Congenital hypertension due to unilateral renal vein thrombosis.

Evans, D J; Silverman, Milton; Bowley, N.

doi:10.1136/adc.56.4.306

Cited by 26 publications

(15 citation statements)

References 5 publications

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“…In particular, PKD and other forms of renal parenchymal disease may continue to cause hypertension throughout childhood [56][57][58]135]. Infants with renal venous thrombosis may also remain hypertensive [45], and some of these children will ultimately benefit from removal of the affected kidney [44,45,49]. Persistent or late hypertension may also be seen in children who have undergone repair of renal artery stenosis or thoracic aortic coarctation [80].…”

Section: Outcomementioning

confidence: 94%

“…Renal venous thrombosis classically presents with the triad of gross hematuria, thrombocytopenia, and palpable renal mass in the clinical setting of high-risk prothrombotic disorders, including infant of a diabetic mother or Factor V Leiden mutation [44][45][46][47][48][49]. Hypertension may be quite severe in such cases and may persist beyond the neonatal period [45,48].…”

Section: Etiologymentioning

confidence: 98%

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Hypertension in infancy: diagnosis, management and outcome

2011

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Advances in the ability to identify, evaluate, and care for infants with hypertension, coupled with advances in the practice of Neonatology, have led to an increased awareness of hypertension in modern neonatal intensive care units. This review will present updated data on blood pressure values in neonates, with a focus on the changes that occur over the first days and weeks of life in both term and preterm infants. Optimal blood pressure measurement techniques as well as the differential diagnosis of hypertension in the neonate and older infants will be discussed. Recommendations for the optimal immediate and long-term evaluation and treatment, including potential treatment parameters, will be presented. We will also review additional information on outcome that has become available over the past decade.

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Section: Outcomementioning

confidence: 94%

Section: Etiologymentioning

confidence: 98%

Hypertension in infancy: diagnosis, management and outcome

2011

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“…We are only aware of one previous case of hypertension reported to have begun during fetal life. 5 However, we believe that three babies previously reported to have presented with early hypertensive heart failure and unilateral renal disease could have been affected as fetuses, rather than perinatally, as postulated by the authors. 6 All the nephrectomy specimens showed some areas lacking normal proximal convoluted tubules, demonstrated both by routine histology and by immunochemical staining using a marker not expressed by fully differentiated proximal tubules.…”

Section: Commentmentioning

confidence: 74%

Renovascular hypertension commencing during fetal life

Hegde

Wright²,

Shenoy³

et al. 2007

Archives of Disease in Childhood - Fetal and Neonatal Edition

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We report three infants with severe, early hypertension due to unilateral renovascular disease, whose cardiovascular changes, or polycythaemia, or both, indicated they had been affected as fetuses. All underwent unilateral nephrectomy, and had a similar histology, with patchy areas having relatively normal glomeruli but immature proximal tubules. This pattern may be a marker for renovascular disease in fetal life. CASE 1A 37 weeks gestation, 3.3 kg girl, born to a mother with insulin-dependant gestational diabetes, required intravenous glucose and glucagon for symptomatic hypoglycaemia at four hours. Polycythaemia (haemoglobin 210 g/l, haematocrit 0.62 l/ l) was present at 24 h, and persisted. On day 3, her systolic blood pressure, measured by Doppler vascular flow detector, was elevated at 80 mm Hg, and she had developed heart failure, with poorly contacting ventricles and asymmetric septal hypertrophy on echocardiography. She had normal femoral pulses, and had not had an umbilical artery catheter. Despite treatment with propranalol 3 mg/kg/d, captopril 0.5 mg/kg/d, and furosemide 1 mg/kg/d, later replaced with spironolactone 1 mg/kg/d and chlorothiazide 15 mg/kg/d, her systolic blood pressure rose to 135 mm Hg by day 7, and 155 by day 14. Her heart failure worsened, and she was transferred to our care.Her hypertension was renin-driven (plasma renin activity 222 pmol/ml/h; normal ,7), and imaging revealed a small (34 mm) left kidney with no perfusion on Doppler ultrasound, and virtually no function on mercaptoacetyltriglycine renography. The 49 mm right kidney was normal on scanning, and produced a normal plasma creatinine for her age and gestation at 68 mmol/l. Her urine contained no blood, protein, or glucose. Her blood pressures remained slightly elevated even when treated with the angiotensin-converting-enzyme inhibitor, captopril, at 5 mg/kg/d. Renal vein blood sampling to measure differential plasma renin activity was not considered justified in view of the invasive nature of this test, combined with the obviously unilateral disease on imaging studies. We therefore removed her left kidney. This showed a patchy histology. Some areas had normal glomeruli, immature poorly differentiated tubules, and marked intimal thickening of the medium sized arteries, while other segments showed old cortical and medullary infarction ( fig 1A). Normal mature proximal convoluted tubules do not express epithelial membrane antigen (EMA), so immunostaining for this marker can indicate incompletely differentiated areas, as is seen in the abnormal areas of her cortex ( fig 1B).She was discharged one week post-nephrectomy with a normal blood pressure, off all drugs. At four months, she was thriving, normotensive, had a plasma creatinine of 46 mmol/l, good biventricular function, and normal fundoscopy. CASE 2A woman with myotonic dystrophy and polyhydramnios delivered a 2.5 kg girl at 36 weeks gestation who was also myotonic, requiring nasogastric feeding. She had continuous positive airway pressure for mild respiratory distress f...

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“…The dissection of the renal artery of the rat is laborious, but both nephrectomy and the ligation of the renal vein are easily performed, as well as the veins in murine models are more suitable for training 10 . Although human right renal vein is smaller and close to the inferior vena cava, the right kidney in rats is more mobile and easier to dissect, as well as the right ovarian vein in the studied rats was a direct tributary of the inferior vena cava (Figure 1-II Evans et al 25 reported the occurrence of congenital unilateral renal vein thrombosis, followed by hypertension and dilution of the urine of the neonate that presented values of specific gravity between 1000 and 1002, weight loss and hemoconcentration, but no change in urea and electrolytes. In the polyuric phase there was a decrease in potassium levels and increased renin, parameters that have been corrected with the removal of the affected kidney in the seventh week of life.…”

Section: Discussionmentioning

confidence: 91%

Experimental models of renal dysfunction in female rats. Functional and histological aspects after unilateral nephrectomy or ligation of right renal vein with kidney preservation

et al. 2015

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PURPOSE:To compare renal dysfunction after right nephrectomy and ligation of the right renal vein with preservation of kidney. METHODS:Animals' weight, pH, density, protein in urine and histological samples of the kidneys were evaluated. Fifteen female rats (Wistar) were divided into three groups. In the control group, right renal vein dissections were performed. In the second group, the right nephrectomy was performed. In the third group, the right renal vein was ligated and the kidney was preserved. Urine samples were taken before, three and seven days after the procedure. On the seventh postoperative day the kidneys were removed to histopathological study.Analysis by Student's t test was performed.RESULTS: weight loss, alterations of urine pH (p<0.05), in specific gravity, proteinuria (p<0.05) were found in groups 2 and 3; hemorrhagic infarction and edema were found after ligation of the right renal vein; changes in the left kidney were also observed on the seventh day. CONCLUSIONS:Unilateral nephrectomy and ligation of the right renal vein produced early changes in glomerular filtration, being more intense in group 3. The contralateral kidney preserved failed to properly maintain renal function in both situations.Key words: Kidney/physiopathology. Acute Kidney Injury/pathology. Proteinuria. Renal Veins. Models, Animal. Rats. Experimental models of renal dysfunction in female rats. Functional and histological aspects after unilateral nephrectomy or ligation of right renal vein with kidney preservation

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Congenital hypertension due to unilateral renal vein thrombosis.

Cited by 26 publications

References 5 publications

Hypertension in infancy: diagnosis, management and outcome

Hypertension in infancy: diagnosis, management and outcome

Renovascular hypertension commencing during fetal life

Experimental models of renal dysfunction in female rats. Functional and histological aspects after unilateral nephrectomy or ligation of right renal vein with kidney preservation

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