Renal function in water snakes

1962 ◽  
Vol 203 (6) ◽  
pp. 995-1000 ◽  
Author(s):  
S. J. LeBrie ◽  
I. D. W. Sutherland

Electrolyte and osmolar concentrations of ureteral urine were compared with serum in several species of water snakes. Hyperosmotic urine was never observed, even after 48 hr of water deprivation. This finding is consistent with the countercurrent theory which precludes urinary concentration when Henle's loops are absent, as in reptilian kidneys. The creatinine/inulin clearance ratio may exceed 2.0, suggesting tubular secretion of creatinine. Tubular secretion is further suggested by the fact that the clearance ratio approaches unity when plasma creatinine concentration is elevated. Variations in glomerular activity are reflected in urine flow in snakes as shown by a direct relationship between clearance of inulin (GFR) and urine flow In snakes solute excretion is dependent on an increase in functional tubular population, with a concomitant increase in filtered load and not a decrease in tubular solute reabsorption. Evidence for this concept is presented and indicates that, over a tenfold increase in GFR, snakes continue to excrete about the same per cent of their filtered load. Water reabsorption, on the other hand, appears to be similar in character to that seen in higher vertebrates. Proximally, it appears to be dependent on solute reabsorption ("obligatory"), whereas distally it is influenced by ADH ("facultative").

1996 ◽  
Vol 17 (5) ◽  
pp. 175-180
Author(s):  
Bassam A. Atiyeh ◽  
Shermine S. Dabbagh ◽  
Alan B. Gruskin

There are several methods to evaluate renal function during childhood. The use of serum creatinine, either alone or in combination with the Schwartz formula, is reliable and quick, but requires knowledge of conceptual age. A plasma creatinine concentration of 88.4 µmol/L (1.0 mg/dL), for example, represents normal renal function in an adolescent but more than 50% loss of renal function in a 5-year-old child. A timed urine collection for creatinine clearance is another evaluative method, but the adequacy of the urine collection always should be determined first. Urea clearance rarely is used to measure GFR because of the complex factors that influence urea excreation. Measurement of the disappearance of radioactive-labeled substances in plasma can be used to determine GFR. Radionuclide renal scans also can be used and offer the advantage of estimating the GFR of each kidney. Although infants and newborns have an intact urine diluting ability, their concentrating ability is impaired. The maximal urinary concentration in the neonatal period is less than 700 mOsm/kg, but reaches adult values of 1200 mOsm/kg by 6 to 12 months of life. Similarly, the infant kidney has a limited capacity for salt regulation, predisposing the infant to salt disturbances.


1984 ◽  
Vol 66 (6) ◽  
pp. 675-681 ◽  
Author(s):  
J. Haylor ◽  
C. J. Lote ◽  
A. Thewles

1. The urinary excretion of prostaglandin E2 (PGE2) was measured in conscious rats under conditions which produced either acid or alkaline urine, but similar change in fluid and solute excretion. 2. Oral isotonic saline increased both urine flow and sodium excretion but did not alter urinary PGE2 output (which remained constant at 80 pmol/3 h per rat) or urine pH (6.2). 3. When the urine was made alkaline (pH 7.8) by oral sodium bicarbonate or carbonate, urinary PGE2 was approximately 3-fold greater (P<0.00l) than the control (pH6.2). The urine flow and sodium output were also increased. 4. When the urine was made acidic (pH 5.7) by oral ammonium chloride, urinary PGE, excretion was reduced (P<0.01) to approximately half the control output. The urine flow and sodium output increased. 5. Within a group of 12 rats receiving oral isotonic saline a positive linear correlation coefficient (P<0.002) was established between urine pH and PGE2 excretion. 6. The results indicate that urine pH may be a determinant of PGE2 excretion in unrestrained, conscious rats. It seems likely that this effect of pH is mediated by a change in the passive reabsorption of PGE, in the distal nephron, although alternative explanations such as altered tubular secretion or synthesis cannot be categorically excluded.


1989 ◽  
Vol 77 (6) ◽  
pp. 637-641 ◽  
Author(s):  
David P. Brooks ◽  
Gerald R. Rhodes ◽  
Paul Woodward ◽  
Venkata K. Boppana ◽  
Francine M. Mallon ◽  
...  

1. Methylguanidine is a suspected uraemic toxin that accumulates in renal failure 2. We measured methylguanidine in the plasma of dogs with acute ischaemic-induced renal failure and in the plasma and urine of dogs with spontaneous chronic renal insufficiency, using a highly sensitive method involving solid-phase extraction followed by h.p.l.c. with post-column fluorescence detection 3. Constriction of the remaining renal artery of four uninephrectomized dogs for 90 min resulted in a significant (P < 0.01) increase in plasma creatinine concentration after 24 h (from 113 ± 3 to 303 ± 50 μmol/l; mean ± sem). Over the next 14 days, plasma creatinine fell towards baseline concentrations. Plasma methylguanidine also increased significantly (P < 0.05) 24 h after renal occlusion (from 0.16 ± 0.04 to 0.86 ± 0.32 μmol/l) and showed a similar pattern to the plasma creatinine concentration 4. In a further four dogs, administration of mannitol (2 g/kg) at the time of reperfusion significantly attenuated these responses 5. Dogs with chronic renal failure demonstrated increased plasma concentrations and urinary excretion of methylguanidine, and the levels appeared to be related to the severity of renal insufficiency. Thus, the dogs with the highest plasma creatinine concentrations and lowest creatinine clearances had the highest plasma methylguanidine concentrations. The clearance of methylguanidine exceeded that of creatinine, indicating that the toxin undergoes renal tubular secretion.


1986 ◽  
Vol 56 (02) ◽  
pp. 229-231 ◽  
Author(s):  
A H Hopper ◽  
H Tindall ◽  
J A Davies

SummaryTBeta-thromboglobulin (βTG) is a platelet-specific protein and since its concentration in plasma rises when platelets are activated, it has been used as an indicator of platelet involvement in vascular disease. Since platelets might be involved in the pathogenesis of diabetic microvascular disease we measured urinary βTG in 20 insulin-dependent diabetics with nephropathy and compared the results with those from 20 normal subjects. Measurement of βTG in urine was undertaken to avoid errors induced by blood sampling and to gain information over a prolonged period using a single assay. Measurements were made of βTG, β2-microglobulin and total protein in urine collected for 24 h and creatinine and β2 microglobulin in plasma. Survival of indium-111-labelled platelets was measured in nine patients. Urinary PTG was significantly (p <0.02) increased in the 20 patients compared with 20 normal volunteers (median value 1.3 vs 0.8 μg/24 h). There was a strong correlation between urinary βTG excretion and plasma creatinine concentration (r = 0.8, p <0.0001) and plasma β2-microglobulin concentration (r = 0.9, p <0.0001). Urinary βTG concentration did not correlate with platelet survival. The results indicate that although urinary βTG is significantly increased in patients with diabetic nephropathy its concentration in urine correlates with indicators of glomerular filtration rather than with a test of platelet activation.


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.


1968 ◽  
Vol 46 (2) ◽  
pp. 275-280 ◽  
Author(s):  
O. Schück ◽  
J. H. Cort

Diuresis was induced in cats by infusion of 3% glucose in 10% ethanol. When urine flow had stabilized at high levels a solution of the Ca salt of ethylenediaminetetraacetate (Na2CaEDTA) was infused as a control for the effect of the EDTA molecule on renal function. The infusion was then changed over to the same molar rate of Na2EDTA, which resulted in a 30% decrease in serum Ca levels. Ca was then repleted rapidly as CaCl2 given intravenously, and the infusion was shifted back to Na2CaEDTA. The decrease in extracellular Ca concentration was associated with a significant antidiuresis. In further experiments on anesthetized dogs, osmotic diuresis was induced either by (a) infusion of hyperosmotic mannitol solutions, which were then shifted over to hypertonic NaCl, or (b) the same solutions in reverse order. Ca excretion correlated in linear fashion with Na excretion, but not with total solute excretion or with filtration rate. When Ca was added to the mannitol infusion, Na excretion increased in linear relation to Ca. It is suggested that Ca (a) decreases tubular permeability for water reabsorption and (b) decreases Na reabsorption, while Na (c) decreases Ca reabsorption. Mechanisms a and b would appear to involve membrane transport directly in the proximal tubule.


PEDIATRICS ◽  
1984 ◽  
Vol 74 (2) ◽  
pp. 265-272
Author(s):  
Robert L. Chevalier ◽  
Fern Campbell ◽  
A. Norman A. G. Brenbridge

Sixteen infants, 2 to 35 days of age, had acute renal failure, a diagnosis based on serum creatinine concentrations &gt; 1.5 mg/dL for at least 24 hours. Eight infants were oliguric (urine flow &lt; 1.0 mL/kg/h) whereas the remainder were nonoliguric. To determine clinical parameters useful in prognosis, urine flow rate, duration of anuria, peak serum creatinine, urea (BUN) concentration, and nuclide uptake by scintigraphy were correlated with recovery. Nine infants had acute renal failure secondary to perinatal asphyxia, three had acute renal failure as a result of congenital cardiovascular disease, and four had major renal anomalies. Four oliguric patients died: three of renal failure and one of heart failure. All nonoliguric infants survived with mean follow-up serum creatinine concentration of 0.8 ± 0.5 (SD) mg/dL whereas that of oliguric survivors was 0.6 ± 0.3 mg/dL. Peak serum creatinine concentration did not differ between those patients who were dying and those recovering. All infants who were dying remained anuric at least four days and revealed no renal uptake of nuclide. Eleven survivors were anuric three days or less, and renal perfusion was detectable by scintigraphy in each case. However, the remaining survivor (with bilateral renal vein thrombosis) recovered after 15 days of anuria despite nonvisualization of kidneys by scintigraphy. In neonates with ischemic acute renal failure, lack of oliguria and the presence of identifiable renal uptake of nuclide suggest a favorable prognosis.


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