Relief Of Unilateral Ureteral Obstruction Research Articles

Metabolic Response in Rabbit Urine to Occurrence and Relief of Unilateral Ureteral Obstruction.

Ureteral obstruction will lead clinically to hydronephrosis, which may further develop into partial or complete loss of kidney function and even cause permanent histological damage. However, there is little knowledge of metabolic responses during the obstructed process and its recoverability. In this study, a complete unilateral ureteral obstruction (CUUO) model was established in the rabbit, and 1H NMR-based metabolomic analysis of urine was used to reveal the metabolic perturbations in rabbits caused by CUUO and the metabolic recovery after the CUUO was relieved. Univariate and multivariate statistical analyses were used to identify metabolic characteristics. The gradually decreased levels of 3-hydroxykynurenine, 3-methylhistidine, creatinine, guanidoacetate, meta- and para-hydroxyphenylacetate, and phenylacetylglycine and the gradually increased levels of acetate, alanine, citrate, glycine, lactate, and methionine in urine could be regarded as potential biomarkers for the occurrence and severity of ureteral obstruction. And the reduced levels of 3-methylhistidine, creatinine, guanidoacetate, hippurate, meta-hydroxyphenylacetate, and methylguanidine and the elevated levels of 2-aminoisobutyrate, acetylcholine, citrate, lactate, lysine, valine, and α-ketoglutarate in urine compared with the obstructed level could characterize the metabolic recovery of ureteral obstruction. Our results depicted the disturbed biochemical pathways involved in ureteral obstruction and demonstrated the practicability of recovering renal functions for the patients with severe hydronephrosis in clinical practice by removing causes for obstruction.

A porcine model of relief of unilateral ureteral obstruction: study on self-repairing capability over multiple time points.

It is still controversial whether renal tubular interstitial fibrosis (TIF) is a reversible process. Although previous studies examining TIF have been carried out in rodents, their kidney size and physiological character differ with humans, and the difference among diverse individuals before and after damage was obvious. Thus an experimental animal model to simulate human kidney disease was urged to be established. In order to clarify whether TIF is reversible, and the exact time points that the kidney has the capacity to be repaired, a porcine relief of unilateral ureteral obstruction (R-UUO) model was developed. Kidney damage and reparation were observed dynamically in vivo over various time points. Pigs were randomized divided into three groups (n=6): UUO 5days group, UUO 7days, and UUO 10days group. Each porcine in that groups underwent UUO and subsequent R-UUO for three time points. Renal function, histological structure, and protein expressions of α-smooth muscle actin (α-SMA), vimentin and E-cadherin were evaluated at different time points. Following R-UUO after 5 and 7days of UUO, compared to UUO, serum creatinine levels were significantly decreased. Renal pathological tissue damage was repaired. The expressions of α-SMA and vimentin were decreased and E-cadherin expression was increased (P<0.05). However, during R-UUO 14, 28, and 56days after 10days of UUO, serum creatinine was not decreased significantly. The expressions of α-SMA and vimentin consistently remained at high levels. Renal damage was unable to be restored and resulted in chronic lesions. Kidney damage induced by UUO can be reversed in early stages. However, longer time of UUO with significant levels of TIF showed limited reversibility. The porcine R-UUO model provides an ideal animal model for the investigation of kidney injury and repair as well as for the evaluation of the effect of drug treatment.

Reversal of Epithelial to Mesenchymal Transition Following Relief of Unilateral Ureteral Obstruction in the Rat

Reversal of Epithelial to Mesenchymal Transition Following Relief of Unilateral Ureteral Obstruction in the Rat

Impact of Biological Gender and Soluble Guanylate Cyclase Stimulation on Renal Recovery After Relief of Unilateral Ureteral Obstruction

Gender difference and nitric oxide deficiency contribute to the progression of many chronic kidney diseases. In a model of unilateral ureteral obstruction relief we analyzed the impact of biological gender and nitric oxide/cyclic guanosine monophosphate signaling stimulation on renal disease severity and restoration. Female and male rats underwent sham surgery or unilateral ureteral obstruction. After 5-day unilateral ureteral obstruction female and male rats were assigned to obstruction relief alone or obstruction relief plus 7-day treatment with the soluble guanylate cyclase stimulator BAY 41-8543. Compared to male rats with obstruction relief renal disease was less severe in female rats, which had significantly less tubulointerstitial matrix accumulation and tubular atrophy. In each gender group α1 and β1-soluble guanylate cyclase was comparably and significantly increased but female rats produced significantly more cyclic guanosine monophosphate after treatment with the soluble guanylate cyclase stimulator. In each group BAY 41-8543 treatment was associated with significant amelioration of renal matrix protein expansion, macrophage infiltration, tubular apoptosis and atrophy. Female gender is protective for unilateral ureteral obstruction relief. This was linked to higher sensitivity of the soluble guanylate cyclase enzyme and cyclic guanosine monophosphate production in response to BAY 41-8543. In these female and male rats enhancing the signaling of nitric oxide/cyclic guanosine monophosphate with BAY 41-8543 significantly accelerated the restoration of renal architecture after obstruction relief and largely ameliorated the differences in disease severity due to the gender disparity.

Formation of atubular glomeruli in the developing kidney following chronic urinary tract obstruction

Congenital urinary tract obstruction is a major cause of progressive renal disease in children. We developed a model of partial unilateral ureteral obstruction (UUO) in the neonatal mouse, in which nephrogenesis at birth is similar to that of the midtrimester human fetus. The proximal tubule responds to UUO by undergoing apoptosis and necrosis, likely due to mitochondrial sensitivity to hypoxia and reactive oxygen species in the face of reduced endogenous antiapoptotic factors such as eNOS. Damage to the glomerulotubular junction is followed by scission and formation of atubular glomeruli and aglomerular tubules. This is an orchestrated process, with atubular glomeruli surrounded by a continuous layer of regenerated parietal epithelial cells. Relief of UUO at 7 days of age results in remodeling of the renal parenchyma by adulthood. In contrast to proximal tubular destruction, collecting ducts remain dilated and patent, with remodeling due to apoptosis and proliferation (a process associated with recruitment of intercalated cells as progenitor cells following UUO in the fetal monkey). Formation of atubular glomeruli occurs in other renal disorders (congenital nephrotic syndrome and cystinosis), and may represent a maladaptive response to proximal tubular injury reflecting an evolutionary adaptation by an ancestor we share with aglomerular marine fish.

Stimulation of soluble guanylate cyclase accelerates renal recovery following relief of unilateral ureteral obstruction

Background Unilateral ureteral obstruction (UUO) is characterized by progressive renal atrophy, tubular apoptosis and tubulointerstitial fibrosis. Pharmacological stimulation of soluble guanylate cyclase (sGC) and subsequent cGMP production have recently been found to be renoprotective. In this study, the sGC stimulator BAY 41-8543 was given to rats after relief of UUO in order to analyze the effects of enhanced NO/sGC/cGMP signaling on the subsequent renal disease recovery, concerning the renal atrophy, tubular apoptosis and tubulointerstitial fibrosis.

Dietary arginine supplementation attenuates renal damage after relief of unilateral ureteral obstruction in rats1

Progression of renal injury after relief of unilateral ureteral obstruction (UUO) has been demonstrated. Nitric oxide (NO) may be an effective intervention due to its vasodilatory, antifibrotic, and anti-apoptotic effects. Herein, we used dietary L-arginine (ARG) supplementation in a UUO relief model. This study comprised group 1, control (no treatment). All other rats were subject to 3-day UUO, which was then relieved, and the rats maintained for 7 additional days. Group 2, no additional treatment; group 3, L-ARG; group 4, L-NAME, NO synthase inhibitor; group 5, ARG and L-NAME. Urinary NO(2/3) was quantified. GFR and ERPF were measured at day 10. Interstitial fibrosis and fibroblast expression, macrophage infiltration, tubular apoptosis, and proliferation, NOS expression, and the levels of tissue TGF-beta were evaluated. Urinary NO(2/3) was significantly increased by ARG treatment and decreased by L-NAME. GFR and ERPF measured 7 days following relief were not significantly different in the previously obstructed kidneys (POK) of groups 2 and 3. L-NAME significantly reduced GFR and ERPF in the POK. ARG significantly reduced apoptosis, macrophage infiltration, and fibroblast expression in the POK. L-NAME exacerbated the effects on apoptosis and fibroblasts. Fibrosis was minimal in groups 1 through 3, but was significantly increased by L-NAME. ARG did not affect renal NOS expression and tissue TGF-beta1 levels. Dietary ARG supplementation during UUO relief did not improve ERPF or GFR. However, renal damage, including fibrosis, apoptosis, and macrophage infiltration was significantly improved by ARG treatment. This suggests that increasing NO availability could be beneficial in the setting of UUO relief.

Renal damage progresses despite improvement of renal function after relief of unilateral ureteral obstruction in adult rats

Progression of renal damage after relief of unilateral ureteral obstruction (UUO) has been demonstrated, especially in neonatal rats. We evaluated renal function and renal damage after relief of 3-day UUO in five groups of adult rats: group 1, no treatment; group 2, 3-day UUO; groups 3-5, 3-day UUO followed by relief; group 3, 7-day relief; group 4, 14-day relief; and group 5, 28-day relief. Glomerular filtration rate (GFR), renal blood flow (RBF), tissue transforming growth factor-beta (TGF-beta), interstitial fibrosis and fibroblast expression, tubular apoptosis, macrophage infiltration, expression of nitric oxide synthases (NOS), and urinary nitrate/nitrite (NO(2)/NO(3)) were evaluated. RBF and GFR were decreased to <10% of baseline by 3 days of UUO. GFR and RBF in a previously obstructed kidney (POK) returned to baseline by 14 days after relief. Both tissue TGF-beta(1) and interstitial fibrosis were significantly higher in POK of groups 3-5 compared with groups 1 and 2 . In group 5, the numbers of infiltrating macrophages, fibroblasts, and apoptotic tubular cells were higher in POK compared with group 1. Urinary NO(2)/NO(3) was significantly higher than baseline from 3 to 27 days after relief of UUO. Expression of NOS isoforms was increased in tubules. As interstitial fibrosis contributes to decreased renal function, these results suggest that the acute recovery in function may be compromised in the long term by the progressive renal fibrosis which was found. Furthermore, pharmacological intervention at the time of relief of UUO, targeted to fibrotic processes, may contribute to long-term recovery of renal function.

Recovery from release of ureteral obstruction in the rat: Relationship to nephrogenesis

Obstructive nephropathy is a major cause of renal insufficiency in infants and children. Despite release of unilateral ureteral obstruction (UUO) in the first five days of life in the rat, renal growth is impaired, while glomerular filtration rate (GFR) is preserved at one month, but decreases markedly by one year. To test the hypothesis that renal recovery from UUO depends on the stage of nephrogenesis at the time of relief of obstruction, renal recovery from relief of five days UUO following completion of nephrogenesis (days 14 to 19) was compared with UUO during nephrogenesis (days 1 to 5). Rats underwent UUO or sham operation at one day of age, with relief five days later. In additional groups of neonatal rats, the operation was at 14 days, with relief at 19 days. Three months later, blood pressure, GFR, urine flow, sodium and potassium excretion, and kidney weight were measured. In addition, the number of glomeruli, glomerular maturation, glomerular diameter, tubular atrophy, and interstitial fibrosis were determined in each kidney. The effects of five-day UUO on number of glomeruli was determined also in adult rats one month following relief of obstruction. Three months following relief of UUO during days 14 to 19, renal growth was decreased by 50%, compared to a 30% reduction following relief of UUO during days 1 to 5 (P < 0.05). The number of glomeruli was reduced by approximately 50% regardless of the timing of UUO, but glomerular size was reduced only in rats with UUO from days 14 to 19. Blood pressure and tubular atrophy were increased, and GFR, urine flow, sodium and potassium excretion were decreased in the postobstructed kidney of both neonatal groups. In the adult rat, the five-day UUO did not result in a decrease in the number of glomeruli. In the period immediately following nephrogenesis, the kidney is particularly susceptible to long-term injury from temporary UUO. This suggests that a delay in relief of significant ureteral obstruction should be avoided if diagnosed in the perinatal or neonatal period.

REDUCED NUMBER OF GLOMERULI IN KIDNEYS WITH NEONATALLY INDUCED PARTIAL URETEROPELVIC OBSTRUCTION IN PIGS

We quantify the structural components of the nephron in adult pig kidneys with neonatally induced unilateral hydronephrosis in comparison with nonobstructed kidneys. The study included 11 pigs with unilateral partial ureteropelvic obstruction induced 2 days after birth and 8 sham operated control pigs. Obstructed kidney glomerular filtration rate was significantly reduced at age 4 weeks but did not differ from control kidneys after 24 weeks. At age 24 weeks the kidneys were perfusion fixed, and the number and volume of glomeruli and tubular lengths were measured using stereological methods. Mean obstructed kidney volume did not differ from that of control kidneys. Mean number plus or minus standard deviation of glomeruli in the obstructed kidneys was reduced by 28% compared to that of control kidneys (502 +/- 163 x 103 versus 697 +/- 161 x 103, p = 0.02), whereas no difference in mean glomerular volume was observed. Mean length of the proximal or distal tubules did not differ between obstructed and control kidneys. Mean number or volume of glomeruli in nonobstructed kidneys contralateral to obstructed kidneys did not differ from that of control kidneys. The individual number of glomeruli in the obstructed kidneys was not associated with function of these kidneys. Neonatally induced unilateral partial ureteropelvic obstruction causes impaired nephrogenesis with a significant reduction in the number of nephrons, which is not reflected in measurements of kidney function in this model. The reduction in the number of glomeruli suggests that congenital unilateral obstruction impairs nephrogenesis.

Unilateral ureteral obstruction in neonatal rats leads to renal insufficiency in adulthood

Although unilateral ureteropelvic junction obstruction is the most common cause of congenital obstructive nephropathy in infants and children, management remains controversial, and follow-up after pyeloplasty is generally limited to the pediatric ages. We have developed a model of temporary unilateral ureteral obstruction (UUO) in the neonatal rat: One month following the relief of five-day UUO, the glomerular filtration rate (GFR) of the postobstructed kidney was normal despite a 40% reduction in the number of glomeruli and residual vascular, glomerular, tubular, and interstitial injury. To determine whether hyperfiltration and residual injury of remaining nephrons leads to progression of renal insufficiency in later life, 31 rats were sham operated or subjected to left UUO at one day of age, with relief of UUO five days later, and were studied at one year of age. GFR was measured by inulin clearance, and the number of glomeruli, tubular atrophy, glomerular sclerosis, and interstitial fibrosis were measured by histomorphometry in sham, obstructed (UUO), and intact opposite kidneys. Intrarenal macrophages and alpha-smooth muscle actin were identified by immunohistochemistry. Despite relief of UUO, ultimate growth of the postobstructed kidney was impaired. The number of glomeruli was reduced by 40%, and GFR was decreased by 80%. However, despite significant compensatory growth of the opposite kidney, there was no compensatory increase in GFR, and proteinuria was increased. Moreover, glomerular sclerosis, tubular atrophy, macrophage infiltration, and interstitial fibrosis were significantly increased not only in the postobstructed kidney, but also in the opposite kidney. Although GFR is initially maintained following relief of five-day UUO in the neonatal rat, there is eventual profound loss of function of the postobstructed and opposite kidneys because of progressive tubulointerstitial and glomerular damage. These findings suggest that despite normal postoperative GFR in infancy, children undergoing pyeloplasty for ureteropelvic junction obstruction should be followed into adulthood. Elucidation of the cellular response to temporary UUO may lead to improved methods to assess renal growth, injury, and functional reserve in patients with congenital obstructive nephropathy.

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Recovery following relief of unilateral ureteral obstruction in the neonatal rat

Obstructive nephropathy is a primary cause of renal insufficiency in infants and children. This study was designed to distinguish the reversible and irreversible cellular consequences of temporary unilateral ureteral obstruction (UUO) on the developing kidney. Rats were subjected to UUO or sham operation in the first 48 hours of life, and the obstruction was removed five days later (or was left in place). Kidneys were removed for study 14 or 28 days later. In additional groups, kidneys were removed at the end of five days of obstruction. Immunoreactive distribution of renin was determined in arterioles, and the distribution of epidermal growth factor, transforming growth factor-beta1, clusterin, vimentin, and alpha-smooth muscle actin was determined in tubules and/or interstitium. The number of glomeruli, glomerular maturation, tubular atrophy, and interstitial collagen deposition was determined by morphometry. Renal cellular proliferation and apoptosis were measured by proliferating cell nuclear antigen and the TdT uridine-nick-end-label technique, respectively. The glomerular filtration rate was measured by inulin clearance. Renal microvascular renin maintained a fetal distribution with persistent UUO; this was partially reversed by the relief of obstruction. Although glomerular maturation was also delayed and glomerular volume was reduced by UUO, the relief of obstruction prevented the reduction in glomerular volume. Although relief of obstruction did not reverse a 40% reduction in the number of nephrons, the glomerular filtration rate of the postobstructed kidney was normal. The relief of obstruction did not improve tubular cell proliferation and only partially reduced apoptosis induced by UUO. This was associated with a persistent reduction in the tubular epidermal growth factor. In addition, the relief of obstruction reduced but did not normalize tubular expression of transforming growth factor-beta1, clusterin, and vimentin, all of which are evidence of persistent tubular injury. The relief of obstruction significantly reduced interstitial fibrosis and expression of alpha-smooth muscle actin by interstitial fibroblasts, but not to normal levels. The relief of obstruction in the neonatal rat attenuates, but does not reverse, renal vascular, glomerular, tubular, and interstitial injury resulting from five days of UUO. Hyperfiltration by remaining nephrons and residual tubulointerstitial injury in the postobstructed kidney are likely to lead to deterioration of renal function later in life.

Unilateral Post-Obstructive Diuresis in the Neonate

A total of 3 neonates exhibited severe post-obstructive diuresis after relief of unilateral ureteral obstruction. Of the neonates 2 had normal kidneys contralaterally while 1 had a contralateral kidney that was dysplastic. Urinary output exceeded oral intake initially in all 3 patients necessitating intravenous supplementation for up to 10 days. Stabilization resulted from an increase in oral intake rather than a decrease in diuresis. Unilateral post-obstructive diuresis is extremely uncommon but it may occur in the neonate because of the unique features of the renal physiology encountered in this age patient.

Counterbalance in functional adaptation to ureteral obstruction during development

Renal counterbalance, as described by Hinman in 1923, is the phenomenon of increased function of the intact kidney in proportion to the loss of function resulting from unilateral ureteral obstruction (UUO). In the neonatal guinea pig, chronic partial UUO results in severe vasoconstriction and growth arrest of the ipsilateral kidney. Angiotensin II appears to contribute significantly to the vasoconstriction, and the renin-angiotensin system is also involved in the hemodynamic response of the intact opposite kidney to UUO and to relief of UUO. Immunolocalization of renin following complete UUO in the neonatal rat revealed extension of renin-containing cells along the length of the afferent arteriole in both the obstructed and the intact opposite kidney. The proportion of juxtaglomerular apparatuses with detectable renin and renin messenger ribonucleic acid (mRNA) (identified by in situ hybridization), as well as renal renin content (a measure of active renin), were increased in the obstructed kidney compared with the intact opposite kidney. Chemical sympathectomy by chronic guanethidine administration reduced the total renin mRNA in the obstructed kidney (determined by Northern blot analysis) and prevented the increased renin immunostaining in both kidneys. Thus, renal counterbalance in the developing kidney subjected to UUO is mediated or modulated by the renal nerves and involves marked alterations in gene expression and cellular processing of renin.

Role of atrial peptide in the natriuresis and diuresis that follows relief of obstruction in rat

The present studies demonstrate that endogenous levels of atrial peptide are significantly elevated in the plasma of rats with bilateral ureteral obstruction (BUO) compared with control rats or rats with unilateral ureteral obstruction. The contribution of endogenous atrial peptide to the natriuresis and diuresis that follows release of BUO was examined by the intravenous infusion of heparin with or without the exogenous administration of atrial peptide. Infusion of heparin, which binds atrial peptide and interferes with its biological effect, decreased the natriuresis and diuresis observed after release of BUO. Heparin administration also markedly blunted the natriuresis and diuresis observed after exogenous administration of atrial peptide following release of BUO in rats. In contrast, heparin administration did not decrease the natriuresis and diuresis seen in the experimental kidney after relief of unilateral ureteral obstruction. The finding of increased plasma levels of atrial peptide in rats with bilateral ureteral obstruction together with the decrease in diuresis and natriuresis observed with the administration of heparin after release of BUO in these animals indicate that endogenous levels of atrial peptide contribute to the natriuresis and diuresis that occur after release of BUO in rats.

Impaired parathyroid hormone receptor-adenylate cyclase system in the postobstructed canine kidney.

The present studies examine the initial events in the action of PTH, namely receptor binding and adenylate cyclase activation in the postobstructed canine kidney. Both kidneys were removed from five mongrel dogs 2 h after relief of unilateral ureteral obstruction (UUO) of 42 h duration. Basolateral membranes (BLM) were prepared from both the UUO and contralateral (control) kidneys. Maximal activation of adenylate cyclase by PTH was 35% lower (P less than 0.01) in BLM from UUO than control kidneys (3869 +/- 200 vs. 5978 +/- 425 pmol cAMP/mg protein X 30 min). The concentration of PTH required for half-maximal activation of the enzyme was unchanged. Addition of 1 mM GTP failed to correct the decreased enzyme activity in response to PTH of BLM from kidneys with UUO. NaF activation, a measure of interaction of the nucleotide regulatory component (G/F) with the catalytic unit of the adenylate cyclase was similar in BLM from UUO and control kidneys. Similarly, activation of the catalytic unit of the enzyme by Mn2+ was not different. Specific binding of [125I]Nle8, Nle8, Tyr34-bovine PTH NH2 was markedly reduced (P less than 0.01) in BLM from UUO vs. control (6.37 +/- 1.20 vs. 2.43 +/- 0.09 fmole bound/microgram protein). There was no change in hormone affinity for the binding site. These data indicate that there is decreased activation of adenylate cyclase by PTH as a consequence of apparent loss of receptors for the hormone in the BLMs of renal tubular cells of postobstructed kidneys. These abnormalities may play a role in the abnormal regulation of phosphorus excretion after ureteral obstruction.

The Mechanism of Unilateral Post-Obstructive Diuresis

We report 2 cases of a pathological urinary water loss of clinical relevance after relief of unilateral ureteral obstruction following pyeloplasty. The mechanism of this unilateral post-obstructive diuresis is based on the combination of preservation of glomerular filtration rate of the obstructed kidney and distal tubular damage.

Obstructive nephropathy in the rat: possible roles for the renin-angiotensin system, prostaglandins, and thromboxanes in postobstructive renal function.

Relief of unilateral ureteral obstruction (UUO) of 24 h duration in rats is followed by severe renal vasoconstriction in the postobstructive kidney (POK). The present study examined possible roles of renal prostaglandins (PG) and thromboxanes (TX), as well as the renin-angiotensin system, in this vasoconstriction. Administration of the cyclooxygenase inhibitor indomethacin, which blocks both PG and TX production, failed to improve POK hemodynamics in UUO rats. To explore the possible role of the TX compounds, which include the potent vasoconstrictor thromboxane A2 (TXA2), UUO rats were infused with imidazole, an agent that blocks synthesis of TX, but not of PG. Imidiazole led to two- to threefold increases in the clearance of both inulin and rho-aminohippuric acid by the POK. This effect of imidazole was abolished by indomethacin, suggesting that the amelioration of POK vasoconstriction by imidazole was a result of inhibition of vasoconstrictor TX synthesis (e.g. TXA2), with PG vasodilators (e.g. PGE2 or PG12) still active. Urea, infused in a solution whose osmolality and volume were identical to the imidazole infusion, failed to improve hemodynamics in the POK, making it unlikely that nonspecific effects of volume expansion or osmotic diuresis mediated the beneficial effect of imidazole. Further studies examined the possible role of the renin-angiotensin systems in the vasoconstriction of the POK. UUO rats infused with the angiotensin II antagonist, Saralasin, exhibited no significant improvement in POK function, a finding that might be at least partly attributable to agonist/vasoconstrictor properties of Saralasin. In other experiments, treatment of UUO rats with the angiotensin-converting enzyme blocker SQ 14225 (Captopril), in order to inhibit angiotensin II formation, led to at least twofold increases in the clearance of both inulin and rho-aminohippuric acid in the POK. It is unlikely that Captopril exerted this beneficial effect by potentiating the vasodilator kinins, because the effect was not diminished by administration of either carboxypeptidase B (which destroys the kinins) or Trasylol (which blocks kinin synthesis). Thus, these results suggest that both angiotensin II, as well as metabolites of the PG-TX system, may be important determinants of postobstructive renal hemodynamics in the rat.

Studies on mechanism of hypophosphaturia after relief of unilateral ureteral obstruction.

The effect of unilateral ureteral obstruction (UUO) of 48 h duration on phosphate excretion was studied in dogs. After the relief of UUO, the fraction of filtered phosphate excreted (FEP) was markedly