The fluid therapy given to 1027 patients during the first 48 hours after burning II. The inputs of sodium and water and the tonicity of the therapy

A survey has been made of the actual amounts of sodium and the volumes of fluid isotonic with respect to the sodium ion and sodium-free water given to 1027 patients of all ages and having burned areas covering between 10 and 90 per cent of the body surface. Our actual inputs have been compared with those actually given in other units treating burned patients and those recommended by the various formulae which are considered to indicate the sodium and water requirements of burned patients.

The inputs of sodium and isotonic fluid were directly related to the severity of the burn and were almost always within the range of inputs given in the majority of other units treating burned patients. Our inputs were often greater than those recommended by the various formulae. In contrast to the sodium and isotonic fluid inputs our relatively large inputs of sodium-free water were not related to the severity of the burn. The tonicity of the therapy given to patients with relatively small burns was therefore markedly hypotonic whereas the patients with the most extensive burns received near isotonic therapy.     

A randomized study of intravenous fluid replacement following living-donor renal transplantation

Fourteen adult recipients of living-donor kidneys preserved with ice-cold intracellular electrolyte solution were randomly assigned to receive either high fluid replacement (total volume of urine output + 30 ml/hr) or low fluid replacement (constant 125 ml/hr) during the first 48 hr after grafting. High replacement recipients had significantly higher fluid intake and urine output than did low replacement recipients. However, net fluid balance at the end of the 48-hr study period was positive for both groups and not significantly different. Fractional excretion of sodium was directly related to urine output in all patients. Serum osmolality, serum sodium concentration, and urine sodium concentration were not significantly different in the treatment groups. Urine osmolality was significantly higher in the low-replacement group at 24 and 36 hr after transplantation. The i.v. replacement of total urinary output is unnecessary in adult recipients of living-donor kidneys preserved with ice-cold intracellular electrolyte solution because such grafts can conserve sodium and water immediately after transplantation.     

Acute Effects of Furosemide and Mannitol on Renal Function in the Early Postoperative Period

The effects of furosemide and mannitol on renal function in the immediate postoperative period were studied in 16 patients, who had undergone upper abdominal surgery under neurolept anaesthesia. Renal function was studied preoperatively and during the first postoperative hour with a standard clearance technique. The patients were then randomly given furosemide, 1 mg/kg b.w., or mannitol, 0.5 g/kg b.w. Renal function was further investigated during the following 6 h in periods of varying duration. The injection of furosemide caused an initial increase of renal plasma flow (RPF), while glomerular filtration rate (GFR) decreased. Striking increases of urine flow, fractional sodium, fractional chloride and fractional osmolal excretion were found. These increases reached maximum levels during the second 20-min clearance period after the injection. Fractional free water reabsorption decreased and during the first 20-min clearance period it changed into free water clearance. These changes had reached or nearly reached the preoperative control levels after 6 h.
The infusion of mannitol caused an initial rise in RPF, while GFR remained stable. Increases were found in urine flow, fractional sodium, fractional chloride, fractional osmolal excretions and fractional free water reabsorption. The changes reached maximum levels during the first 20-min control period and then gradually returned to the preoperative control levels.
Mannitol did not impair GFR and had a milder effect on renal function than furosemide. The losses of sodium and water were much smaller in the mannitol group than in the furosemide group. It is therefore concluded that mannitol should be used as the diuretic of choice in the treatment of postoperative oliguria in patients without known cardiovascular disease associated with increased preload and/or left ventricular insufficiency.     

Urinary nitrite excretion and urinary variables in patients with primary nocturnal frequency of micturition: effects of indomethacin suppositories

Urinary nitrite excretion was measured in patients with primary nocturnal frequency of micturition (PNFM) and in normal individuals. Effects of indomethacin suppository on urine volume and other urinary variables were evaluated. The study comprised seven patients with PNFM and seven healthy control (age range 30–45 years). Nitrite was assayed in spot morning urine samples; urine volume, urine osmolality and electrolytes, serum osmolality and electrolytes and functional bladder capacity (FBC) were assayed. Both groups were then given 100 mg of indomethacin suppository daily for a maximum of 10 days and urinary variables were re-evaluated during day 10. Results showed that urinary nitrite excretion of patients with PNFM was greater than that of the normal subjects (230±62 umol/l vs. 42±30 umol/l, P<0.05). The mean (SD) 24 h urine volume and osmolality, the night urine volume and osmolality, serum osmolality, FBC, creatinine clearance, fractional excretion of sodium (FENa), fractional excretion of potassium (FEK), and urinary excretion of glucose and potassium were lower in patients with PNFM as compared with normal individuals, although not statistically significantly so, except for FBC that was significantly lower in the patients. Urinary excretion of sodium, calcium, chloride, phosphorus, magnesium, day-night urinary volume ratio, spot morning osmolality, nocturnal index, and nocturnal polyuria index were higher in patients with PNFM. Indomethacin decreased the 24 h urinary volume by 21%, creatinine clearance by 12%, osmolar clearance by 14% and urinary protein excretion by 38% in the patients. These variables decreased by 26, 45, 17 and 12% respectively in the healthy subjects, whereas 24 h urinary protein excretion increased mildly by 9%. Indomethacin increased day-night urinary volume ratio by 73% in the healthy subjects. It might be concluded that urinary nitrite excretion, urinary excretion of sodium, chloride, phosphorus, calcium, and magnesium increased and FBC decreased in patients with PNFM; Indomethacin decreased urinary volume, FENa, FEK, osmolar clearance, and free water clearance in the healthy subjects and the patients. These might explain the mechanism of action of indomethacin to reduce frequency of voiding. The possible interaction of prostaglandin and NO in the pathogenesis of PNFM is discussed.     

Emergency Treatment of Lithium-Induced Diabetes Insipidus with Nonsteroidal Anti-Inflammatory Drugs

Thiazides and amiloride are the most often suggested treatment for nephrogenic diabetic insipidus. We found this ineffectual in a patient with acute problems and reviewed the literature to see if there were other more efficient approaches. A 47-year-old woman on lithium had polyuria. When inadvertently fasted for 48 h she became confused, had a seizure, and her sodium was 170 mmol/L. Urinary output was 24 L/day. Large volumes of intravenous fluids were given but sodium remained >170 mmol/L. Treatment with DDAVP, thiazides, and amiloride did not decrease urinary output. Indomethacin 150 mg was started and urine volume immediately fell to one-half. However, because of persistent high urine output the patient was then fluid depleted, with further reduction to normal in urine volume, and Na decreased to 140 mmol/L. Creatinine rose from 135 μmol/L to 173 μmol/L, but decreased to 152 μmol/L when indomethacin was decreased to 75 mg q.d.; urinary output remained stable around 2 L/day. The literature described 22 patients with nephrogenic diabetes insipidus (16 congenital, 6 lithium) treated with nonsteroidal anti-inflammatory drugs. Urine flow was reduced to 1/3, within hours. Rarely, mild renal failure ensued, improving in all but one case when nonsteroidal anti-inflammatory drugs were reduced. Indomethacin (and controlled volume reduction if continued high urine output), while observing renal function, appears the emergency treatment of choice for serious complications of nephrogenic diabetes insipidus.     

Factors affecting urine volume in chronic renal failure

Twenty-four-hour urine volume was studied in 80 determinations from 12 patients with chronic renal failure (creatinine clearances between 7.1 and 38.9 L/d) hospitalized on a metabolic ward. Urine volume ranged from 0.91 to 4.51 L/d. Various components of urine that might affect urine output, ie, osmolar excretion, sodium excretion, urea nitrogen excretion, free water clearance, and potassium excretion, were correlated with urine volume to determine their relative effects. Total osmolar excretion correlated highly with urine output (r = .92, P less than .001), while correlation with free water clearance was weak. Of the three osmotic components, total urea nitrogen excretion correlated best with urine volume (r = .86, P less than .001), while the correlation with sodium excretion was less pronounced (r = .75, P less than .001). The relatively greater impact of urea excretion on urine volume was confirmed by multiple regression analysis. However, total cation excretion (sodium plus potassium) gave nearly as good a regression with urine volume (r = .83, P less than .001). Our findings confirm that total osmolar excretion is a major determinant of urine volume in chronic renal failure and suggest that urea excretion may play the most important role in determining output.     

A comparison of the effects of potassium citrate and sodium bicarbonate in the alkalinization of urine in homozygous cystinuria

For many years, urine alkalinization has been one of the cornerstones in the treatment of homozygous cystinuria. Because of the relationship found between the excretion of urinary sodium and cystine, potassium citrate has emerged as the preferred sodium-free alkalizing agent. To evaluate the usefulness of potassium citrate for urine alkalization in cystinuric patients, sodium bicarbonate and potassium citrate were compared in 14 patients (10 on tiopronin treatment and four without treatment with sulfhydryl compounds). The study started with 1 week without the use of any alkalizing agents (Period 0) followed by 2 weeks with sodium bicarbonate (Period 1) and 2 weeks with potassium citrate (Period 2). Urinary pH, volume, excretion of sodium, potassium, citrate and free cystine, as well as the plasma potassium concentration, were recorded. Potassium citrate was shown to be effective as an alkalizing agent and, in this respect, not significantly different from sodium bicarbonate. Even though a normal diet was used, a significant increase in urinary sodium excretion was observed with sodium bicarbonate (Period 1). Urinary potassium and citrate excretion increased with potassium citrate (Period 2). A significant correlation was found between urinary sodium and cystine in the tio-pronin-treated patients. No significant differences in cystine excretion were recorded in Periods 0, 1 and 2. Plasma potassium was significantly higher during Period 2, but only one patient developed a mild hyperkalemia (5.0 mmol/l). The use of potassium citrate for urine alkalization in homozygous cystinuria is effective and can be recommended in the absence of severe renal impairment.     

Early anuria prevention in human kidney transplantation. Advantage of fluid load under pulmonary arterial pressure monitoring during surgical period.

In human kidney transplantation, a high blood flow established through the graft immediately upon clamp release is usually associated with immediate satisfactory renal function. One hundred consecutive kidney transplant patients were thus provided with a large volume of fluid during surgery. To avoid pulmonary edema, fluid load was given under mean pulmonary arterial pressure (PAP) monitoring, and controlled ventilation was maintained during the early postoperative period. Whether initial PAP value was within normal range or elevated, all patients required an equivalent fluid load to reach the best hemodynamic condition upon clamp removal. The mean intraoperative fluid load consisted of 2406 +/- 968 ml of water with 22.8 +/- 9.4 g of sodium chloride, 5.9 +/- 1.8 units of albumin, and 2.6 +/- 1.8 units of packed red blood cells. Immediately before clamp release patients were given furosemide and mannitol. During the postoperative period, i.v. infusions consisted of water and sodium chloride (6 g/liter) to match urine output, provided that diuresis was equal to or above 400 ml/hr. If diuresis remained or decreased below this level, diuresis replacement was associated with PAP-controlled infusion of saline, albumin, and red blood cells if needed. Furosemide was eventually given if diuresis did not increase above 400 ml/hr with fluid loading. With this protocol a good early diuresis was established in 95% of the cases. Ten patients required dialysis before the 5th postoperative day, one of them because of fluid overload and anuria. Concurrently, a decreased mortality rate and an increased graft survival rate were observed.     

Atrial natriuretic polypeptide after burn injury: blood levels and physiological role in rats

To define the relationship between atrial natriuretic polypeptide and the physiological changes of water and electrolytes after burns, the changes in plasma hormonal levels, including atrial natriuretic polypeptide, and urinary water and sodium excretions were examined in burned rats. Further, to elucidate the physiological significance of atrial natriuretic polypeptide after burns, the effects of a specific antiserum against atrial natriuretic polypeptide were determined in burned rats. Plasma atrial natriuretic polypeptide levels in rats following 30 per cent BSA full skin thickness burns were elevated for sustained periods (432.3 +/- 156.5 pg/ml, P less than 0.01 on day 1 postburn, 244.5 +/- 73.7 pg/ml, P less than 0.05 on day 3 postburn). Urine volume and sodium excretion decreased significantly during the first 72 h after burns. On day 3 postburn, urine volume and sodium excretion began to increase significantly. Specific rabbit antiserum against atrial natriuretic polypeptide was injected into the burned rats during this diuretic phase. Significant inhibition of diuresis and natriuresis was observed after the injection of antiserum (27.5 +/- 2.4 per cen decrease in urine volume, 57.1 +/- 10.4 per cent decrease in sodium excretion). These results suggest that atrial natriuretic polypeptide plays a physiological role in the regulation of urinary water and sodium excretion after burns.     

Increased natriuretic ability and hypotensive effect during short-term high calcium intake in essential hypertension

The present study has investigated whether an increased natriuresis could account for the hypotensive effect of a high calcium diet which has been reported by others. A calcium supplement (equivalent to 1 g of elemental calcium) was given for 5 days to 18 patients with essential hypertension in a randomized single-blind, placebo-controlled, cross-over trial. In 15 of the patients, 2 liters of isotonic saline were infused intravenously over 4 h during the last day of each test period and hourly urine collections were taken. Calcium supplementation produced a mild but significant hypercalcemia as well as increased urinary calcium excretion. Body weight and systolic blood pressure decreased significantly. The blood pressure decrease was indirectly related to the pretreatment plasma renin activity (r = -0.61, p less than 0.01). Urinary sodium excretion increased during calcium diet (80 mmol/day negative balance, p less than 0.01). During saline infusion under calcium supplementation the urine volume, osmolality and sodium excretion were significantly higher compared with placebo. The changes in urinary sodium excretion correlated positively with the changes in urinary calcium excretion (r = 0.68, p less than 0.01) in patients given the high calcium diet, when infused with saline. We conclude that calcium supplementation induces a considerable sodium loss in the urine which is very likely to result in the hypotensive effect.     

Parenteral fluid therapy in septic shock: An evaluation of crystalloid and colloid

A retrospective review of 25 patients with bacteremic shock was undertaken to evaluate and compare the quality of resuscitation with infusion of either crystalloid or colloid solutions. The average improvement in systolic pressure in the crystalloid infusion group was 23 mm of Hg, whereas the colloid group achieved a mean rise in pressure of 48 mm. Colloid was also superior to crystalloid in terms of speed and magnitude of response measured. In the group of 8 patients given colloid, central venous pressure was recorded over the 24-hour infusion period with a mean rise of 8 cm of water produced, vs. 2 cm of water in the crystalloid group. Crystalloid administration aggravated arterial hypoxemia, whereas colloid infusion did not worsen respiratory function. All 25 patients were oliguric or anuric before beginning therapy; adequate urine flow was quickly restored by expanding blood volume alone, with the fusion of a large volume of salt and water unnecessary. Hence, it is concluded that salt solutions should not be given in cases of bacteremic shock, unless clear indications of deficits or continuing losses of sodium and water are present. Excessive sodium administration was an unreliable and ineffective blood volume expander, accentuated hypoalbuminemia, and increased pulmonary shunting and hypoxemia. Prompt blood pressure and central venous pressure elevation, and restoration of urine flow, can be achieved with colloid solution.     

Comparison of the diuretic effect of furosemide mixed with human albumin or fresh frozen plasma for patients with hypoalbuminemia in the intensive care unit

BACKGROUND: Diuretics are commonly used in the intensive care unit (ICU) for patients with fluid over-loading. Hypoalbuminemia is a major cause of diuretic resistance. Albumin mixed with furosemide can promote diuresis and sodium excretion in patients with hypoalbuminemia. The purpose of this study is to compare the diuretic effect of furosemide (FU) mixed with human albumin (HA) or fresh frozen plasma (FFP) in ICU patients with hy-poalbuminemia. METHODS: Patients with fluid overloading and hypoalbuminemia who needed diuretic treatment were enrolled and were divided into 2 groups: the first group having clearance of creatinine (CCr) >20 ml/min, and the second group having CCr < or = 20 ml/min. FU (60 mg) mixed with HA (HA group), 60 mg FU mixed with FFP (FFP group) and water (placebo group) were given intravenously to these patients for 60 minutes in random order on the first, third and fifth day. After drug administration, 8-hour urine was collected, and urine amount and urinary sodium excretion were checked. RESULTS: Both the HA group and the FFP group had significantly higher urinary volume and sodium excretion than the placebo group in the patients with CCr >20 ml/min or CCr < or = 20 ml/min (p < 0.01). In the patients with CCr >20 ml/min, there was no difference in the amount of urine excretion and cumulative urinary sodium excretion between the HA group and FFP group. In the patients with CCr < or =ml;20 ml/min, the HA group had a significantly higher urine output and urinary sodium excretion than the FFP group (p < 0.05). CONCLUSIONS: In ICU patients, 60 mg FU mixed with HA or FFP has a similar diuretic effect in patients with CCr >20 ml/min. FFP is an effective alternative choice for improving diuresis for ICU patients with hypoalbuminemia. In patients with CCr < or = 20 ml/min, albumin mixed with 60 mg FU has a superior diuretic effect compared with FFP mixed with FU.     

Urine electrolytes in the assessment of extracellular fluid volume contraction

The purpose of this study was to determine which urine electrolytes should be measured to confirm that the extracellular fluid (ECF) volume is depleted. ECF volume contraction was induced by furosemide administration to rats consuming an electrolyte-free diet. An external potassium balance was achieved by replacing potassium losses with KHCO3 and KCl so that the sodium and chloride deficits were comparable (equivalent to a 30% reduction in ECF volume). As expected, the urine sodium and chloride concentrations fell to 2 +/- 0.3 mmol/l and 3 +/- 0.3 mmol/l, respectively. Rats were then randomized to receive 50-75% of their sodium or chloride deficit as either: NaCl (control group), NH4Cl or NaHCO3 to mimic clinical situations associated with ECF volume contraction. In the NaCl group, the urine sodium and chloride concentrations remained low (6 +/- 2 mmol/l and 7 +/- 2 mmol/l), consistent with persistent ECF volume contraction. Although the NH4Cl group continued to have a low urine sodium concentration (2 +/- 0.2 mmol/l), there was now a marked increase in the urine chloride concentration (51 +/- 7 mmol/l; p less than 0.01 vs. NaCl group). In contrast, although the NaHCO3 group continued to have a low urine chloride concentration (2 +/- 1 mmol/l), there was a significant increase in the urine sodium concentration (19 +/- 3 mmol/l; p less than 0.01 vs. NaCl group). We conclude that the clinical assessment of ECF volume by urine electrolytes requires an evaluation of both the urine sodium and chloride concentrations.     

Low-dose dopamine treatment of patients in nonketotic hyperosmolar hyperglycemic coma

In the acute neurosurgical setting, nonketotic hyperosmolar hyperglycemic coma (NHC) is thought to be caused by cerebral dehydration therapy and administration of steroids, glycerol, or mannitol. The mortality of this complication is reportedly very high, and is due to acute renal and/or cardiac failure. The authors evaluated the effect of low-dose dopamine (LDD; 1 to 5 micrograms/kg/min) administration in 10 patients with this syndrome. LDD was given to five patients. In these cases, hypovolemia was treated under central venous pressure monitoring with an iso-osmolar hyponatremic lactate solution given in a volume greater than the urine output. After the hypovolemia was corrected, the fluid was administered in a volume equal to the urine output until the serum osmolarity was normalized. In the five patients not given LDD, a large quantity of hypotonic solution was rapidly administered. In all patients treated with LDD, the urinary sodium increased and the urinary output stabilized. Consequently, the excess urea-nitrogen and serum sodium were quite easily washed out. The total net intake volume for the normalization of serum osmolarity was small and the duration of treatment was much shorter than that of patients not treated with LDD. The LDD regimen was not associated with complications, such as aggravation of cerebral edema, renal failure, or cardiac failure. On the other hand, three of the five patients not given LDD died of acute renal and/or cardiac failure without normalization of laboratory data. It is emphasized that this therapy, which results in beta-effect of catecholamine, sodium diuresis, and increased renal blood flow, is a practical means of managing acute neurosurgical cases complicated by NHC.     

Principles of quantitative water and electrolyte replacement of losses from osmotic diuresis

Osmotic diuresis results from urine loss of large amounts of solutes distributed either in total body water or in the extracellular compartment. Replacement solutions should reflect the volume and monovalent cation (sodium and potassium) content of the fluid lost. Whereas the volume of the solutions used to replace losses that occurred prior to the diagnosis of osmotic diuresis is guided by the clinical picture, the composition of these solutions is predicated on serum sodium concentration and urinary sodium and potassium concentrations at presentation. Water loss is relatively greater than the loss of sodium plus potassium leading to hypernatremia which is seen routinely when the solute responsible for osmotic diuresis (e.g., urea) is distributed in body water. Solutes distributed in the extracellular compartment (e.g., glucose or mannitol) cause, in addition to osmotic diuresis, fluid transfer from the intracellular into the extracellular compartment with concomitant dilution of serum sodium. Serum sodium concentration corrected to euglycemia should be substituted for actual serum sodium concentration when calculating the composition of the replacement solutions in hyperglycemic patients. While the patient is monitored during treatment, the calculation of the volume and composition of the replacement solutions for losses of water, sodium and potassium from ongoing osmotic diuresis should be based directly on measurements of urine volume and urine sodium and potassium concentrations and not by means of any predictive formulas. Monitoring of clinical status, serum sodium, potassium, glucose, other relevant laboratory values, urine volume, and urine sodium and potassium concentrations during treatment of severe osmotic diuresis is of critical importance.     

Sodium and potassium excretion in patients with ileostomies.

The output of sodium and potassium from urine and ileostomy was investigated in 35 healthy patients with ileostomies; 17 had undergone proctocolectomy for ulcerative colitis and 18 for Crohn's colitis. Fifteen of the patients with Crohn's disease had also had small bowel resections, varying from 15 to 46% of the original bowel length. The patients were investigated at home because most studies of sodium and water balance in patients with ileostomies have been done in hospital wards, which may not reflect actual conditions. Mean (SD) ileostomy output was 565 (152) ml in patients with ulcerative colitis and 1,267 (540) ml in patients with Crohn's disease. The intrapatient variation was limited, whereas the interpatient variation was significant and correlated with the length of small bowel resected. The sodium concentration in the ileostomy discharge was 110 (9.2) mmol/l and did not change consistently with ileostomy volume. The potassium concentration was 10 (2.1) mmol/l. There was a significant inverse correlation between daily ileostomy sodium output and urinary sodium concentration (r = -0.44, p less than 0.01), and a significant correlation between the daily output of sodium in ileostomy contents and the sodium:potassium ratio in urine. We conclude that patients with ileostomies are at risk of sodium and water depletion, particularly those who have had small bowel resections. Increased sodium output from the ileostomy is associated with a reduction in the sodium:potassium ratio in the urine. To screen patients at risk, an estimate of the sodium balance can be made by measuring sodium and potassium concentrations in a single specimen of urine.     

Effects of increased intra-abdominal pressure and volume expansion on renal function in the rat.

BACKGROUND: The effects of increased intra-abdominal pressure (IAP) and volume expansion on renal function in the rat were studied to gain more knowledge of the oliguria seen during laparoscopic procedures and to reduce the detrimental renal effects of IAP. METHODS: IAP was elevated to 5 or 10 mmHg by insufflation of CO(2) and maintained for 2 h in anaesthetized and mechanically ventilated rats. Rats with normal IAP served as controls. An angiotensin II receptor I antagonist, candesartan, was given as a bolus injection and a 5% volume expansion was achieved by i.v. saline infusion. An angiotensin-converting enzyme (ACE) inhibitor was also given. Renal parameters were the glomerular filtration rate (GFR), urine production, the urinary concentrations of sodium and potassium and the osmolality in the urine. The arterial acid-base balance and blood pressure were also monitored. RESULTS: The GFR deteriorated by 70% during pneumoperitoneum (PP) of 10 mmHg. There was a dramatic drop in sodium excretion (88-97%). With candesartan and elevated IAP, there was a drop in mean arterial pressure (from 90 to 55 mmHg) and the negative renal effects were very pronounced. Renal function was better preserved during elevated IAP in combination with volume expansion. CONCLUSIONS: Capnoperitoneum suppresses renal function, especially in combination with angiotensin II receptor 1 blockade and ACE inhibition. Volume expansion reduces the deleterious effects of PP on renal function during elevated IAP. The results suggest that patients should not be given pharmaceuticals blocking the renin-angiotensin-aldosterone system prior to procedures that may increase IAP. It may be beneficial, however, to reduce angiotensin II tension by volume expansion.     

Hormonal, renal, and autonomic nerve factors involved in the excretion of sodium and water during dynamic salt and water loading in hypoxaemic chronic obstructive pulmonary disease.

BACKGROUND--Some patients with hypoxaemic chronic obstructive pulmonary disease (COPD) develop sodium and water retention and a subclinical autonomic neuropathy. The possibility that these might be associated has been investigated. METHODS--The ability of 24 patients with COPD to excrete a 6 ml/kg 2.7% intravenous saline or 15 ml/kg oral water load was studied and changes in plasma electrolyte levels, osmolality, plasma aldosterone and vasopressin levels, urinary volume and sodium content, glomerular filtration rate, renal blood flow, and cardiovascular autonomic nerve function were measured. Patients were divided into groups of eight: those in group A (controls) had mild COPD with a Pa02 of > 9 kPa and no oedema, patients in group B were more hypoxaemic but had never been oedematous, whilst those in group C were hypoxaemic and mildly oedematous at the time of the study. RESULTS--Patients in groups B and C excreted less sodium and water during saline loading and a lesser proportion of the water load. Patients in group C had a reduction in renal blood flow and glomerular filtration rate and all had a subclinical autonomic neuropathy, which was also found in three patients in group B. Their plasma aldosterone level was raised but did suppress appropriately on saline loading. Vasopressin levels were abnormally raised for the osmolality in patients in group C and in those with autonomic dysfunction throughout the water load and at 240 minutes after the salt load. Sodium and urine excretion was highly correlated with autonomic dysfunction, aldosterone levels at time zero, and renal blood flow. The 11 patients with autonomic dysfunction were more likely to be oedematous, more hypoxaemic, excreted much less urine and sodium, had lower glomerular filtration rate and renal blood flow, and higher aldosterone and vasopressin levels than the remaining patients. CONCLUSIONS--In patients with COPD the inability to excrete sodium and water is multifactorial. This is the first study to show that autonomic dysfunction is at least associated and might play an important part in the impaired sodium and water homeostasis seen in patients with severe COPD.     

Changes in urine volume accomplished by physicians treating nephrolithiasis

PURPOSE: We quantified the changes in urine volume and sodium accomplished in various practice settings and the consequent effects on calcium oxalate supersaturation. MATERIALS AND METHODS: We determined comprehensive urine stone risk factors in 2,877 patients treated in 14 practices, including a university referral center and private sector practices. Changes in urine volume and stone risk factors were measured. RESULTS: In a wide range of practice settings the volume increase was about 0.3 l. daily. Urine sodium excretion increased with volume for unexplained reasons, as did urine calcium excretion. As expected, thiazide lowered calcium excretion but the effect progressively decreased as urine volume increased. Therefore, urine calcium and calcium oxalate supersaturation changes were the result of opposing forces. The net effect was a decrease partly offset by sodium and calcium excretion increases. CONCLUSIONS: Urine volume increments are modest in practice and they are modestly offset by increases in urine sodium due to increased sodium intake. Clinicians should strive for higher volume increases than are currently achieved and be vigilant concerning what seems to be a strong tendency toward a higher sodium intake with more fluids.     

去甲肾上腺素对肾移植术患者肾功能的影响

目的 探讨去甲肾上腺素对肾移植术患者肾功能的影响.方法 同种异体肾移植术患者32例,ASA分级Ⅲ或Ⅳ级,年龄22～64岁,随机分为多巴胺组(D组)和去甲肾上腺素组(N组),每组16例.麻醉诱导后D组静脉输注多巴胺1～10μg·kg-1·min-1,N组静脉输注去甲肾上腺素0.03～0.3μg·kg-1·min-1,持续至术毕,维持术中MAP波动幅度不超过基础水平的10%.分别于术毕及术后12 h时取中心静脉血样及尿样,测定血清半胱氨酸蛋白酶抑制因子C(Cystatin C)、β2-微球蛋白(β2-MG)及尿α1-微球蛋白(α1-MG)、β2-MG的浓度,并记录术中输液总量、肾血管开放至术毕时的尿量、术后12 h内的尿量及呋塞米的用量.结果 两组术中输液总量、尿量及呋塞米用量和各时点血清Cystatin C、β2-MG及尿α1-MG、β2-MG浓度比较差异无统计学意义(P＞0.05);与术毕时比较,术后12 h时两组患者血清Cystatin C、β2-MG及尿α1-MG、β2-MG浓度均降低(P＜0.05).结论 静脉输注去甲肾上腺素0.03～0.3μg·kg-1·min-1对移植肾功能无不良影响,可用于肾移植术患者.