709

Case Report

A Case of Hyperreninemic Hypertension after

Extracorporeal Shock-Wave Lithotripsy

Manabu SASAGURI, Keita NODA, Takemasa MATSUMOTO, Kazuyuki SHIRAI, Emiko TSUJI, Yuji TSUJI*, and Kikuo ARAKAWA

A 53-year-old male was found to have hypertension caused by the significant secretion of renin from an

atrophic left kidney. He had undergone extracorporeal shock-wave lithotripsy (ESWL) for left renal lithiasis

11 years previously. A renal dynamic study with 99mTc-diethylenetriaminepentaacetic acid (DTPA) indicated

that the rate of renal excretion and uptake was decreased in the left kidney and normal in the right kidney.

Renal angiography demonstrated a normal right renal artery and a small but nonstenotic left renal artery.

The ratio of PRA in the left renal vein to that in the right renal vein was 1.7. Blood pressure could be low-

ered to the range of 140-150180-90 mmHg with imidapril, an ACE inhibitor. ESWL may cause hypertension via the well-known Page kidney effect. In this case, the kidney, atrophic probably due to ESWL, released a

significant amount of renin. (Hyperfens Res 2000; 23: 709-712)

Key Words: hyperreninemic hypertension, renovascular hypertension, extracorporeal shock-wave lithotrip-

sy, Page kidney

Introduction

Hypertension in unilateral renal disease can be caused by renovascular hypertension, but also by chronic atrophic

pyelonephritis, congenital hypoplasia, tuberculosis, renal cyst, renal encystment (Page kidney), hydronephrosis, and tumors (1). Renovascular hypertension may give rise to renal artery stenosis or renal ischemia in response to atherosclerosis, fibromuscular dysplasia, Takayasu's arter-itis, middle artery syndrome, neurofibromatosis, aortic dissection, renal artery aneurysm, dissection of the renal artery, renal arteriovenous fistula, radiation arteritis, re-nal artery embolus, renal transplantation or extrinsic ob-struction (2). Extracorporeal shock-wave lithotripsy (ESWL) is wide-

ly applied for the treatment of renal lithiasis. The side effects of ESWL include hemorrhage, edema, and acute tubular necrosis of the kidney. ESWL is also associated with hypertension, which can either occur immediately or

be delayed by several weeks or months (3). report describes a case of hyperreninemic after ESWL.

The present

hypertension

Case Report

A 53-year-old male was seen in our hospital for elevated blood pressure (1681102 mmHg) on June 22nd, 1999. He had come to our hospital in 1988 due to general malaise. At that time, high blood pressure (150/100 mmHg) and a stone-like shadow on abdominal X ray had been found. Plasma renin activity (PRA) was 2.1 ng/ml/h and the plas-ma aldosterone concentration was 110 pg/ml. On ultra-sonography, hydronephrosis due to ureterolithiasis was observed in the left kidney; however, the size of the left kidney was the same as that of the right kidney. Subse-quently, the patient underwent extracorporeal shock-wave lithotripsy for left renal lithiasis at another hospital. Although he had been taking a 2-mg dose of trichlor-methiazide once a day for 2 months, an, antihypertensive

From the Department of Internal Medicine, and * Department of Urology, Fukuoka University School of Medicine,

Address for Reprints: Manabu Sasaguri, M.D., Department of Internal Medicine, Fukuoka University School

Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan.

Received March 31, 2000; Accepted in revised form May 1, 2000.

Fukuoka, Japan.

of Medicine, 7-45-1

710 Hypertens Res Vol. 23, No. 6 (2000)

drug was not administered until this visit from 1988 to 1999. Since 1997, blood pressure has been found to be elevated at regular annual check-ups. According to his family history, only his elder brother has exhibited signs of hypertension.

In our outpatient clinic, the patient's blood pressure was found to be 170/104 mmHg. Left ventricular hyper-trophy was observed on electrocardiogram (SV1 + RVS= 4.87 mV) and echocardiography (interventricular septum =12 mm, left ventricular posterior wall thickness= 12 mm, left ventricular end-diastolic diameter =39 mm). Five milligrams of imidapril, an ACE inhibitor, was initially administered. Three weeks later, the daily dose of imi-dapril was increased to 10 mg. Blood pressure decreased to a range of 150-156/80-90 mmHg. A renal dynamic study with 99mTC-diethylenetriaminepentaacetic acid

(DTPA) was performed because the plasma renin activity was 3.0 ng/ml/h and the plasma aldosterone concentration was 261 pg/ml on the patient's first visit, indicating that renal uptake and the excretion rate were decreased in the left kidney and normal in the right kidney (Fig. 1). The

glomerular filtration rate of the left kidney was 32 ml/ min, and that of the right kidney was 82 ml/min. The

patient was admitted to our hospital with a tentative di-agnosis of renovascular hypertension. Renal angiography

demonstrated a normal right renal artery and a small but nonstenotic left renal artery (Fig, 2B, C). On nephro-

gram, the right kidney measured 10.5 X 4.8 cm, while the left kidney was 8.0 X 4.4 cm with an irregular margin (Fig. 2A). PRA was 7.7 ng/ml/h in the peripheral blood, 13.6 in the left renal vein, 8.0 in the right renal vein, 10.9 in the upper vena cava, and 9.2 in the lower vena cava. In-travenous pyelography showed that the left kidney was smaller than the right kidney, with its double pelvis, and caliceal stones were observed in the left kidney without any evidence of hydronephrosis (Fig. 3). In this case, it is

possible that subsequent to ESWL the treated kidney may have been damaged and released renin, resulting in a further elevation of blood pressure. At present, blood

pressure in this patient can be controlled within a range of 140-150/80-90 mmHg with imidapril, an ACE inhibi-tor.

Discussion

ESWL is widely applied in the treatment of renal lithiasis. The side effects of ESWL include hemorrhage, edema, and acute tubular necrosis of the kidney. This form of re-nal trauma is associated with an immediate decrease in renal function of the treated kidney. ESWL is also associ-ated with hypertension, which may occur immediately or can be delayed by several weeks or months. Approx-imately 8% of patients develop hypertension requiring

pharmacological treatment 1 year after ESWL (3, 4). Re-cently, Ashida et al, have shown that hypertension (>160 mmHg) can develop in 3 of 97 patients as a late complica-tion associated with ESWL (S). However, the mechanism of hypertension after ESWL is unclear. Williams et al. have suggested that it could be due to a long-term decrease in effective renal plasma flow caused by renal fibrosis, as has been observed in canine kidneys after ESWL (6). Peterson and Finlayson (7) have suggested that renal trauma caused by ESWL may cause hypertension as a result of a perirenal hematoma via the well-known Page kidney effect. Page has observed that constriction of the renal parenchyma itself without com-

promise of the main renal vessels alters intrarenal hemodynamics to produce renal ischemia leading to renin release (8). When Grant et al. followed 33 patients with renal trauma, they observed hypertension in 13 of these 33 from 9 weeks to 16 years. Four of these 13 patients had subcapsular hematomas (9). The mechanism of hypertension in these cases is the same as that in the Page kidney. It has actually been shown by sensitive MRI methods that 63% of post-ESWL patients exhibit some abnormalities such as a loss of corticomedullary dif-ferentiation, perirenal fluid, subcapsular hematoma, and hemorrhage into a renal cyst (10, 11). In our case, the left kidney was atrophic, probably due to ESWL, since atrophy of the left kidney was not observed on ultrasono-

Fig. 1. Renal dynamic study with 99mTc-diethylenetri-aminepentaacetic acid (DTPA). (A) Uptake of 99mTc-DTPA was low in the left kidney. (B) Uptake and the ex-cretion curve for 99mTc-DTPA were decreased in the left kidney.

Sasaguri et al: A Case of Hyperreninemic Hypertension after ESWL 711

graphy before ESWL. Ashida et al. have observed renal atrophy in 5 of 97 patients as a late complication associ-ated with ESWL (5).

In our case, PRA was 13.6 ng/ml/h in the left renal vein and 8.0 in the right renal vein, with a ratio of 1.7. A renal vein renin ratio over 1.5 reportedly indicates that the affected kidney secretes renin into the total circula-tion, resulting in elevations in blood pressure (12, 13). In our case, the atrophic left kidney secreted a significant amount of renin. In the Page hypertension model using rabbits, i. e. , one wrapped kidney, PRA in the peripheral vein was not elevated, but rather was observed to in-

crease only when a low-salt diet was administered (14). However, three patients presenting with a remediable form of hypertension caused by Page kidney showed a significant increase in the renal venous renin ratio, sug-

gesting that hypertension in these cases was of renovascu-lar origin (15-17). Moreover, their blood pressure re-turned to normal after nephrectomy of the affected kid-ney. Patients with hypertension caused by the same mechanism have been shown to exhibit hydronephrosis and renal infarction, where the affected kidney secretes a significant amount of renin (13, I8). One of the under-lying mechanisms of hypertension in our case is similar to

Fig. 2. (A) Aortography. There was no stenosis in either of the main renal arteries. The left kidney was atrophic. In digital subtraction arteriography (B, C), instead of being stenotic, the left renal artery was atrophic in appearance, while there were no abnormalities in the right renal artery or kidney.

712 Hypertens Res Vol. 23, No. 6 (2000)

that in these cases because the co-existence of essential

hypertension cannot be ruled out. The atrophy of the left

kidney was probably due to ESWL, as other causes such

as stenotic renal artery and hydronephrosis were not

observed.

In conclusion, ESWL may cause hypertension via the

well-known Page kidney effect. In the case reported here,

the kidney, which was probably atrophic due to ESWL,

released a significant amount of renin, resulting in hyper-

reninemic hypertension. At present, the blood pressure in

this patient can be controlled within the range of 140-1501

80-90 mmHg with an ACE inhibitor.

Fig. 3. Intravenous pyelography. The left kidney was smaller than the right kidney. Caliceal stones, but no evi-dence of hydronephrosis, were observed in the left kidney, and the right kidney had a double pelvis.

1.

2.

3.

4.

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