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The aims of the present study were to examine the effects of urea and isotonic saline loads separately and together on urea handling in the medullary collecting duct and surface distal tubules of the rat kidney. Microcatheterization of the medullary collecting duct during isotonic saline diuresis (saline at 5% of body weight per hour, plasma urea 4.3 mM/L), showed an increase in the remaining fraction of filtered urea from 56.2% at the beginning (corticomedullary junction) to 68.5% at the end (papillary tip) of the medullary collecting duct (n = 17 paired samples in six rats, p less than 0.05). There was no change in the fraction of filtered urea along the medullary collecting duct during urea diuresis (plasma urea 87 mM/L, n = 15 paired samples in six rats) or during urea--saline diuresis (plasma urea 103 mM/L, n =32 paired samples in nine rats). Micropuncture of surface distal tubules in the same animals showed an increase in the fraction of filtered urea between end-distal samples and the beginning of the medullary collecting duct from 28.9 to 56.2% during isotonic saline diuresis (p less than 0.001), and from 53.6 to 75.3% during urea--saline diuresis (p less than 0.01), but no change during urea diuresis (63.6 to 60.0%, p = NS). Our conclusions are as follows. (1) Urea entry into the medullary collecting duct during steady-state diuresis occurs at low intratubular urea contractions (isotonic saline diuresis) but not at high concentrations (urea--saline diuresis and urea diuresis). (2) Urea entry between the surface distal tubule and the beginning of the medullary collecting duct occurs during saline diuresis (isotonic saline diuresis and urea--saline diuresis) but not urea diuresis. The latter finding suggests that isotonic saline loads affect urea transport differently in juxtamedullary nephrons compared to superficial nephrons.
OBJECTIVES: To determine whether results similar to a previous study, in which sucrose-induced diuresis started before creating partial outlet obstruction resulted in protection of bladder contractile function in obstructed animals, would be obtained if diuresis were begun after creation of partial outlet obstruction. METHODS: Thirty-six rats were separated into six groups of 6 rats each: group 1, control; group 2, diuresis; group 3, obstructed; group 4, obstructed immediately after diuresis; group 5, obstructed with diuresis beginning 10 days after obstruction; and group 6, obstructed before diuresis. Diuresis was induced by feeding 5% sucrose instead of water. After 3 weeks of obstruction, all bladders were excised, cut into longitudinal strips, and mounted in isolated muscle baths for physiologic study. RESULTS: Sucrose-induced diuresis resulted in a statistically significant increase in bladder mass and a mild increase in smooth muscle contractility compared with the control water-fed group. Obstruction resulted in a fourfold increase in bladder weight and substantial decreases in the responses to all forms of stimulation. The bladder weights of the obstruction plus diuresed groups were all similar to the diuresis-alone group and significantly lower than those of the obstructed group. All diuresed groups showed protection of the contractile responses compared with the obstruction-alone group. Unexpectedly, the group that began diuresis 1 day after obstruction showed the strongest protection. CONCLUSIONS: Diuresis significantly reduced the increase in bladder mass induced by obstruction and also reduced the level of contractile dysfunction. Diuresis begun 1 day after obstruction resulted in the greatest level of protection.
Medullary collecting duct function was studied by direct microcatheterization techniques in rats undergoing postobstructive diuresis. Significant net addition of water and sodium to the duct was demonstrated during postobstructive diuresis after relief of 24-h bilateral ureteral ligation. This striking abnormality in function was associated with reduced delivery of sodium and water to the collecting duct compared to sham-operated controls. To examine the role of circulating factors in this phenomenon, another group of rats was studied that underwent 24 h of total urine reinfusion into the femoral vein. Natriuresis and diuresis were similar to the postobstructive group, but absolute collecting duct reabsorption of sodium and water was normal. The natriuresis and diuresis in rats with urine reinfusion resulted from increased delivery of fluid and sodium to the medullary collecting duct. A third group of rats was studied with 24-h unilateral ureteral ligation as well as urine reinfusion from the contralateral normal kidney. Without urine reinfusion there was no diuresis-natriuresis but with urine reinfusion the diuresis and natriuresis after relief of unilateral obstruction was similar to that after relief of bilateral obstruction. Moreover, net addition of sodium and no significant water reabsorption were demonstrated in the medullary collecting duct of such animals. The results indicate that (a) the medullary collecting duct is the critical nephron segment affected by ureteral obstruction, since postobstructive diuresis occurred despite reduced delivery of fluid from the more proximal nephron; (b) the net addition of sodium to the medullary collecting duct observed during postobstructive diuresis is probably a direct effect of obstruction, since it was found during postobstructive diuresis after relief of bilateral or unilateral ureteral ligation, but not with urine reinfusion alone; and (c) blood-borne factors are important in the development of postobstructive natriuresis and diuresis, and probably act by increasing the fraction of filtered sodium and water delivered from the proximal and distal tubule to the collecting duct.
OBJECTIVE: To evaluate the effect of saline (0.9% NaCl) solution administered IV to induce diuresis on 15 dimensional variables of the kidneys, size of renal pelvis, and diameter of the cranial part of the ureters. ANIMALS: 25 dogs without evidence of renal disease that were undergoing chemotherapy for various neoplasms. PROCEDURE: The kidneys, cranial aspect of the ureters, and trigone area of the urinary bladder of each dog were examined ultrasonographically before and during IV administration of saline solution (2.7 to 18.8 ml/kg of body weight/h). RESULTS: Ultrasonography revealed unilateral and bilateral pyelectasis during diuresis in 16 of 23 (70%) dogs but unilateral pyelectasis in only 1 dog before diuresis. Unilateral pyelectasis during diuresis was observed in 11 of 16 (69%) dogs. Pyelectasis during diuresis was categorized as slight in 15 of 21 (71%) kidneys. Degree of pyelectasis during diuresis was not identical in both kidneys of 13 of 16 (81 %) dogs. Diuresis did not induce ureterectasis, and it did not cause changes in 15 dimensional variables of the kidneys. CONCLUSIONS: In nonsedated, nonazotemic dogs, IV administration of saline solution to induce diuresis may cause slight pyelectasis without evidence of ureterectasis. CLINICAL RELEVANCE: When dilatation of the cranial part of the ureter is > 2 mm at the same time that ipsilateral pyelectasis is detected during ultrasonographic examination of the urinary tract system of a nonsedated, nonazotemic dog receiving IV administration of saline solution to induce diuresis, additional examinations are recommended to determine the possibility of early obstructive nephropathy or pyelonephritis.
PURPOSE: The pleural fluid that accumulates secondary to congestive heart failure is almost always a transudate based upon its level of protein and lactic acid dehydrogenase (LDH). Previous work has suggested that the characteristics of the fluid may change into those of an exudate with diuresis. The purpose of the present study was to determine whether aggressive diuresis does result in this change in pleural fluid characteristics. PATIENTS AND METHODS: Twelve patients with severe congestive heart failure (ejection fraction 23.9 +/- 9.6%) and pleural effusions were studied serially as they underwent diuresis. After an initial thoracentesis was performed, the patients then underwent aggressive diuresis for 12 to 48 hours with one or two follow-up thoracentesis. RESULTS: The mean weight loss during the study period was 4.5 +/- 2.8 kg. With diuresis the LDH level, LDH ratio, protein level, and protein ratio all increased significantly (p less than 0.05). All 12 patients had transudative pleural effusions at the onset of diuresis. However, despite the increases in the levels of protein and LDH with diuresis, only one patient's pleural fluid attained values compatible with an exudate. CONCLUSION: From this study we conclude that it is uncommon for a transudative pleural effusion due to congestive heart failure to develop the characteristics of an exudative pleural effusion with rapid diuresis.
BACKGROUND: Hypoxia of the renal medulla has been implicated in the development of renal injury, particularly acute renal failure, and its regulation in humans may therefore be relevant to certain renal disorders. Changes in oxygenation of the renal medulla can now be monitored noninvasively with blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI). Using this method, water diuresis has been shown to improve medullary oxygenation in young persons. Urinary excretion of prostaglandin E2 (PGE2) likewise increases during water diuresis in younger but not in older people. We used BOLD MRI to measure the effects of aging and of inhibiting prostaglandin synthetase on the renal response to water diuresis in healthy human subjects. METHODS: Nine younger (25 to 31 years) and nine older (59 to 79 years) female volunteers were studied with BOLD MRI during antidiuresis in the postabsorptive state and during water diuresis. Simultaneously, urinary excretion of PGE2 was determined. PG synthetase was inhibited by administering ibuprofen. RESULTS: Renal medullary oxygenation, initially low, greatly improved during diuresis in younger subjects, whereas PGE2 excretion increased. In older women, however, water diuresis elicited no change in oxygenation of renal medulla or PGE2 excretion. Ibuprofen inhibited excretion of PGE2 and blocked the increase in medullary oxygenation normally produced by water diuresis in the young. CONCLUSIONS: The increase in oxygenation of the renal medulla accompanying water diuresis depends on PGE2 synthesis. Attenuation of renal PGE2 synthesis in older people is probably responsible, at least in part, for the loss of the ability to improve medullary oxygenation that younger subjects possess. Inability to improve renal medullary oxygenation might predispose to hypoxic renal injury in older patients.