Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Animal and human studies suggest that fetal oliguria is a normal physiologic response to hypoxemia. To assess the clinical significance of this observation, we studied (before their admission) 51 fetuses of women whose pregnancies were complicated by oligohydramnios at greater than or equal to 38 weeks' gestation. We found that the mean hourly fetal urine production decreased significantly in relation to the severity of subsequent intrapartum fetal compromise. The mean antepartum rate was 95 ml/hr in the 21 fetuses with a normal intrapartum heart rate pattern; this fell to 59 ml/hr in the 18 fetuses who had an abnormal intrapartum heart rate pattern but who responded to intrauterine resuscitation. The rate was 33 ml/hr in the 12 fetuses who were delivered by cesarean section as a result of fetal distress. These findings suggest that oligohydramnios associated with fetal oliguria may be used to identify those fetuses who have less intrinsic or uteroplacental reserve than do those of women with oligohydramnios who have a higher rate of fetal urine production.
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PMID:Oligohydramnios: antepartum fetal urine production and intrapartum fetal distress. 831 42

Renal tubular dysgenesis (RTD), with hypoplasia especially of renal proximal convoluted tubules and clinical neonatal anuria or oliguria, has been reported as a congenital familial (autosomal recessive) disease, variably with features of oligohydramnios, Potter syndrome, or pulmonary hypoplasia. A similar tubular lesion due to antenatal tubular atrophy has been reported for conjoined twins with twin-twin transfusion syndrome or acardia and in infants of mothers given antihypertensive agents, including angiotensin-converting enzyme (ACE) inhibitors, during pregnancy, and it has been seen as a unilateral lesion in young infants with renal artery stenosis due to arteritis or medial arterial calcinosis. The renal tubular changes in RTD are very like those of the "endocrine kidney" in experimental animals and resemble those of the renal tubular atrophy of end-stage kidney diseases such as glomerulonephritis, tubulointerstitial kidney disease, obstructive uropathy/pyelonephritis, graft rejection of transplanted kidneys, or the renal parenchymal changes seen with protracted dialysis therapy. Labeled lectins that differentially mark proximal convoluted, distal convoluted and connecting, and collecting tubules showed no distinctive differences in staining patterns of the hypoplastic renal tubules of infants and children with RTD, postnatal renal artery obstruction, or the various types of end-stage renal disease with the lectins used (PNA, GSLI, UEA, and LTA). The findings suggest that the renal tubular changes in some if not all the conditions studied are the result of renal ischemia. The reported familial RTD with hypernephronic nephromegaly may be a specific disorder, but other forms could reflect renal ischemia acquired in utero or in early or later postnatal life.
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PMID:Labeled lectin studies of renal tubular dysgenesis and renal tubular atrophy of postnatal renal ischemia and end-stage kidney disease. 815 24

Renal failure in the newborn infant is mainly determined by vascular causes. In this report we describe a patient with a particular vascular cause of renal failure. The patient was the product of a twin pregnancy in which the twin partner died in utero. In retrospect, the twins appeared to be monozygotic. As the pregnancy was studied carefully prenatally by ultrasound, we were able to observe the development of this condition, characterized by oliguria, oligohydramnios, and lung hypoplasia: the oligohydramnios sequence. After organ development had been normal initially, renal function was lost and the oligohydramnios sequence developed in the survivor after the co-twin had died in utero.
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PMID:Renal failure in the surviving monochorionic twin after death of the co-twin in utero. 861 56

In a fetal autopsy series, we have explored the occurrence of renal tubular dysgenesis in twins. Renal tubular dysgenesis was found exclusively among those monozygotic twins with evidence of twin transfusion syndrome, particularly in those donor twins with oligohydramnios and growth restriction. We infer that hypotension in the donor twin of the twin transfusion syndrome pair is responsible for the failure of proximal convoluted tubule differentiation, and the disturbance of renal function is manifested as oligohydramnios prenatally, and either oliguria or tubular dysfunction postnatally.
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PMID:Renal tubular dysgenesis in twins. 968 62

Therapy for obstructive uropathy is largely determined by whether the obstruction involves one or both kidneys, and by the age of the patient. In the infant and child, obstructive uropathy is almost always due to a congenital malformation of the ureter, bladder, or urethra. Ultrasonographic prenatal diagnosis has permitted early detection and even fetal intervention for posterior urethral valves, although this form of treatment must be considered experimental at present. More important to the affected infant than optimal renal development is the prevention of pulmonary hypoplasia, which is a consequence of fetal oliguria and oligohydramnios. Congenital ureteropelvic junction (UPJ) obstruction is generally unilateral, and although there is controversy regarding the timing of surgical correction, current evidence favors early pyeloplasty. In the adult, obstructive nephropathy is often acquired, with ureteral obstruction usually a consequence of nephrolithiasis. Removal of the stone can be accomplished surgically or by lithotripsy. Bladder outlet obstruction is usually secondary to prostatic hyperplasia, which may progress slowly, allowing a delay in surgical intervention. Neurogenic bladder may require intermittent catheterization or cholinergic therapy; those with hypertonic bladder may benefit from anticholinergics. Regardless of the patient's age, prompt and accurate diagnosis is essential to planning an optimal strategy for the management of obstructive uropathy.
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PMID:Therapeutic approaches in obstructive uropathy. 981 56

Twin-twin transfusion syndrome (TTTS) complicates one in five monochorionic pregnancies and is generally associated with high mortality and morbidity. One twin (the recipient) grows appropriately and has polyhydramnios while the other (the donor) may have a reduced growth velocity and severe oligohydramnios. The disparities in amniotic fluid volumes represent differences in fetal urine output. These differences occur secondary to hemodynamic changes, in which the vascular arrangement of placental anastomoses in TTTS leads to unidirectional flow from the donor to the recipient twin. A better understanding of the pathophysiology may contribute to improved management of this morbid condition. We studied three consecutive prospectively diagnosed stillborn twin pairs affected by early-onset TTTS. Renin gene expression was studied in sections of fetal kidneys with immunocytochemistry using a renin antiserum and with in situ hybridization using riboprobes complementary to renin mRNA, and renin-secreting cells (RCC) were counted. The overall maturation of the renal cortex was assessed by the percentage of immature glomeruli. The donor twin kidneys were smaller than those of the recipients, but the maturation of the renal cortex was not significantly different (28.2% immature glomeruli in the donor and 24.4% in the recipient kidney). The donor kidney showed increased renin gene expression with hyperplastic juxtaglomerular apparatuses (JGAs) that contained excess RCCs (median 20.02 [25th-75th centiles, 5.4, 25.1 RCCs per 100 glomeruli]). In contrast, the recipient kidney was virtually devoid of these cells (0.04 [0, 0.36] RCCs per 100 glomeruli; P < 0.05). In the donor kidney, increased renin release may, by a local action, contribute to renal vasoconstriction and oliguria. Increased renin and/or angiotensin II in the blood passing through the placental anastomoses may, by an endocrine action, suppress renin synthesis in the recipient kidney, thereby increasing renal blood flow and causing polyuria and polyhydramnios. These changes in the renal RAS could thus contribute to the pathogenesis of TTTS. The renal renin changes noted here may represent a contributory or compensating mechanism, the success of which may dictate the overall survival of the twin pregnancy and allow better understanding of the pathophysiology and perhaps therapy that may be employed in this condition.
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PMID:Renin gene expression in fetal kidneys of pregnancies complicated by twin-twin transfusion syndrome. 1117 34

Despite advances in treatment, twin-to-twin transfusion syndrome (TTTS) still carries a high risk for perinatal mortality and morbidity. Simple blood transfer from the donor to the recipient twin cannot explain all of the features of this disease, in particular the recipient's hypertensive cardiomyopathy. We report a case in which TTTS resulted in preterm delivery with early neonatal death of both twins, allowing assessment of the renin angiotensin system (RAS) status of each fetus, both by cord blood renin and aldosterone assay and by renal immunohistochemistry. The donor had severe oliguria/oligohydramnios, whereas the recipient, in addition to severe polyuria/polyhydramnios, had cardiomyopathy, atrioventricular regurgitation, and ascites. Although immunohistochemistry demonstrated that renal secretion of renin was up-regulated in the donor and down-regulated in the recipient, cord blood levels of renin and aldosterone were similar, with high renin levels in both twins. This observation supports the hypothesis that despite renal RAS down-regulation, the recipient is exposed to RAS effectors elaborated in the donor and transferred via placental shunts. This may contribute to cardiomyopathy and hypertension in the recipient, which cannot be accounted for by hypervolemia alone. We thus hypothesized that in TTTS, the recipient's hypertensive cardiomyopathy could be due to a mechanism similar to the classical model of hypertension referred to as "2 kidneys-1 clip." Thus the hypovolemic donor twin, comparable to the clipped kidney, produces vasoactive hormones that compromise the recipient, comparable to the normal kidney, causing hypertension and cardiomyopathy.
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PMID:Paradoxic activation of the renin-angiotensin system in twin-twin transfusion syndrome: an explanation for cardiovascular disturbances in the recipient. 1618 93