Nonrenovascular renal hypertension in children

NONRENOVASCULAR

RENAL HYPERTENSION

IN CHILDREN STEPHEN

R. SHAPIRO,

RAYMOND HENRY

M.D.

D. ADELMAN,

TESLUK,

M.D.

M.D.

From the Departments of Urology, Pediatrics, and Pathology, University of California School of Medicine, Davis, California

ABSTRACT - Hypertension in children has been reported with increasing frequency because of increased awareness of its occurrence by clinicians. Renovascular lesions have been stressed in the past. However, in recent years, a number of nonrenovascular renal lesions have received attention and form the basis fn- this report. Unilateral chronic atrophic pyelonephritis, segmental unilateral pyelonephritis, the Ask-Upmark kidney, and unilateral renal hypoplasia have been associated with curable hypertension. The subject of juxtaglomerular cell hyperplasia, which has variably been reported in these cases, is reviewed. Ureteral obstruction, in the form of ureteropelvic or ureterovesical junction obstruction, solitary renal cysts, the unilateral multicystic kidney, renal trauma, and renal tumors (Wilms’ tumor and juxtaglomerular cell tumors) may also be associated with hypertension in children. Pheochromocytoma must be ruled out in all cases. Because of renewed interest, these nonrenovascular renal causes of hypertension are now likely to be diagnosed with increased frequency.

and mortality in children as well as adults.‘,* The exact significance of elevations in systolic blood pressure in children is not clear. Actuarial studies in adults show a decreased survival rate with systolic hypertension, regardless of the level of the diastolic pressure.’ In children, further information, in the form of long-term follow-up studies, is required to assess the risk of systolic hypertension.

It has been only in recent years that clinicians have become more aware of persistent systemic hypertension in infants and children.’ The precise incidence of hypertension in the pediatric age group is not known, since there is not yet uniform agreement on the definition of normal values.1-4 Estimates range from 1 to 10 per cent.5 Blood pressure in children varies with age and sex and, therefore, tables of normal values must be consulted (Table I).’ The importance of blood pressure measurements in children must be emphasized. In a recent survey at three pediatric teaching hospitals, 62 per cent of 143 hospitalized children had their blood pressures recorded, and only 5.3 per cent of 1,156 outpatients had blood of finding pressure recorded. 6 The importance asymptomatic children with significant diastolic cannot be overemphasized. hypertension Moderate to severe diastolic hypertension is associated with the risk of significant morbidity

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I. Maximal normal values (mean -I- 2 S. D.) for systolic and diastolic blood pressures in

TABLE

infants and children Age (Years)

0 to % 3

8 11 15

6

(from Adelman2)

Systolic

IXastolic

110 120 125 135 140

65

70 80 80 85 ~__

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The various techniques for blood pressure measurement are described in detail by Stickler and Kelalis.‘O It is important that the proper cuff size be used to avoid spuriously high blood pressures (the so-called “small cuff syndrome”). This caution regarding cuff size also applies to use of the Doppler method. The cuff length should adequately encircle the arm; the cuff width should be two-thirds the length of the upper arm; and the patient should be quiet and not agitated. Anxiety and crying will elevate Fifty per cent of hyperthe blood pressure. tensive children may be asymptomatic.’ When symptoms are present, they may include headaches, visual disturbances, irritability, abdominal pain, anorexia, hemiplegia, Bell’s palsy, convulsions, or congestive heart failure. The etiology for hypertension in children can be determined in most cases. Figures vary, but it is possible that in half of the cases the hypertension will be curable.“~” The many causes of persistent hypertension in infants and children are listed in Table II. Renal vascular lesions have been stressed in the literature 1,8,g~11~13and reviews are available. 14-17 Recent reports of curable nonrenovascular renal hypertension have prompted the present review. Hypertension due to end stage renal disease, reviewed elsewhere, has been excluded. 18,1g Unilateral Chronic Atrophic Pyelonephritis The experiments of Goldblatt et al. in 193420 and the subsequent use of the Stamey2r and Howard and Connor tests (1961 and 1962), focused attention on unilateral renal artery stenosis as a cause of persistent systemic hypertension. However, in recent years, the availability of reliable, accurate, and reproducible venous renin assays have allowed study and documentation of other forms of renal hypertension. 23 Unilateral chronic atrophic pyelonephritis has been known to be an occasional cause of renal hypertension for many years. Cure rates, with unilateral nephrectomy, reported in the earlier literature, have ranged from 26 to 40 per cent.24-26 Luke et al. in 196827 reported a 50 per cent cure rate in an unselected population of 28 adults with unilateral pyelonephritis. They noted that results were best in younger patients with a shorter history of hypertension and in cases in which function of the damaged

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TABLE II.

Causes of persistent hypertension in infants and children

Renal parenchymal disease Chronic pyelonephritis Unilateral Bilateral Segmental Chronic glomerulonephritis Post-renal transplant Cystic disorders of kidneys Renal hypoplasia dysplasia Ask-Upmark kidney Hypoplastic kidney Unilateral multicystic kidney Neoplasms Wilms’ tumor Juxtaglomerular cell tumor Trauma Renal artery thrombosis Focal renal infarction Page kidney Renal artery aneurysm Renal vascular disease Renal artery stenosis Renal artery thrombosis Renal artery embolism Arteritis Aneurysm Arteriovenous fistula Cardiovascular Coarctation of aorta Thoracic aorta Abdominal aorta Endocrine disorders Pheochromocytoma Neuroblastoma Cushing’s syndrome Hyperaldosteronism Adrenogenital syndrome Miscellaneous Small cuff syndrome Increased intracranial pressure Toxins (lead, mercury) Metabolic (hypercalcemia, hypernatremia) Essential hypertension Drugs (amphetamines, oral contraceptives, steroids)

kidney contributed less than 25 per cent of the total function. Cure of hypertension with nephrectomy for chronic atrophic pyelonephritis has also been reported in children.‘*s*g,13~28 Haycock in 197S2’ reviewed the literature and found 45 children under the age of fifteen at the time of operation. Of these, 34 (76 per cent) were cured of hypertension. Measurements of renal vein renin ratios have been made in an attempt to improve selection of

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FIGURE 1. (A) lntrauenous pyelogram showing hypertrophied right kidney and small, poorly visualized left kidney. (B) Cystogram showing left vesicoureteric reflux. (C) Renal arteriogram demonstrating tiny left kidney with small left renal artery and poor arborization. Right kidney had two renal arteries but ias otherwise normal.

cases for operation since this method has proved reliable in the diagnosis of renovascular hypertension. Although not yet proved, the current ratio of involved to uninvolved side of 1.5 : 1 may be as valid for parenchymal disease as it has been for renal vascular hypertension.30 Vesicoureteric reflux can be associated with atrophic pyelonephritis and hypertension and, occasionally, with elevated plasma renin activity (PRA).3*“3 In Still and Cottom’s* series of hypertensive children, vesicoureteric reflux was demonstrated in half of the patients with chronic pyelonephritis who underwent voiding cystourethrography. The occurrence of hypertension and parenchymal scarring have been demonstrated in the presence of sterile vesicoureteric reflux in the piglet model by Hodson.34 Hicks et aL31 reported 8 patients with the triad of hypertension, pyelonephritis, and vesicoureteric reflux and suggested that antireflux surgery cured or ameliorated the hypertension in selected cases. This conclusion is not warranted by the data presented. In fact, the causative relationship between vesicoureteric reflux and hypertension in humans remains to be proved. Until further data become available, antireflux surgery, solely for improvement of hypertension, cannot be recommended. Children with bilateral disease generally have not been cured of hypertension when nephrectomy has been performed on the worst

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kidney. 28zg It has been stated that unilateral nephrectomy will never be successful in relieving hypertension even if mild scarring is present in the contralateral kidney.2g However, predictability of cure in such cases may improve with availability of more sophisticated and discriminating tests. Accordingly, patients with bilateral disease may warrant further study. The prognosis with medical management of the hypertension in these children is not entirely hopeless.35 Blood pressure can be significantly ameliorated with appropriate antihypertensive therapy. Case presentation A thirteen-year-old white female, seen in the emergency department for a tendon laceration, was noted to have a blood pressure of 176/130 mm. Hg. She was asymptomatic, with normal findings on physical examination including funduscopic and cardiac evaluation. Findings on chest x-ray film, electrocardiogram, and serum electrolytes were also normal. Blood urea nitrogen was 12 mg. and creatinine 1 mg. per 100 ml.; twenty-four-hour urinary excretion of 17_ketosteroids, 17-ketogenic steroids, vanilmandelic acid, metanephrines, and normetanephrines were normal. Urinalysis revealed 100 to 150 white blood cells per high-power field and 4 plus bacteriuria. A urine culture was negative (while on antibiotics). Intravenous

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pyelogram showed a large but normally shaped right kidney and a small, poorly visualized left kidney. Left vesicoureteric reflux was demonstrated by voiding cystourethrography (Fig. 1A). Angiography was performed (Fig. 1B). Left renal vein renin activity was 25.5 ng. per milliliter per hour; right renal vein renin activity was 6.5 ng. per milliliter per hour; inferior vena cava renin activity was 5 ng. per milliliter per hour. The patient underwent a left nephrectomy and subsequently has remained normotensive. The left kidney weighed 21 Gm. and measured 5 by 2.5 by 1.4 cm.; frequent areas of thyroidization of glomeruli were present. The interstitium contained a hypocellular fibrous connective tissue interspersed with intense infiltrates of plasma cells and lymphocytes, compatible with a diagnosis of chronic pyelonephritis. Segmental

unilateral

pyelonephritis

Segmental lesions such as focal pyelonephritis may cause hypertension. Although comparison of renin activities in the main renal veins has provided prognostic information in the therapy of renal parenchymal or renal vascular disease,36 it may be of limited value in assessing a segmental parenchymal lesion. However, selective segmental renal vein catheterization to obtain venous blood draining an abnormal renal segment has proved useful in cases of segmental lesions such as focal pyelonephritis, as well as segmental renal artery branch stenosis, the hypoplastic or Ask-Upmark kidney, infarction, and juxtaglomerular or other renin-secreting from tumors.37-40 PRA, the diseased segment, is often significantly higher than that from the main renal vein. Javadpour et a1.41 found significantly elevated renin activity from the diseased segment in 2 cases with focal unilateral pyelonephritic scarring secondary to vesicoureteric reflux, despite no significant difference between right and left main renal vein renin activities. Each case was cured of the hypertension by segmental nephrectomy. Selective segmental renal vein catheterization is technically feasible and diagnostically rewarding and may reveal a significant source of renin not apparent in samples from the main renal vein.42 For example, it is well known that on the left side dilution by the gonadal and adrenal veins can result in low renal vein renin ratios in the presence of severe unilateral renal parenchymal or vascular disease.43 It is unclear why

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an elevated segmental renin level which is diluted to a normal value in the main renal vein should be associated with systemic hypertension. Indeed, the role of renin in the maintenance of chronic unilateral renal hypertension is still not entirely clear. Peripheral levels of renin are within normal limits in approximately half the patients in whom the blood pressure is reduced after surgery for renal hypertension.44 It is the combination of a renal vein renin (or segmental renal vein renin) ratio greater than 1.5 with evidence of contralateral renin suppression rather than the peripheral PRA alone which has the most prognostic value. Normal values for peripheral PRA, which vary with age, have recently been determined in children.46*47 Unilateral segmental renal hypoplasia (Ask-Upmark kidney) and renal hypoplasia Ask-Upmark in 192g4* described segmental renal hypoplasia in 6 patients with malignant nephrosclerosis, 5 of whom were adolescents.

FIGURE 2. Ask-Upmark kidney. Grossly, kidney weighs less than 80 Gm. and, typically, grooves are noted on capsular surface overlying hypoplastic segment. Entire kidney in that area is affected by anomaly, and that segment of renal pelvis is abnormal. (Adapted from Ask-Upmurk.4a)

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The hypoplastic kidney was small in size and had few pyramids and a deep groove on its surface, beneath which a calyx-like recess of the renal pelvis terminated without the normal relationship to a pyramid. One or several renal lobules may be affected (Fig. 2). Histologically, within the hypoplastic zone, the tubules show a pseudothyroid appearance, vessels are thick walled, and glomeruli are difficult to find and usually sclerotic. 4g,50 There are no signs of inflammation in this area differentiating this lesion from chronic pyelonephritis. The remainder of the kidney is microscopically normal. AskUpmark considered these structural alterations to be congenital in origin. His description has been confirmed by other authors51-53 but has generally been considered to be somewhat rare. Royer et al. 53 have encountered 38 cases since 1963. Girls are affected twice as often as boys, and most cases presented after the age of ten years. The usual clinical presentation is with the symptoms of severe hypertension. Urography reveals a hypoplastic kidney with the calyceal abnormalities confined to the involved segments. Of particular interest is the fact that in 23 cases there was “bilateral” involvement, in some cases severe enough to warrant consideration of removal of the worst kidney and segmental nephrectomy in the better kidney.54 Fikri et ~1.~~ presented a typical case of unilateral AskUpmark kidney in 1973 except that, pathologically, there was pyelonephritis within the hypoplastic transverse groove. This finding is supported by a recent report by Johnston and Mix5’j which postulates that the Ask-Upmark kidney may well be related to infection and vesicoureteric reflux. Until recently, a unilateral small kidney with hypertension has been attributed in the English medical literature to either pyelonephritis or “primary hypoplasia.” Hypoplastic kidneys, without the features of the Ask-Upmark kidney, have also been reported in association with hypertension. 25,27~2g~57-5g As with the Ask-Upmark kidney, Bengtsson et a1.60 found, in many cases, that it was difficult to give a clear-cut microscopic description of the hypoplastic “kidney” unaffected by infection and vascular disease, since pyelonephritis and hypertensive disease are often superimposed. Angiographically, the artery of the hypoplastic kidney is described as uniformly narrow in its whole length, while in pyelonephritis, the point of the artery, where it arises from the aorta, is said to have a normal width, although the rest of the artery may be narrow.61

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The hypertension associated with hypoplastic kidneys and the Ask-Upmark kidney may be associated with hyperreninemia, but this has been documented in only a few cases.54,62 However, Royer et ~1.~~ point out that in other cases the results have been normal or contradictory. Brosman and Lindstrom63 reported a case of Ask-Upmark kidney with documented elevated segmental renal vein renin. Hypertension was cured by nephrectomy. Juxtaglomerular hyperplasia has been reported in a hypoplastic kidney described by Meares and Gross,5g and this was taken as evidence of hyperreninemia. Further reports of the relationship of PRA and renal vein renin ratios are required to prove, finally, that excessive renin production is related to the hypertension in these cases. Juxtaglomerular

Cell Hyperplasia

The role of the juxtaglomerular apparatus (JGA) in the maintenance of vascular tone has been firmly established. Correlation of structural changes with functional variations has been examined and well demonstrated in other species, particularly in rodents.64-67 Numerous attempts have also been made in humans but with lesser degrees of success. Part of this is due to the fact that the structure of the JGA in humans is not as well defined; in normal kidneys, it is inconspicuous and difficult to orient in sections. The granular cells of the JGA are an important special feature, since they are presumed to be related to the presence of renin; however, they stain poorly in humans in the normal kidney. The best technique in studying this aspect is the Bowie stain6* which requires Helly fixation for satisfactory results making retrospective studies impossible. The Bowie stain itself is not particularly reliable without considerable experience. Attempts to quantitate size and cellularity changes in routine hematoxylin and eosinstained material have been difficult because of poorly defined limits of the JGA. Turgeon and Sommers6g have been pioneers in this study of the correlation between JGA hyperplasia and Others have been unable to hypertension. match this enthusiasm. Many recent workers have fallen back on rough estimations about the size or cellularity of this structure. A good example of this is a fairly thorough study by hyperBarajas et al. ‘O who studied renovascular tension treated surgically. They used the Bowie

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stain as well as estimation of size and cellularity rather than quantitative counts because of the difficulties mentioned previously. There was evidence of both increase in granularity and hyperplasia of the JGA in the ischemic kidney, but no correlation with cure by surgical repair et ~2.~~ also used could be shown. Itskovitz Helly fixation and the Bowie stain and concentrated on the degree of granulation using a scale of 1 to 10. They were able to show that the degree of JGA hyperplasia measured in this way paralleled renovascular hypertension and curability. Similar studies in chronic pyelonephritis cases failed to reveal JGA hyperplasia. Cracker et al. 72 were also able to correlate JGA hyperplasia (using Sommer’s cell counting technique)6g with response to surgical repair of vascular problems. They believed that the JGA hyperplasia was so obvious that a prediction of curability of renovascular lesions could be made from frozen sections prepared during surgery. They also studied Bowie stained preparations but with formalin fixation. There have been numerous studies in which evaluation of size and cellularity have been made from routine sections with some degree of usefulness.73,‘4 This is certainly possible with well-handled material in which the changes are fairly marked such as in unilateral rapidly progressive renal hypertension. JGA hyperplasia is not likely to be found in cases with unilateral chronic pyelonephritis. The finding of JGA hyperplasia is probably a valid and significant observation in cases of unilateral renal hypoplasia and the Ask-Upmark kidney with hypertension, as well as in clear-cut cases of unilateral renal ischemia. It has also been reported with unilateral hydronephrosis and in a multicystic kidney (vide in&z). JGA hyperplasia should be looked for pathologically in these situations, although special handling of the surgical material is required, and a fair sampling, plus adequate experience with control material, is also required. In interpreting the data, it must be kept in mind that JGA hyperplasia has also been observed in other conditions not associated with unilateral renal hypertension such as the crush syndrome, eclampsia, Bartter’s syndrome, and congestive heart failure. 75-77 Ureteral

Obstruction

and Hypertension

Sporadic case reports of hypertension associated with hydronephrosis have appeared in the earlier literature.78-80 Smith in 195625 was

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able to find 23 cases of unilateral hydronephrosis in the literature from 1937 to 1956 cured of their hypertension by nephrectomy. As recently as 1968, when Belman, Kropp, and Simona reported an abdominal pregnancy with unilateral ureteral obstruction and hypertension, it was frequently stated that unilateral hydronephrosis is not a frequent cause of renal hypertension. Since then, a number of cases of hyperreninemic hypertension due to unilateral ureteropelvic junction obstruction have been reported in infants and childrens2 as well as in adults.83-85 Renal hypertension can often be classified as either volume dependent or renin dependent. With renin dependent hypertension, the PRA is markedly elevated and the PRA and blood pressure may rise higher in response to salt and water removal. To the contrary, diuresis improves the situation when the hypertension is volume dependent.s6 Vaughan, Buhler, and Laragh 87 found a normal PRA in adults with hypertension associated with unilateral chronic hydronephrosis and suggested that it was volume dependent. Palmer, Sweiman, and Assaykeen” reported the first case of renal hypertension due to hydronephrosis (UPJ obstruction) in a solitary kidney. The PRA was normal and, after pyeloplasty, there was a massive postobstructive diuresis and a 5Kg. weight loss. Hypertension, possibly volume dependent in this case, improved. Some animal experiments may be helpful in understanding the relationship between ureteral obstruction and hypertension. A series of experiments in dogs8g-g1 suggest that hypertension occurs primarily in younger animals and with relatively acute ureteral obstruction. Rabbit studies85 have shown that decreased renal blood flow with unilateral hydronephrosis stimulates renin production by the obstructed kidney. Experiments in rats g2 have shown that a normal contralateral kidney is necessary for renin secretion to occur with partial ureteral occlusion. However, this does not appear to be the case in humans, since Davis et aLg3 reported a hypertensive child with ureteropelvic junction obstruction in a solitary kidney with elevated PRA. After pyeloplasty, there was only a moderate diuresis, but the PRA, as well as the blood pressure, returned to the normal range. JGA hyperplasia has been reported in a hypertensive twenty-one-year-old male with severe ureteropelvic junction obstruction of the right side of a horseshoe kidney who underwent a right nephrectomy. g4

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FIGURE 3. (A)Initial intravenous pyelogram shows bilateral hydronephrosis. (B) Voiding cystourethrogram shows vesicoureteric rejlux and contrast medium trapped in both renal pelves due to ureteropelvic junction obstruction. (C) Severe exacerbation of right ureteropelvic junction obstruction during episode of right pyelonephritis.

Reports of ureteral obstruction from causes other than ureteropelvic obstruction associated with hypertension have also appeared. Shown and Mooreg5 reported a thirty-five-year-old male with hypertension due to obstruction of a right retrocaval ureter. Klein, Lupu, and Brosmang6 reported a thirty-six-year-old male with hypertension due to traumatic ureteral occlusion. Garret, Polse, and Morrow” reported a four-year-old boy with hypertension and unilateral ureteral obstruction at the ureterovesical junction. It is likely that further reports of a similar nature will appear with increased recognition of the association between hydronephrosis and hypertension. A case of bilateral hydronephrosis and hypertension relieved by surgical repair of the obstructive uropathy is presented. Case

mild hypertension again developed after bilateral ureteral reimplantation some months later (Fig. 4). S imilar cases have been reported.”

presentation

A five-year-old boy was seen with hematuria after a fall from a slide. Intravenous pyelogram and voiding cystourethrogram demonstrated bilateral ureteropelvic junction obstruction as well as bilateral vesicoureteric reflux (Fig. 3B). After cystoscopy, a right pyelonephritis developed with acute exacerbation of the obstruction on the right side (Fig. 3C). Hypertension developed with elevated PRA which was relieved only by percutaneous nephrostomy drainage and bilateral pyeloplasties. Transient

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FIGURE 4. prior to bilateral pyelo{A) Hypertension of plasties demonstrated graphically. (B) Reoccurrence transient mild hypertension after bilateral ureteral reimplantation.

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Solitary Renal Cyst with Segmental Ischemia and Hypertension High renin hypertension due to a solitary renal cortical cyst in adults has been reported recently.gg,‘OO Babka, Cohen, and Sode,“’ and Hoard and 0’Brienlo2 described the same lesion in a fourteen-year-old and a thirteen-year-old boy, respectively. Arteriograms in some of these cases suggest that segmental ischemia may be the cause of the high renin hypertension which is relieved by either cyst decompression surgically,gg,‘ol excision, lo2 or by needle aspiration.ioO Lateralizing renal vein renin ratios greater than 1.5:l.O were documented in each case.gg-102 Peripelvic cysts associated with hypertension103*‘05 have also been reported, although hyperreninemia has not yet been documented. The mechanism of hypertension is presumably similar. Unilateral Multicystic Kidney and Hypertension Unilateral renal dysplasia has rarely been reported in association with hypertension. Javadpour et al. ‘0~ reported the first such case in 1970 in a six-year-old girl with a unilateral multicystic kidney and systemic hypertension which was relieved by nephrectomy. Unfortunately, PRA was not documented. However, pathologically, hyperplasia of the JGA in available nephrons was noted, suggesting a renin-mediated hypertension. The possible association between hypertension and unilateral multicystic kidney is mentioned by Gwinn and Landing, lo’ although no cases are cited. In a recent clinical survey by Bloom and Brosman,lO* the association with hypertension was again noted in some cases, although the magnitude of the blood oressure elevations were not fully defined. L

Renal Trauma

and Hypertension

The true incidence of the development of hypertension after significant renal trauma is not known, but it is estimated at less than 5 per cent. log-lll It has been known, since the report of Braasch and Strom in 1943112 that removal of the damaged kidney may relieve the hypertension. Causes for the hypertension include perirenal fibrosis and compression (the socalled Page kidney),‘13 renal artery thrombosis, renal artery aneurysm, and segmental renal scarring. ‘lo Brosman and Lindstrom63 demon-

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strated segmental excess renin production from a focal renal scar in a hypertensive child with increased PRA after trauma. There was no lateralization of main renal vein renin ratios. The child was cured of the hypertension by segmental nephrectomy. In 1962, Downs and Hewett1i4 were able to find in the literature 7 cases of post-traumatic subcapsular hematoma with hypertension due to renal compression (Page kidney). A number of recent reports have appeared documenting elevated venous renins lateralizing to the side of renal trauma in these cases.115-11* Fluid collections in either the subcapsular or perirenal space beneath Gerota’s fascia can result in renal compression. Fluid or hematoma in the pararenal space outside Gerota’s fascia is unlikely to compress the renal parenchyma. Reported cases of the Page kidney are equally divided between subcapsular and perirenal masses compressing the kidney. Hematomas (85 per cent) or urinomas (15 per cent) are the usual cause for the mass. Neoplasm, renal biopsy, anticoagulation therapy, and so forth may also result in the hematoma.“’ Surgical treatment, when necessary, for persistent hypertension consists of removal of the perirenal or subcapsular mass, or partial or total nephrectomy. that In contrast, Maling et al.“’ suggested there is no increased incidence of hypertension after renal trauma. They followed 63 children and adults with significant renal trauma along with age and sex matched controls for six to one hundred-thirty-eight months and found a similar incidence of the development of hypertension in both groups. In spite of this wellcontrolled study, most evidence suggests that the blood pressure must be checked periodically after renal trauma since documented cases of hypertension have occurred many years after the traumatic episode. log The degree of renal damage is usually established within a year of the renal trauma and may allow estimation of the required intervals for subsequent blood pressure measurement.

Renal Tumors

and Hypertension

Wilms’ tumor The association between Wilms’ tumor and hypertension was first reported in 1937 by Pincoff and Bradley120 who found 4 such patients. In 2 patients, the hypertension recurred after nephrectomy with recurrence of the

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tumor. It is now well appreciated that moderate hypertension is found in most cases of Wilms’ tumors. lzl Sukarochana, Tolentino, and Kiesetheir cases of wetter in 1972122 reviewed Wilms’ tumor and found 63 per cent with documented elevations of both systolic and diastolic Nephrectomy controlled the blood pressures. blood pressure in all cases, which was usually mild. In 7 cases, they documented elevated renal vein renin assays at surgery suggesting that compression of the normal renal parenchyma by the tumor was responsible for the hyperreninemia. In these cases it is unlikely that the tumor itself produced the renin, since patients with metastases remained normotensive. Severe hypertension associated with a Wilms’ Mitchell et tumor is unusual. 123,124 However, al. in 1970125 reported a two-year-old girl with malignant hypertension, increased renin in both tumor and plasma, with relief of hypertension after removal of the tumor. Similarly, a four-year-old boy with severe hypertension, a Wilms’ tumor and an elevated PRA was described by Ganguly et al. in 1973.‘26 The renin content of the tumor was very high, whereas the renin content of the adjacent renal cortex was negligible, proving that the tumor, not the compressed adjacent kidney, was the source of renin in this case. Juxtaglomerular

cell tumors

A rare and highly unusual renal tumor, apparently derived from the JGA,40,‘28-‘31 has recently been described by Robertson et al. 12’ Eight of these tumors63 have now been reported, including one in a fourteen-year-old female.‘32 These tumors form a homogeneous group. The lesions are well circumscribed and show a microscopic pattern partly tubular and partly stromal. The stromal or matrix cells show granularity and have staining features in common with granulated cells of the juxtaglomerular apparatus. Other similarities to the JGA are seen by electron microscopy. 4o Bioassay of tumor extracts indicate presence of renin. Since multiple elements of the juxtaglomerular apparatus are present, most authors believe that this lesion is a hamartoma. Clinically, the patients are young and present with hypertension, hypokalemia, and secondary hyperaldosteronism. Because of the small size of the tumors, failure to study renin secretion in these patients may result in misdiagnosis as primary aldosteronism. Failure to suppress elevated aldosterone excretion with deoxycortico-

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sterone acetate in a patient with elevated PRA is suggestive of a renin-secreting tumor.‘33 The lesion has led to fatal central nervous system hemorrhage in 2 of these 8 reported cases. In the case reported by Schambelan et ~1.~’ prior subtotal adrenalectomy demonstrated that severe hypertension can occur in these cases without excessive aldosterone secretion. Resection of the lesion has always produced immediate resolution of symptoms and hypertension in surviving patients. Pheochromocytoma Chrispin and Scatliff in 1973134 reported a twelve-year-old boy with hypertension and congestive heart failure who was found to have a pheochromocytoma which intimately involved the left renal hilum. More importantly, however, an elevated PRA has now been documented in more than 70 per cent of patients with pheochromocytoma in whom it has been measured.135 Goodman and Roberts’36 reported a patient in whom the PRA was elevated and unilateral chronic pyelonephritis was present. A pheochromocytoma was discovered only accidentally at surgery, which nearly resulted in the death of the patient. The elevated PRA may be due to either catecholamine stimulation or volume depletion which is present in most of these patients. ‘37 It is therefore, necessary to screen all hypertensive’children for pheochromocytoma prior to any major surgical procedure. 4301 X Street, Suite 249 Sacramento, California 95817 (DR. SHAPIRO) ACKNOWLEDGMENTS.

permission for advice

To

to include his case, and assistance.

Anthony E. Way, M.D., for and to John M. Palmer, ht. D.

References 1. Rance

systemic

CP, Arbus BS, Balfe JW, and Kogh SW: Persistent hypertension in infants and children, Pediatr. Clin. North

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