The hourly pattern of urine solute and electrolyte excretion following standard surgical trauma

Although urine volume (and, less frequently, concentration) is often measured in the perioperative period, little attempt has been made to separate temporal phases of the intra- and postoperative response to surgery. In 7 patients undergoing standard severe single trauma and managed by a conventional regimen which included intraoperative Hartmann's solution, we have investigated the hourly pattern of urine solute and electrolyte excretion over the first 48 h. Contrary to expectation, in the first 5 h Na+ excretion increases in association with overall solute excretion, and thereafter progressively diminishes. K+ excretion increases 4 h postoperatively and remains elevated for 24 h, after which it returns to normal, even though Na+ excretion remains low. Free water excretion is negative for the first 24 h, though urine osmolality does not suggest a maximal antidiuretic response by the kidney--the highest concentration achieved being just below 800 mosmol/kg. In order to distinguish between the physiological adaptive changes due to starvation and those due to injury, the hourly pattern of urine solute and electrolyte excretion was further investigated in 12 healthy volunteers mimicking postoperative conditions. Apart from the early postoperative period, the hourly pattern of Na+, K+ and osmolar excretion shows no discernible difference from the operated group. These results show that, particularly in relation to Na+, the changes seen in the post-injury patient, even after major uncomplicated surgery, are largely adaptive, and this is especially striking at 24 h after surgery.     

The effect of vasopressin on solute and water excretion during and after surgical operations.

The relationship between the concentration of plasma arginine vasopressin (AVP), urine volume, and osmolality during and after an abdominal operation was studied in nine patients. In all patients the AVP level rose well above that necessary for maximal antidiuresis (5 fmol ml-1) and then returned to within the normal range (0.5-5.0 fmol ml-1) usually over the next 24 hours. During this period of raised AVP concentration the urine volume, which varied considerably, was closely related to osmolar excretion. With the fall of AVP to normal levels, all but one of the patients eventually exhibited positive free water clearance. However, in most patients the urine remained hypertonic for some hours and its volume continued to be determined mainly by osmolar load which was itself apparently related to glomerular filtration rate. At no time was there a significant relationship between changes in plasma AVP concentration and urinary volume.     

Polyuria of thyrotoxicosis: downregulation of aquaporin water channels and increased solute excretion

Thyrotoxicosis is a common disorder causing cardiovascular and renal irregularities. In this study, thyrotoxicosis was produced in rats by 14 days of daily thyroxine injection. This was associated with an increase in cardiac index, mean arterial pressure, and renal blood flow compared with euthyroid controls. Food and water intake along with urine output were significantly increased in the thyrotoxic rats compared with control animals associated with a significant increase in solute excretion. Polyuria and increased solute excretion still occurred even when food and water intake was equivalent. These renal responses were associated with significant decreases in AQP1 and AQP2 water channel expression in both the ad lib and paired intake studies in the cortex and inner medulla. The downregulation of AQP2 protein occurred in spite of equivalent plasma arginine vasopressin (AVP) in the ad lib and increased AVP in the paired feeding studies. Solute-free water reabsorption was greater in both the ad lib and paired thyrotoxic than euthyroid rats and was associated with increased Na-K-2Cl cotransporter expression. We propose that the AVP-independent downregulation of AQP2, the observed increase in renal arterial pressure, and decrease in filtration fraction contribute to polyuria the increased solute excretion in spite of enhanced ion transporters in thyrotoxicosis.     

Inositol hexakisphosphate in urine: the relationship between oral intake and urinary excretion

OBJECTIVE: To study the relationship between the oral intake of inositol hexakisphosphate (InsP6, phytic acid, an inhibitor of urinary crystallization) and its urinary excretion, to establish their possible mutual influence. MATERIALS AND METHODS: Two groups of male Wistar rats (six animals each) received either; tap water and normal rat food pellets (controls); or a liquid diet in which InsP6 was absent and which then received gradually increasing amounts of InsP6. The urinary levels of InsP6 were then assessed regularly in both groups. RESULTS: When InsP6 was absent from the diet, urinary excretion declined to undetectable levels after 22 days. The addition of increasing amounts of InsP6 to the liquid diet caused an increase in its urinary excretion after about 10 days. Adding InsP6 in amounts > 425 mg/L caused no further increases in urinary excretion. Adding inositol (with no InsP6) to the liquid diet caused only a slight increase in the urinary excretion of InsP6. CONCLUSION: These results showed that InsP6 urinary levels were related to its oral intake; consequently, a low consumption of InsP6 would cause a urinary deficit of this crystallization inhibitor and thus an increase in the risk of developing urinary calcium stones. Although urinary excretion was dose-dependent, there was an ingested amount (20.9 mg/kg) above which there was no increase in the amount excreted. This intake is easily obtained by consuming a normal diet (rich in InsP6) indicating that to maintain appropriate urinary levels of InsP6, the consumption of InsP6 supplements is only necessary when the diet is particularly poor in InsP6.     

Variation of urate excretion with urine flow in normal man.

In normal persons, a decrease in urine flow following the injection of small amounts of vasopressin was accompanied by a significant decrease in the clearance and excretion of urate. When vasopressin and a small natriuretic dose of mannitol were administered together, urine flow and urate excretion again decreased. The recovery of urine flow to control values was accompanied by a similar recovery of urate excretion. Because a natriuretic dose of mannitol did not reverse the antiuricosuric effect of the flow decline, it is postulated that the flow effect probably reflects changes in a component of urate efflux distal to the loop of Henle.     

Control of renal solute excretion by enteric signals and mediators

Renal solute excretion is important for the homeostasis of various ions. It is widely believed that hormones such as aldosterone, parathyroid hormone, the vitamin D endocrine system, and growth factors are responsible for alterations in renal ion transport in response to increased absorption of enteric solutes. In the cases of sodium, potassium, and phosphorus, moieties produced in the gastrointestinal tract alter renal ion transport when foods that have high concentrations of cognate ions are ingested. The gastrointestinal tract senses the presence of increased luminal concentrations of these ions, presumably via specific "sensors," and responds by releasing effector substances into the intestinal wall and portal circulation. These substances rapidly increase renal excretion or reduce renal tubular reabsorption and thus blunt large increases in the serum concentrations of these ions. The characterization of enteric solute sensors and mediators will greatly advance our understanding of physiologic mechanisms that control solute homeostasis and will allow the development of specific drugs that stimulate or inhibit these pathways.     

Impact of acute reduction in chronically elevated left atrial pressure on sodium and water excretion

To test the hypothesis that a reduction in chronically elevated left atrial pressure would decrease sodium and water excretion in humans, we studied 61 carefully selected patients who underwent cardiac surgery for valvular or coronary artery disease or both. The immediate postoperative decrease in left atrial pressure (from 16.7 +/- 1.0 to 9.4 +/- 0.4 mm Hg; p less than 0.001) was inversely correlated with postoperative urine output (r = -0.69; p less than 0.001) and sodium excretion (r = -0.51; p less than 0.005). There was no significant relationship between postoperative urine output or sodium excretion and other hemodynamic or nonhemodynamic variables. A significant postoperative decrease in plasma atrial natriuretic factor (from 150 +/- 22 to 65 +/- 14 pg/ml; p less than 0.01) and increase in plasma renin activity (from 2.5 +/- 0.6 to 8.7 +/- 3.2; p less than 0.05) occurred in patients with a 7 mm Hg or greater postoperative decrease in left atrial pressure. Thus, an acute reduction in left atrial pressure results in significant reductions in urine output and sodium excretion, the magnitude of which are related to the degree of reduction in left atrial pressure.     

Effects of an acebutolol-hydrochlorothiazide combination on urinary solute excretion in healthy adults

Ten healthy adult male volunteers were studied to assess the urinary effects of a single dose of a combination of hydrochlorothiazide 12.5 mg and acebutolol 200 mg (HZAL). The formation induced a significant increase in the 24-hour urinary output of sodium. Outputs of fluid, chloride, potassium, calcium, magnesium, zinc, total inorganic phosphate and creatinine were unaffected. With the exception of Mg2+ flow, times to maximal urinary flows of fluid and solutes were shortened by HZAL. These qualitative changes resemble those induced by hydrochlorothiazide but did not achieve quantitative significance, either because the constituent diuretic dose was too small or because acebutolol compensated for some of its effects.     

Impact of the endothelin system on water and sodium excretion in patients with liver cirrhosis.

BACKGROUND: Impaired renal function in patients with liver cirrhosis is a serious complication and is characterized by sodium and water retention in the absence of identifiable specific causes of renal dysfunction. The endothelin system has been shown to be activated in liver cirrhosis and might contribute to impaired renal function. However, the mechanisms leading to an activation of the endothelin system in these patients and the effects of an activated endothelin system on renal function in these patients are as yet unknown. METHODS: To determine the correlation between the activity of the endothelin system and the ability to excrete water and sodium in patients with liver cirrhosis, we measured plasma endothelin-1 concentrations by reversed phase-HPLC followed by an endothelin RIA and performed an oral water load tests in 10 healthy control subjects and 43 patients with liver cirrhosis. In addition, we analysed possible mechanisms/factors like plasma endotoxin that might contribute to the activation of the endothelin system in liver cirrhosis. RESULTS: This study showed that the endothelin system is activated in patients with liver cirrhosis in a disease-stage-dependent manner. Patients with Child C liver cirrhosis have a 5.45-fold increased plasma ET-1 concentration compared to healthy controls, whereas plasma ET-1 is only increased 2.74-fold in Child A patients. An oral water load test revealed a highly significant (P < 0.0001) inverse correlation between the plasma endothelin-1 concentrations and the ability to excrete a given water load. Plasma endotoxin, a well-known stimulus of ET-1, is significantly (P < 0.03) correlated with plasma ET-1 in cirrhotic patients. The ET-1 concentrations in the ascites of patients with liver cirrhosis were lower and not related to plasma ET-1. CONCLUSION: The activity of the endothelin system in patients with liver cirrhosis depends on the severity of liver impairment. Plasma endotoxin might be an important stimulus of the endothelin system in liver cirrhosis. We observed a highly significant inverse correlation between the plasma endothelin-1 concentrations and the ability to excrete a given water and sodium load, suggesting that the endothelin system plays a role in the regulation of water excretion in patients with liver cirrhosis.     

Glycosaminoglycans and urine flow rate

The value of glycosaminoglycans determination in urine has been challenged because the relation between the glycosaminoglycans concentration and other signs of kidney damage is a matter of controversy. It is quite possible that the observed discrepancies could be due to the influence of the urine flow rate, the urine concentration and the time of day on the glycosaminoglycans concentration. Therefore, standardization of the urine sampling time and selection of the most appropriate unit to quantify glycosaminoglycans excretion seem to be essential.     

Impact of renal cryoablation on urine composition

Objectives. To examine prospectively serial urine biochemical parameters in 14 patients (9 men, 5 women) undergoing laparoscopic cryoablation of a small, exophytic solid renal mass. Prior studies have shown that various types of renal injury may predispose to the formation of urinary calculi. The metabolic effects of cryoenergy on the surrounding normal renal parenchyma are unknown.Methods. Timed 24-hour urine collections were obtained preoperatively and postoperatively on days 1, 30, and 60 to evaluate the following parameters: light microscopic findings, volume, pH, creatinine, protein, beta₂-microglobulin, calcium, citrate, oxalate, phosphate, uric acid, sodium, and potassium.Results. Urinary beta₂-microglobulin excretion increased from a preoperative baseline value of 114.8 to 1931.2 μg/L on postoperative day 1, an increase of more than 15-fold (P = 0.05), thus confirming major renal injury. These values sharply decreased at 30 days and returned to near-baseline levels at 60 days postoperatively (P = 0.76). Nevertheless, all lithogenic parameters remained within the normal range throughout the follow-up period, with no significant change in any value.Conclusions. Our findings suggest that renal cryoablation does not adversely alter urine composition with respect to lithogenic parameters for up to 2 months after surgery. Elevated beta₂-microglobulin levels indicating significant renal injury immediately postoperatively spontaneously revert to baseline levels within 2 months.     

Lack of effect of salt intake on urinary uric acid excretion

Although it has been established that acute expansion of the extracellular fluid volume results in enhanced uric acid clearance, the effect of chronic volume expansion by a high salt diet on urinary uric acid excretion has not been examined. Eleven normal subjects were placed on a constant diet containing 10 mEq. sodium per day for 10 days, followed by 240 mEq. sodium daily for another 10 days. Measurements were performed on the final 3 days of each phase. Urinary sodium increased from 9 plus or minus 3 standard error to 221 plus or minus 9 mEq. per day (p less than 0.001), and uric acid clearance increased from 5.9 plus or minus 0.4 to 7.1 plus or minus 0.6 ml. per minute (p less than 0.01). However, serum uric acid decreased from 6.4 plus or minus 0.4 to 5.5 plus or minus 0.3 mg./dl. (p less than 0.001). Total urinary excretion of uric acid did not change (533 plus or minus 24 to 535 plus or minus 26 mg. per day). A high salt diet does not result in sustained hyperuricosuria, although it may predispose to kidney stone formation in other ways.     

Solute-free water excretion and electrolyte-free water excretion are better terms than solute-free water clearance and electrolyte-free water clearance

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