Hypertension due to segmental infarction of the kidney

Hypertension Due to Segmental Infarction of the Kidney* J . ALEX HALLER, JR ., M .D ., LEO R. RADIGAN, M .D . and ANDREW G . MORROW, M .D .

Bethesda, Maryland xIE.ATERAl, renal disease as the causative factor in severe hypertension is a well established clinical entity . In remarkably few instances, however, has the time relationship between the kidney disease and the onset of hypertension been well documented . In the cases reported by I toward and associates` in one patient hypertension developed seventeen days after a possible renal embolus . With non-operative treatment this patient's blood pressure gradually returned to normal . In Perera's survev 2 there is a single case in which hypertension is known to have developed within a year following renal artery obstruction . This patient's blood pressure returned to normal after nephrectomy . Poutasse' has recently reported another case in which hypertension' developed within five months following an embolus to the renal artery . This patient's blood pressure also returned to normal following nephrectomy. We have recently had the opportunity to study a patient in whom the time relationship between renal infarction and subsequent hypertension was exceptionally well documented .

the abdomen was soft and she was afebrile . A specimen of urine contained no cells or albumin . A diagnosis of splenic infarction was made and the patient was given dicumarol . Within eighteen hours

U

CASE REPORT A forty-two year old housewife was admitted to the Surgical Service of the National Heart Institute on September 20, 1954 with the diagnosis of mitral stenosis . She complained of progressive shortness of breath and marked fatigability . During the previous four years she had had three arterial emboli, one cerebral and two to the lower extremities . The blood pressure was 120/70 . There was slow atrial fibrillation and the characteristic murmur of mitral stenosis . This diagnosis was substantiated by angiocardiography, right heart catheterization and transbronchial left heart catheterization . At 5 A .M . on October 2, 1954, two days prior to proposed cardiac surgery, the patient was awakened by intense non-radiating pain in the left flank . She was slightly nauseated . Peripheral pulses were unchanged,

Fie . 1 . Retrograde renal arteriogram demonstrating occlusion of the segmental artery to the lower pole of the left kidney . the pain had diminished and in three days disappeared entirely . A specimen of urine collected four days after the onset of pain contained a trace of protein but no cells or casts . A mitral commissurotomy was performed on October 19, 1954, seventeen days after the attack . The postoperative course was benign and the blood pressure remained normal . Whole blood urea nitrogen values of 15 and 17 mg . per 100 cc . were recorded in the postoperative period . The patient was

" From the Clinic of Surgery, National Heart Institute, Bethesda 14, Maryland . FEBRUARY, 1957

303

304

Hypertension Due to Renal Infarction-Haller el al.

Fle . 2. The left kidney which was removed at operation . The lower pole is small and the segmental artery is occluded by a thrombus . discharged to the care of her referring physician on November 24, 1954 . She experienced a gradual increase in exercise tolerance and had no dyspnea or pain . Frequent determinations of the blood pressure by her physician were normal . She remained well until January 2, 1955 . On this day she experienced the first of daily frontal headaches . On January 5, she saw her physician and was found to have a blood pressure of 160/110 . There were no retinal changes . It had been ninety-five days since the episode of embolic pain . The headaches increased in severity and frequency and on January 10 her systolic blood pressure was 220 mm . Hg. She was found to have retinal hemorrhages and exudates . Specimens of urine at this time contained no cells or protein . She was readmitted on January 13, 1955 . The blood pressure at this time was 210/116 . The pulse was 80 . There was marked retinal arterial spasm and numerous globular and flame-shaped hemorrhages . There was striking A-V nicking but no papilledema . Examination of the urine was again normal . Blood urea nitrogen was 16 mg . per 100 cc . An intravenous pyelogram showed prompt bilateral dye excretion but there was diminished concentration on the left where the calyces were poorly visualized . A urine concentra-

Fm . 3 . Section through transition zone of left kidney showing necrotic glomeruli of the infarct partially replaced by infiltrating fibrous tissue . The adjacent viable structures show segmental glomerular hyalinization and moderate endothelial proliferation of the smaller arterioles . Lion test revealed a maximum specific gravity of 1 .035 . An intravenous regitine® test was negative . Hexamethonium (15 mg .) was given intravenously over a fifteen minute period with a dramatic fall in blood pressure to 120/80. The patient was maintained on subcutaneous hexamethonium, 15 mg . every four hours for forty-eight hours . During this period the systolic blood pressure was maintained below 180 mm . Hg and she remained free of headaches . Retrograde pyelography revealed contraction of the calyceal system on the left, compatible with a small left kidney . Differential volumetric urine samples showed that the volume excreted by the right kidney was ten times that of the left . The two hour phenolsulfonphthalein excretion was 54 per cent . During the second forty-eight hours of hospitalization it was necessary to increase the hexamethonium dosage to 25 mg . every three hours in order to maintain a systolic pressure below 180 mm . Hg . There was intermittent return of frontal headaches . A retrograde aortagram was performed percutancously by means of a catheter passed via the femoral artery to the level of the renal vessels . Twenty cc . of 70 per cent urokon ® were injected at this site and serial films revealed occlusion of the inferior branch of the left renal artery . (Fig . 1 .) A diagnosis of renal infarction secondary to AMERICAN JOURNAL

OF

MEDICINE

Hypertension Due to Renal arterial occlusion seemed established . In the next forty-eight hours adequate blood pressure control became snore and more difficult despite increasing doses of hexamethonium . On January 20, 1955, a left nephrectomy was perfor tried . The lower pole of the excised kidney was replaced by adipose and fibrous tissue in the infarcted area . The renal artery to this pole was occluded by organized thrombus . (Fig . 2 .) Microscopically, this portion of the kidney showed almost complete medullarv fibrosis . The tissue from the superior portion of the kidney revealed thickening of numerous glomeruli while others were hyalinized or scarred . The microscopic characteristics of acute infarction were observed in the transition zone . (Fig . 3 .) I'ostoperalively, the blood pressure did not exceed 130 systolic: for the first four days, but the blood urea nitrogen rose to 40 rug . per 100 cc . on the fifth postoperative dav . At this time the patient again coruplained of mild headache and the blood pressure was 210/100 . The urinary output exceeded 2,000 cc . daily with a specific gravity of 1 .008 to 1 .010 . On the sixth day alter operation the blood urea nitrogen was 56 mg . per 100 cc . and the highest blood pressure was 180 .95 . Thereafter the blood urea nitrogen slowly fell and The blood pressure became stabilized at 140-160, 85-90 . On the eighteenth day an intravenous pyelogram showed normal function of the right kidney . On the tweuty-first day she was discharged . The blood urea nitrogen at this tine was 30 mg- per 100 cc . and the blood pressure 140/80 . The patient has been asymptoniatic- for the past fourteen months and has gained eight pounds . Her blood pressure is 100/60 . The urinalysis and blood urea nitrogen are normalCOMMENTS The postoperative course of this patient, complicated by transient return of elevated blood pressure, polyuria and azotemia, may in part reflect secondary vascular changes in the remaining kidney . This assumption is based upon the extensive glomerular lesions observed in the viable portion of the excised kidney . These

FEBRUARY, 1957

Infarction--Halter el a/ .

305

changes were apparently secondary to the hypertensive state . The patient's subsequent recovery emphasizes the reversibility of these lesions_ In his original experimental studies, Goldblatt1 demonstrated the necessary- role of parenchvmal ischemia in the production of hypertension . In this patient there was considerable viablee tissue adjacent to the infarciod area and this may have represented such art area of renal ischemia . Pererat has emphasized the rapid and , malignant" course of hypertension associated with unilateral renal disease as contrasted with that seen in essential hypertension or bilateral renal disease . Eleven days after hypertension was first detected in this patient, she was seriously ill with conslant headache, marked hypertension and retinopathv . SUMMARY

A case is presented of unilateral renal infarction resulting in hypertension ninety-five clays later . The segmental arterial occlusion was demonstrated by retrograde aortography . Following nephrectomy, the patient's blood pressure returned to normal and has remained so for a period of fourteen months . REFERENCES

1 . IIOwIARD, J . E ., BERTHRONG, M ., COULD, 1) . M. and YrsnT, f. . R . Hypertension resulting from unilateral renal vascular disease and its relief by nephrectomy . Bull. Jilu Hopkins Hnr(, 94 : 51, 1954 . 2 . PERERA, C . A. and HAELIG, A . W . Clinical characteristics of hypertension associated with unilateral renal disease . Circulation, 6 : 549, 1952 . 3 . POLTASSE, E . F . Occlusion of a renal artery as a cause of hypertension . Circulation, 13 : 31, 1956 . 4 . Gonnst .Arr, H . The Renal Origin of Hypertension . In American Lectures in Pathology, American Lecture. Series Publication 14, Cannon, P . R ., ed . Springfield, Ill ., 1948 . Charles C Thomas .