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A case of spontaneous rupture of the renal pelvis during postobstructive diuresis following spontaneous relief of anuria in a patient with postpyelolithotomy retroperitoneal fibrosis, is described. The unusual etiopathological setting which predisposed to the occurrence of such a rare phenomenon and its treatment implications are discussed.
Stimulation of renal dopamine-1 (DA1) receptors for 3 hours produces an increase in renal plasma flow and sustained natriuresis. The present study was designed to assess the response of renal hemodynamic and tubular function to long-term DA1 receptor stimulation. Fenoldopam, a selective DA1 receptor agonist, was infused intravenously for 24 hours in 10 normal male subjects in metabolic balance at 150 mEq sodium and 60 mEq potassium intake in a single-blind, vehicle-controlled protocol. During DA1 receptor activation, urine flow rate and fractional excretion of sodium increased for the first 5 hours, 16.9 +/- 0.9 ml/min compared with a vehicle control value of 12.4 +/- 0.5 ml/min (p less than 0.001) and 2.0 +/- 0.1% compared with a vehicle control value of 1.1 +/- 0.1% (p less than 0.005), respectively. Urinary sodium excretion rose at 5 hours, 0.27 +/- 0.02 mEq/min compared with a vehicle control value of 0.14 +/- 0.01 mEq/min (p less than 0.01). Renal plasma flow increased during fenoldopam at 5 hours, 505 +/- 47 ml/min compared with a vehicle control value of 397 +/- 25 ml/min (p less than 0.01), and was sustained for 24 hours, 523 +/- 40 ml/min compared with 432 +/- 31 ml/min (p less than 0.05). The distal sodium load increased and the percentage of distal sodium reabsorption decreased during fenoldopam. Glomerular filtration rate, blood pressure, heart rate, plasma aldosterone concentration, plasma renin activity, and fractional excretion of potassium were unchanged. Selective DA1 receptor activation produced sustained 5-hour diuresis and 11-hour natriuresis without kaliuresis or a systemic hemodynamic effect.(ABSTRACT TRUNCATED AT 250 WORDS)
Fractional reabsorption of water, sodium, and potassium at proximal and distal tubular sites within the nephron was studied by recollection-micropuncture experiments on dogs undergoing hypertonic mannitol diuresis. After an initial control hydropenic phase, 16% mannitol in modified Ringer's solution was administered intravenously, resulting in marked increases in fractional excretion of water (28.7%), sodium (12.6%), and potassium (63.9%). Inulin clearance decreased significantly from 35.1 to 25.2 ml/min. Analysis of paired micropuncture data revealed a significant decrease in tubule fluid to plasma (TF:P) inulin ratios in both the proximal tubule (1.63-1.45) and distal tubule (5.38-1.94). There was also a significant decrease in proximal TF:P sodium ratios (0.99-0.93) and potassium ratios (1.05-0.98). Distal TF:P sodium ratios, in contrast, rose significantly (0.38-0.59), while TF:P potassium ratios tended towards unity whether initially greater or less than one. Fractional reabsorption of sodium and water decreased by 5% and 10% respectively in the proximal tubule, but to a lesser extent than the resulting increases in fractional urinary excretion. The nonreabsorbed fraction, however, had increased sharply at the point of distal puncture for water (32%), sodium (26%), and potassium (26%), indicating a large inhibitory effect within the loop of Henle in addition to the smaller proximal effects.
The hypotensive, natriuretic, and diuretic actions of human atrial natriuretic factor-(99-126) (hANF) are accompanied by an elevation of cyclic guanosine monophosphate (cGMP) in plasma and urine. However, the oxidized hANF analogue, human [Met-O110]ANF-(99-126) (Met-O-ANF), has been reported to be unable to increase cGMP (Biochem. Biophys. Res. Commun. 128: 538-546). We employed this oxidized peptide to evaluate the relationship between its biological effects and cGMP generation, with cGMP serving as a marker of the recognized property of ANF to stimulate particulate guanylate cyclase. Met-O-ANF appeared to be a partial agonist, exhibiting a decreasing order of relative potency of hypotensive, vasorelaxant, diuretic, and natriuretic functions compared to hANF. A lower degree of cGMP increases was achieved by this analogue in cultured smooth muscle and endothelial cells. Met-O-ANF doses, which led to a significant increase in diuresis, were neither natriuretic nor accompanied by an increase of urinary cGMP. We were thus able to dissociate the diuretic and natriuretic effects of ANF. High doses of the oxidized analogue were required to elevate cGMP levels in plasma and urine. In isolated kidney fractions, Met-O-ANF's action on cGMP was significantly lower in glomeruli (fivefold less), virtually absent in the collecting duct, yet only slightly different (20% less) in thick ascending limb. Our results indicate that the diuretic and natriuretic effects are exerted at distinct sites, with only the natriuresis being related to an increase of extracellular cGMP. The variability of differential potency of biological and biochemical effects from tissue to tissue of these two forms of human ANF support the notion of the heterogeneity of the ANF effector system.
The ionic contrast medium diatrizoate used in high-dose unilateral nephroangiography in dogs produced an abnormal nephrogram, 'patchy contrast medium retention', and a marked decrease in renal blood flow in five of eight injected kidneys. Increased glomerular permeability (albuminuria), reduced glomerular filtration rate (creatinine clearance), and reduced osmotic diuresis were demonstrated in all selectively injected kidneys.
The non-ionic ratio 3.0 contrast media metrizamide and iohexol used in high-dose unilateral nephroangiography in dogs produce homogeneous nephrograms and no marked effects on renal blood flow, glomerular filtration rate, and osmotic diuresis, in contrast to previously reported results using the same technique with iodine-equivalent doses of the ionic ratio 1.5 contrast medium diatrizoate (25). Iohexol affected glomerular permeability significantly less than metrizamide and diatrizoate.
Urine volumes and flows as functions of time after oral administration of placebo, furosemide 80 mg and tizolemide 100 mg to sixteen healthy male adults at 08.00 a.m. are described through mathematical models. Accumulated urine volumes after dosing, V, as functions of time, t, are accounted for by sigmoid functions and urine flows are described as dV/dt. No significant differences were found between the 24-hour urine volume mean values after furosemide (2457 ml) and tizolemide (2283 ml) and both were significantly higher than the corresponding mean value after placebo (1369 ml) ( p less than 0.001). Peak diuresis after dosing occurs about 1.5 hours for furosemide, 4 hours for tizolemide and 6 hours for placebo. Fourteen hours after dosing, urine volume amounts to 90% of the 24-hour urine volume after furosemide and to 76% after tizolemide, so that both substances may be regarded as diurnal diuretics.
We have studied Malpighian tubules of Aedes aegypti using a variety of methods: Ramsay fluid secretion assay, electron probe analysis of secreted fluid, in vitro microperfusion and two-electrode voltage clamp. Collectively, these methods have allowed us to elucidate transepithelial transport mechanisms under control conditions and in the presence of diuretic peptides. Mosquito natriuretic peptide (MNP), a corticotropin-releasing factor (CRF)-like diuretic peptide, selectively increases transepithelial secretion of NaCl and water, meeting the NaCl loads of the blood meal. The intracellular messenger of MNP is cAMP, which increases the Na+ conductance and activates the Na+/K+/2Cl- -cotransporter in the basolateral membrane of principal cells. Leucokinin non-selectively increases transepithelial NaCl and KCl secretion, which may deal with hemolymph volume expansions or reduce the flight pay load upon eclosion from the aquatic habitat. The non-selective NaCl and KCl diuresis stems from the increase in septate junctional Cl- conductance activated by leucokinin using Ca2+ as second messenger. Fundamental to diuretic mechanisms are powerful epithelial transport mechanisms in the distal segment of the Malpighian tubules, where transepithelial secretion rates can exceed the capacity of mammalian glomerular kidneys in the renal turnover of the extracellular fluid compartment. In conjunction with powerful epithelial transport mechanisms driven by the V-type H+-ATPase, diuretic hormones enable hematophagous and probably also phytophagous insects to deal with enormous dietary loads, thereby contributing to the evolutionary success of insects.
The blood-sucking insect Rhodnius prolixus rapidly eliminates a Na(+)-rich K(+)-poor urine after its large meals. K(+)-rich fluid is first secreted by the upper Malpighian tubules and passes to the lower tubules where most of the potassium is reabsorbed. During the initial stimulation of the tubules, the lower tubules must be activated first to avoid loss of potassium. The major element in this is that they respond more rapidly than do the upper tubules to particular hormonal concentrations rather than that they react to lower hormonal concentrations than do the upper tubules. During subsequent diuresis, regulation of the haemolymph potassium concentration depends on three cooperative homoeostatic mechanisms in the tubules. A fall in potassium concentration of the medium bathing the tubules causes (i) a decrease in the rate of fluid secretion by the upper tubules, (ii) a decrease in potassium concentration in the fluid secreted by the upper tubules and (iii) an increase in the rate of potassium absorption by the lower tubules. The tubules respond in the opposite direction to an increase in potassium concentration of the medium. As a result, the potassium concentration of the urine can be adjusted to match the potassium concentration of the fluids absorbed from the gut, so that the potassium concentration of the insect's haemolymph remains unaltered.
The rate of secretion of the Malpighian tubules of Glossina austeni is controlled by a diuretic hormone. This hormone is present in the nervous tissue of the fly together with a degradative enzyme that can be activated by boiling. It is demonstrated that the Malpighian tubules are able to destroy the diuretic hormone; they may therefore participate in the control of diuresis. The diuretic hormone appears to be a heat-stable, non-dialysable, alcohol-soluble molecule, containing amino acid, glucose and sialic acid residues.
The diuresis which follows the pupal-adult ecdysis of Pieris brassicae is hormonally controlled. Use of the isolated Malpighian tubules as a bioassay shows the presence of substantial diuretic activity in homogenates of the brain and corpus cardiacum-corpus allatum complex. The hormone is probably produced in the brain and released from a storage site in the corpora cardiaca. The tubules of the butterfly are maximally responsive to the diuretic hormone at the time of eclosion.
Control of post-feeding diuresis in females of the mosquito Aëdes aegypti has been studied by means of a weighing technique and simple surgical procedures. The primary controlling factor is (as in the larva) a nervous feedback mechanism and not an increased production of diuretic hormone. As the mosquito ingests blood, sensory information from the distending abdomen reaches the mid gut via the nerve cord, brain and stomatogastric system. This information probably inhibits retroperistaltic movements of the mid gut allowing fluid from the Malpighian tubules (which seems to be produced continually) to be moved back to the rectum for subsequent excretion, instead of being re-cycled to the haemolymph via the mid gut. Such a control does not preclude a role for the diuretic hormone, continual secretion of which may cause the continual production of fluid from the Malpighian tubules.
Effects of alpha-human atrial natriuretic polypeptide (alpha-hANP) on renal function were studied in anesthetized dogs and isolated perfused rat kidneys. Two doses of alpha-hANP were used to determine whether renal hemodynamics or tubular reabsorption is tha major factor in the diuretic action of alpha hANP. The excretion rates of sodium (Na) and inorganic phosphate (PO4) were evaluated to determine the site of diuretic action in the renal tubule. In dogs that received the smaller dose of alpha-hANP (5 ng.kg-1.min-1) infused into the renal arteries without changes in systemic or renal hemodynamics, urine volume (UV) and urinary Na excretion (UNaV) increased significantly. Fractional excretion of Na (FENa) was increased, while fractional excretion of PO4 (FEpo4) was unchanged, following the infusion of alpha-hANP. The calculated fractional Na reabsorption in the distal tubule (DTRNa) during the infusion of alpha-hANP was significantly suppressed. In dogs that received the a larger dose of alpha-hANP (50 ng.kg-1.min-1), the glomerular filtration rate (GFR), UV, and FENa were increased and DTRNa was decreased. In isolated rat kidneys perfused at a constant pressure, a lower concentration of alpha-hANP (0.5 ng.ml-1) in the perfusate caused diuresis and increased Na and PO4 excretion without any renal hemodynamic alterations. A higher concentration of alpha-hANP (5 ng.ml-1) increased GFR, Na and PO4 excretion. Since PO4 reabsorption is believed to occur primarily in the renal proximal tubule, these findings suggest that the diuretic action of alpha-hANP in smaller doses in induced by direct action on renal distal nephron.(ABSTRACT TRUNCATED AT 250 WORDS)
A simple and inexpensive rat diuresis cage is described. It may be constructed from thin aluminium sheeting in combination with a standard laboratory holding cage. Application of a low resistance PTFE coating reduces urine losses to a level better than a leading commercial design. Some physiological strain comparison data obtained using the cage are given.
One hundred and one young-adult female Sprague-Dawley rats were acclimatized to metabolic cages for 2 days. After that time 24-hour urine was collected at a constant cooling temperature of 0-4 degrees C. After gel filtration the enzyme activities were determined, and the resulting values were used to calculate 24-hour excretions. The following reference ranges (2.5 and 97.5 percentiles) were determined (in mU/24 h): lactate dehydrogenase 43-181; phosphohexoseisomerase 45-1445; glutathione-S-transferase 1-299; alkaline phosphatase 27-1239; leucine arylamidase 72-377; gamma-glutamyltransferase 1334-9188; arylsulphatase A 59-309; beta-galactosidase 76-305; beta-glucuronidase 20-2756; beta-N-acetyl-D-glucosaminidase 66-491; glutamate dehydrogenase 7-711. There was a significant (though not very high) correlation with diuresis for the lysosomal enzymes beta-N-acetyl-D-glucosaminidase, arylsulphatase A and beta-galactosidase, and for glutamate dehydrogenase, lactate dehydrogenase, phosphohexoseisomerase and alkaline phosphatase. The relation to creatinine excretion was markedly close for the lysosomal enzymes beta-N-acetyl-D-glucosaminidase, arylsulphatase A and beta-galactosidase (r = 0.71-0.83), as well as for alkaline phosphatase, leucine arylamidase and gamma-glutamyltransferase. There was a relatively high correlation between the excretion of beta-N-acetyl-D-glucosaminidase, arylsulphatase A and beta-galactosidase among themselves (r = 0.63-0.81) as well as between leucine arylamidase and gamma-glutamyltransferase (r = 0.75).
Diurnal variation in blood melatonin levels and renal melatonin excretion was monitored in five ewes by blood sampling and quantitative urine collection at 2-h intervals. A typical secretory pattern of melatonin was seen both in blood and urine levels and in the renal excretion of melatonin. Serum melatonin levels increased from daytime values of approximately 200 pmol/l to a mean of 800 pmol/l during darkness. Urine flow rate and urine osmolality did not show any clear diurnal rhythm. To examine whether urine flow rate affects renal melatonin excretion at night, urine was collected in three consecutive 30-min fractions, and blood was sampled in the middle of each urine collection period when the sheep were in normal water balance or after hydration. Hydration increased urine flow rate over sixfold and decreased urine osmolality well below plasma osmolality. Glomerular filtration rate, measured as creatinine clearance, did not change. Serum melatonin concentrations did not differ between hydrated and non-hydrated sheep. However, urinary melatonin excretion was 1.1 +/- 0.3 (S.E.M.) pmol/min at midnight in normal water balance, and significantly higher (2.6 +/- 0.4 pmol/min) in the hydrated state. In this study, the validity of urinary melatonin determinations as an indicator of pineal function was confirmed in normal water balance. In addition, our results suggest that a high tubular fluid load during diuresis increases urinary melatonin excretion because of decreased tubular reabsorption.(ABSTRACT TRUNCATED AT 250 WORDS)
The effect on water and electrolyte balance of stress, simulated by intravenous infusion of cortisol, was studied using 24 18-mo-old Merino wethers (37.0 +/- 0.94 kg mean body weight [BW]) over 72 h. The sheep were allocated to one of four groups: 1) no water/no cortisol (n = 6); 2) water/no cortisol (n = 4); 3) no water/cortisol (n = 6); and 4) water/cortisol (n = 4). Animals allocated to the two cortisol groups were given 0.1 mg x kg BW(-1) x h(-1) of hydrocortisone suspended in isotonic saline to simulate stress for the duration of the experiment. Total body water, plasma cortisol, osmolality and electrolytes, and urine electrolytes were determined at 24-h intervals for 72 h. In the presence of cortisol, total body water was maintained in the face of a water deprivation insult for 72 h. Water deprivation alone did not induce elevated plasma concentrations of cortisol, in spite of a 13% loss of total body water between 48 and 72 h. Infusion of cortisol was found to increase urine output (P = 0.003) and decrease total urinary sodium output (P = 0.032), but had no effect on plasma electrolyte levels or water intake. Water deprivation was found to increase plasma sodium concentrations (P = 0.037). These results indicate that sheep given cortisol to simulate stress suffer from a loss of body water in excess of that associated with a loss of electrolytes, and support the hypothesis that elevated physiological concentrations of cortisol induce a diuresis in ruminants that contributes to dehydration.
The role of the renin-angiotensin-aldosterone system in the development of tolerance to the diuretic effect of furosemide was investigated in 12 healthy male volunteers. Furosemide in a dose of 40 mg daily for one week had a brisk acute diuretic effect, but did not lead to dehydration, hyponatremia or fall in blood pressure. The reason for this was a reduction in sodium excretion between doses (rebound effect) and a decrease in sensitivity to furosemide from day 1 to day 7. The latter phenomenon is referred to as delayed tolerance to furosemide. Inhibition of angiotensin converting enzyme with lisinopril 20 mg daily did not change the renal furosemide excretion rate, the renal sensitivity to furosemide or the tolerance development. Thus, delayed tolerance to furosemide diuresis was not related to dehydration or activation of the renin-angiotensin-aldosterone system. Other mechanisms, probably intrarenal, will have to be looked for.