop of Henle in hypertensives is mainly an abnormal response to extracellular fluid expansion rather than an intrinsic defect in the loop to handle increased tubular loads of sodium. It is possible that the abnormality in sodium reabsorption in the loop of Henle is due to the transmission of the abnormally elevated blood pressure of the hypertensives to the medullary vasa recta during saline loading.