Does a high concentration of calcium in the urine cause an important renal concentrating defect in human subjects?

2000 ◽  
Vol 98 (3) ◽  
pp. 313-319 ◽  
Author(s):  
George S. S. LAM ◽  
John R. ASPLIN ◽  
Mitchell L. HALPERIN

The objective of this study was to evaluate the hypothesis that a high concentration of ionized calcium in the lumen of the medullary collecting duct causes an osmole-free water diuresis. The urine flow rate and osmolality were measured in normal human subjects, as well as in patients with a history of nephrolithiasis who excreted more than 5 mmol of calcium per 24 h. There was an inverse relationship between the concentration of calcium in the urine and the 24 h urine volume both in normal subjects and in patients with a history of nephrolithiasis. When the concentration of calcium in the urine was greater than 5 mmol/l, the urine volume was less than 1 litre per day in the majority of subjects. After 16 h of water deprivation, when the concentration of calcium in the urine was as high as 17 mmol/l (ionized calcium 7.4 mmol/l), urine osmolality was 1258 mOsm/kg of water and the urine flow rate was 0.30 ml/min. We conclude that, although a calcium receptor may be present in the lumen of the medullary collecting duct in human subjects, an extremely high concentration of urinary total and ionized calcium does not cause a clinically important defect in the renal concentrating process.

1997 ◽  
Vol 8 (6) ◽  
pp. 880-886
Author(s):  
S D Soroka ◽  
S Chayaraks ◽  
S Cheema-Dhadli ◽  
J A Myers ◽  
S Rubin ◽  
...  

Antidiuretic hormone leads to an increase in the permeability for water and urea in the inner medullary collecting duct. Hence, urea may not be an "effective" osmole in the inner medulla during maximal renal water conservation. Accordingly, the purpose of this study was to evaluate whether differences in the rate of urea excretion would influence maximum renal water conservation in humans. In water-deprived rats, the concentration of urea and total osmolality were somewhat higher in the urine exiting the inner medullary collecting duct than in interstitial fluid obtained from the entire papillary tip. Nevertheless, the "nonurea" (total osmolality minus urea in millimolar terms) osmolality was virtually identical in both locations. Chronically fasted human subjects that were water-deprived for 16 h had a lower rate of urea excretion (71 +/- 7 versus 225 +/- 14 mumol/min) and a somewhat lower urine osmolality (745 +/- 53 versus 918 +/- 20 mosmol/kg H2O). Nevertheless, they had identical urine flow rates (0.5 +/- 0.01 and 0.5 +/- 0.02 ml/min, respectively), and their nonurea osmolality also was similar (587 +/- 25 and 475 +/- 14 mosmol/kg H2O, respectively) to the water-deprived normal subjects. The composition of their urine differed in that the principal nonurea osmoles became NH4+ and beta-hydroxybutyrate rather than Na and C1. During water deprivation in normal subjects, the ingestion of urea caused a twofold rise in urine flow rate, a fall in the nonurea osmolality, and a rise in the rate of excretion of nonurea osmoles. The nonurea osmolality of the urine, and presumably the medullary interstitial fluid as well, was inversely related to the urea excretion rate. In chronic fasting, the nature, but not the quantity, of nonurea osmoles changed. The similar minimum urine volume was predictable from an analysis based on nonurea osmole considerations.


1994 ◽  
Vol 112 (2) ◽  
pp. 551-554 ◽  
Author(s):  
Ricardo Marques Dias ◽  
Carlos Stabile ◽  
Pedro Dotto ◽  
José Roberto Jardim

In order to analyze the effect of intermittent negative pressure ventilation (NPV) on renal function, we studied 20 healthy male volunteers (mean age 29±4.1 years). NPV was performed with an "Emerson Chest Respirator Pump", adjusted to a breathing frequency of 10 respirations per minute, with inspiratory time/total respiratory time ratio of 0.4 and negative pressure of 25 cmH2O. The experimental protocol was carried out in two phases of two hours each - spontaneous breathing and NPV breathing. At the end of each phase, urine volume of the whole period was collected as well as venous blood sample for biochemical determinations. During NPV there was significant increase (P<0.05) in urine flow rate (1.43±0.81 to 2.76±1.95 ml/min) as well as in natriuresis (258±201 to 389±175 mcEq/min), kaliuresis (61±45 to 98±49 mcEq/min), fractional sodium excretion (1.38±0.88 to 1.96±0.98%), osmolar clearance (3.13±1.82 to 4.32±1.24 ml/min) and pH (7.37± 0.04 to 7.41±0.07) with unchanged creatinine and free water clearances. We concluded that NPV increases urine flow rate, kaliuresis and natriuresis but the data we have do not allow us to explain the mechanisms underlying such a phenomenon.


Author(s):  
Mark T Houser

To substantiate the effects of urine flow rate on renal lysozyme handling and N-acetyl-β-d-glucosaminidase (NAG) excretion, experiments were performed in normal human subjects. Urine flow rate was varied by overnight fluid deprivation and progressive diuresis induced by oral water loading. Lysozyme measurements were made using an improved turbidimetric method and NAG determinations using a modified fluorometric assay utilising individual recovery techniques. Fractional lysozyme clearance and lysozyme excretion demonstrated a nearly linear relationship with urine flow rate ( r=0·78, r=0·80, P<0·0005), and both were elevated significantly in samples obtained during diuresis. NAG excretion, however, demonstrated a significant but weak correlation ( r=0·47, P<0·005) with fractional urine flow rate. A significant ( P<0·05) difference in NAG activity occurred only during the period of hydropenia, when a decrease in excretion was observed. These findings suggest that the effect of diuresis on lysozyme excretion should be considered in studies utilising this enyzyme as a marker of renal injury.


2003 ◽  
Vol 284 (1) ◽  
pp. F199-F208 ◽  
Author(s):  
Sophie Combet ◽  
Nancy Geffroy ◽  
Véronique Berthonaud ◽  
Bernhard Dick ◽  
Laurent Teillet ◽  
...  

Senescent female WAG/Rij rats exhibit polyuria without obvious renal disease or defects in vasopressin plasma level or V2 receptor mRNA expression. Normalization of urine flow rate by 1-desamino-8-d-arginine vasopressin (dDAVP) was investigated in these animals. Long-term dDAVP infusion into 30-mo-old rats reduced urine flow rate and increased urine osmolality to levels comparable to those in control 10-mo-old rats. The maximal urine osmolality in aging rat kidney was, however, lower than that in adult kidney, despite supramaximal administration of dDAVP. This improvement involved increased inner medullary osmolality and urea sequestration. This may result from upregulation of UT-A1, the vasopressin-regulated urea transporter, in initial inner medullary collecting duct (IMCD), but not in terminal IMCD, where UT-A1 remained low. Expression of UT-A2, which contributes to medullary urea recycling, was greatly increased. Regulation of IMCD aquaporin (AQP)-2 (AQP2) expression by dDAVP differed between adult and senescent rats: the low AQP2 abundance in senescent rats was normalized by dDAVP infusion, which also improved targeting of the channel; in adult rats, AQP2 expression was unaltered, suggesting that IMCD AQP2 expression is not regulated by dDAVP directly. Increased AQP3 expression in senescent rats may also be involved in improved urine-concentrating capacity owing to higher basolateral water and urea reabsorption capacity.


1998 ◽  
Vol 275 (3) ◽  
pp. F400-F409 ◽  
Author(s):  
David Marples ◽  
Birgitte Mønster Christensen ◽  
Jørgen Frøkiaer ◽  
Mark A. Knepper ◽  
Søren Nielsen

To examine the involvement of vasopressin and dehydration in the regulation of aquaporin-2 (AQP2) expression in rat kidney, we investigated the effects of treatment for 60 h with the specific V2-receptor antagonist OPC-31260 (OPC), alone and in conjunction with dehydration for the last 12 h. Changes in AQP2 protein and mRNA expression in kidney inner medulla were determined by Western and Northern blotting, and AQP2 distribution was analyzed by immunocytochemistry and immunoelectron microscopy. Treatment with OPC increased urine output fourfold, with a reciprocal decrease in urine osmolality. AQP2 expression decreased to 52 ± 11% of control levels ( n = 12, P < 0.05), and AQP2 was found predominantly in intracellular vesicles in collecting duct principal cells. This is consistent with efficient blockade of the vasopressin-induced AQP2 delivery to the plasma membrane and with the observed increased diuresis. Consistent with this, AQP2 mRNA levels were also reduced in response to prolonged OPC treatment (30 ± 10% of control levels, n = 9). Five days of treatment with furosemide, despite producing even greater polyuria than OPC, was not associated with downregulation of AQP2 levels, demonstrating that AQP2 downregulation is not secondary to increased urine flow rate or loss of medullary hypertonicity. During 12-h thirsting in the continued presence of OPC, urine output dropped dramatically, to levels not significantly different from that seen in (nonthirsted) control animals. In parallel with this, AQP2 levels rose to control levels. Control experiments confirmed continued effective receptor blockade. These results indicate that the V2-receptor antagonist causes a modest decrease in AQP2 expression that is not a consequence of increased urine flow rate or washout of medullary hypertonicity. However, this decrease is much less marked than that seen in some forms of acquired nephrogenic diabetes insipidus. In conjunction with the effects of thirsting, this suggests that modulation of AQP2 expression is mediated partly, but not exclusively, via V2 receptors.


1972 ◽  
Vol 15 (4) ◽  
pp. 338-346 ◽  
Author(s):  
Herbert S. Diamond ◽  
Robert Lazarus ◽  
David Kaplan ◽  
David Halberstam

1988 ◽  
Vol 254 (2) ◽  
pp. R357-R380 ◽  
Author(s):  
L. Rabinowitz ◽  
D. M. Green ◽  
R. L. Sarason ◽  
H. Yamauchi

In unanesthetized adult sheep, following intake of a daily meal, there was a peak in K excretion. The maximum and minimum rates of K excretion following meals were directly related to meal K content. On days without meals, no peak in K excretion occurred. Changes in K excretion on fed and fast days occurred without changes in the low levels of plasma aldosterone and were poorly correlated with urine or blood pH, urine flow rate, Na excretion, or the filtered load of K, but they correlated well with fractional K excretion. Plasma K did not change on fast days. Plasma K increased on some, but not all, fed days. Increases in plasma K that occurred on fed days were insufficient to account for the concurrent kaliuresis. Infusion of aldosterone or isotonic NaCl failed to alter K excretion in fed or fasted sheep. Infusion of isotonic NaCl + aldosterone hypertonic Na2SO4 + aldosterone increased K excretion in fasted but not fed sheep. Infusion of K in the rumen of fed and fasted sheep elevated rumen K concentration and led to increases in K excretion that could not be explained by increases in plasma K. The mechanisms responsible for the homeostatic changes in K excretion on fed and fast days were not ascertained but may importantly depend on sensors of enteric K content.


Author(s):  
Katja M. Gist ◽  
Jamie Penk ◽  
Eric L. Wald ◽  
Laura Kitzmiller ◽  
Tennille N. Webb ◽  
...  

AbstractA standardized, quantified assessment of furosemide responsiveness predicts acute kidney injury (AKI) in children after cardiac surgery and AKI progression in critically ill adults. The purpose of this study was to determine if response to furosemide is predictive of severe AKI in critically ill children outside of cardiac surgery. We performed a multicenter retrospective study of critically ill children. Quantification of furosemide response was based on urine flow rate (normalized for weight) measurement 0 to 6 hours after the dose. The primary outcome was presence of creatinine defined severe AKI (Kidney Disease Improving Global Outcomes stage 2 or greater) within 7 days of furosemide administration. Secondary outcomes included mortality, duration of mechanical ventilation and length of stay. A total of 110 patients were analyzed. Severe AKI occurred in 20% (n = 22). Both 2- and 6-hour urine flow rate were significantly lower in those with severe AKI compared with no AKI (p = 0.002 and p < 0.001). Cutoffs for 2- and 6-hour urine flow rate for prediction of severe AKI were <4 and <3 mL/kg/hour, respectively. The adjusted odds of developing severe AKI for 2-hour urine flow rate of <4 mL/kg/hour was 4.3 (95% confidence interval [CI]: 1.33–14.15; p = 0.02). The adjusted odds of developing severe AKI for 6-hour urine flow rate of <3 mL/kg/hour was 6.19 (95% CI: 1.85–20.70; p = 0.003). Urine flow rate in response to furosemide is predictive of severe AKI in critically ill children. A prospective assessment of urine flow rate in response to furosemide for predicting subsequent severe AKI is warranted.


1983 ◽  
Vol 105 (1) ◽  
pp. 351-362 ◽  
Author(s):  
A. J. MCVICAR ◽  
J. C. RANKIN

1. Improved estimates of urine flow rates of lampreys in various salinities were obtained by the collection of urine for periods of up to 48 h from minimally-stressed, unanaesthetized fish, following catheterization of the urinogenital papilla. 2. The mean urine flow rate of freshwater lampreys was 200.7 ±14.3 ml kg−1 day−1. 3. Urine flow in freshwater lampreys was correlated with spontaneous changes in gill ventilation rate. MS222 anaesthesia reduced both ventilation and urine flow rates, but pronounced effects were only observed at concentrations greater than those needed to induce light anaesthesia (50–55 mg 1−1). Urine flow rate in unanaesthetized fish was extremely sensitive to rapid (6°Ch−1) changes in temperature and Q10 (6–16°C) was approximately 5. 4. Urine flow rate decreased rapidly as the osmotic difference between the body fluids and environment approached zero, and the rate of flow in 30% seawater lampreys was only 7.6% that of freshwater fish. 5. There was no evidence for an effect of environmental calcium concentration on branchial osmotic permeability. 6. Extensive tubular reabsorption of ions occurred in freshwater lampreys. The total daily excretion rate of sodium ions generally decreased in salinities hyperosmotic to the plasma, indicating enhanced reabsorption, but secretion of magnesium and sulphate ions was greatly increased. Urine osmolarity was significantly increased in lampreys in hyperosmotic salinities. 7. Present data compare favourably with data obtained previously from anaesthetized animals, indicating that renal function in lampreys is not significantly impaired by light MS222 anaesthesia.


1995 ◽  
Vol 7 (5) ◽  
pp. 1311 ◽  
Author(s):  
EM Wintour ◽  
R Riquelme ◽  
C Gaete ◽  
C Rabasa ◽  
E Sanhueza ◽  
...  

Samples of maternal and fetal plasma, fetal urine, and amniotic fluid were collected from 8 chronically cannulated pregnant llamas, in the last third of gestation. The samples were obtained for up to 18 days post-surgery. Osmolality, sodium (Na), potassium (K), chloride (Cl), and urea were measured on 40 samples collected on days 1, 2, 3, 4-5, 6-7, 8-9, and 10-19. The osmolalities of maternal and fetal plasma, fetal urine and amniotic fluid, averaged over these 7 time periods, were, respectively, 312 +/- 2, 311 +/- 1, 484 +/- 14, and 317 +/- 1 mosmol kg-1. Values are given as mean +/- s.e. The major differences from fetal fluid values in the ovine fetus (from previously published values) were the higher osmolality and urea concentration of llama fetal urine. Urine flow rate measured in 6 fetuses, 4.5-6.5 kg body weight, was 5.8 +/- 0.4 mliter h-1; urea clearance rate was 55.5 +/- 11.8 mliter h-1. Glomerular filtration rate (GFR), measured with 51Cr-EDTA in 5 fetuses on 1-4 occasions, was 111.4 +/- 23.3 mliter h-1. Fractional reabsorptions (FR) of Na, K and Cl were 97.9 +/- 1, 75.9 +/- 13.5 and 97.7 +/- 0.4% respectively. The GFR (25 mliter kg-1 h-1) and urine flow rate (1 mL kg-1 h-1) were less than half and about one-tenth the respective values in ovine fetuses. As Na reabsorption is the major oxygen-consuming activity of the kidney, the llama fetal kidney requires only half the oxygen needed by the ovine fetal kidney to reabsorb the filtered sodium load. The reason for the formation of hypertonic, rather than hypotonic, urine in the fetal llama may be due to both greater morphological maturity of the kidney and the excretion of as yet unidentified osmotically active organic substances.


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