Idiopathic segmental renal infarction
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CASE REPORTS IDIOPATHIC SEGMENTAL RENAL INFARCTION KATHY WALSH, M.D. NEIL BAUM, M.D. HARRIS HYMAN, III, M.D. JOHN BALL, M.D. SALVADOR VELAZQUEZ, M.D. From the Touro Infirmary, New Orleans, Louisiana ABSTRACT-A case qf segmental renal infarction is presented. The discussion includes the dif- ferential diagnosis and-management. Segmental renal infarction is usually caused by emboli, arteriosclerosis, and trauma. We report a case of segmental renal artery infarction with no identifiable etiology occurring in a thirty- year-old man. Case Report A thirty-year-old white man was admitted with a chief complaint of sudden onset of con- stant radiating right flank pain, which radiated to the right lower quadrant and right testicle. There is no history of antecedent trauma or hy- pertension. On admission his blood pressure was 120/82 mm Hg, and findings on physical examination were normal except for right cos- tovertebral angle tenderness. The urinalysis on admission and several hours later was negative for red blood cells and protein. A KUB film revealed no opacities over the urinary tract. An excretory urogram was normal and without obstructive uropathy (Fig. 1A). The initial laboratory studies revealed: blood urea nitrogen (BUN) 6.7 mg/dl, creatinine 0.8 mg/dl, SGOT 305 mu/ml (normal less than 230 mu/ml). Findings on chest x-ray film and elec- trocardiogram were normal. Twenty-four hours after admission the pa- tient’s blood pressure was 180/120 mm Hg. The hypertension was associated with increased flank pain that required injectable analgesics. No decrease in the blood pressure occurred with relief of the flank pain. The patient was given 10 mg of intravenous hydralazine, and no change in the blood pressure was noted. Capto- pril, an angiotensin converting enzyme inhibi- tor, was given, 25 mg, PO tid, and the blood pressure decreased promptly from 180/120 to 140180 mm Hg. Because the blood pressure responded to an angiotensin enzyme inhibitor, a renovascular origin of hypertension was suspected. A triple renal scan was obtained. This study demon- strated a focal abnormality in the lateral infe- rior region of the right kidney compatible with a segmental renal infarction (Fig. 1B). A repeat intravenous pyelogram with tomog- raphy revealed nonvisualization of the inferior lateral aspect of the right kidney (Fig. 1C). Be- cause a renal infarct was suspected, an arterio- gram was obtained, which confirmed an avas- cular segment to the inferior lateral aspect of the right kidney (Fig. 1D). The patient was on a regimen of bedrest and antihypertensive medication consisting of cap- topril and hydrochlorothiazide for one week. He was discharged on a regimen of hydroch- lorothiazide with a blood pressure of 120/80 mm Hg. Two months after his discharge he was normotensive without medication. 164 UROLOGY / AUGUST 1985 / VOLUME XXVI, NUMBER 2
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Transcript of Idiopathic segmental renal infarction
CASE REPORTS
IDIOPATHIC SEGMENTAL RENAL INFARCTION
KATHY WALSH, M.D. NEIL BAUM, M.D. HARRIS HYMAN, III, M.D. JOHN BALL, M.D. SALVADOR VELAZQUEZ, M.D.
From the Touro Infirmary, New Orleans, Louisiana
ABSTRACT-A case qf segmental renal infarction is presented. The discussion includes the dif- ferential diagnosis and-management.
Segmental renal infarction is usually caused by emboli, arteriosclerosis, and trauma. We report a case of segmental renal artery infarction with no identifiable etiology occurring in a thirty- year-old man.
Case Report A thirty-year-old white man was admitted
with a chief complaint of sudden onset of con- stant radiating right flank pain, which radiated to the right lower quadrant and right testicle. There is no history of antecedent trauma or hy- pertension. On admission his blood pressure was 120/82 mm Hg, and findings on physical examination were normal except for right cos- tovertebral angle tenderness.
The urinalysis on admission and several hours later was negative for red blood cells and protein. A KUB film revealed no opacities over the urinary tract. An excretory urogram was normal and without obstructive uropathy (Fig. 1A).
The initial laboratory studies revealed: blood urea nitrogen (BUN) 6.7 mg/dl, creatinine 0.8 mg/dl, SGOT 305 mu/ml (normal less than 230 mu/ml). Findings on chest x-ray film and elec- trocardiogram were normal.
Twenty-four hours after admission the pa- tient’s blood pressure was 180/120 mm Hg. The hypertension was associated with increased
flank pain that required injectable analgesics. No decrease in the blood pressure occurred with relief of the flank pain. The patient was given 10 mg of intravenous hydralazine, and no change in the blood pressure was noted. Capto- pril, an angiotensin converting enzyme inhibi- tor, was given, 25 mg, PO tid, and the blood pressure decreased promptly from 180/120 to 140180 mm Hg.
Because the blood pressure responded to an angiotensin enzyme inhibitor, a renovascular origin of hypertension was suspected. A triple renal scan was obtained. This study demon- strated a focal abnormality in the lateral infe- rior region of the right kidney compatible with a segmental renal infarction (Fig. 1B).
A repeat intravenous pyelogram with tomog- raphy revealed nonvisualization of the inferior lateral aspect of the right kidney (Fig. 1C). Be- cause a renal infarct was suspected, an arterio- gram was obtained, which confirmed an avas- cular segment to the inferior lateral aspect of the right kidney (Fig. 1D).
The patient was on a regimen of bedrest and antihypertensive medication consisting of cap- topril and hydrochlorothiazide for one week. He was discharged on a regimen of hydroch- lorothiazide with a blood pressure of 120/80 mm Hg. Two months after his discharge he was normotensive without medication.
164 UROLOGY / AUGUST 1985 / VOLUME XXVI, NUMBER 2
gross hematuria. Elevated serum glutamic- oxaloacetic transaminase and lactate dehydro- genase may be present for twenty-four to forty- eight hours after renal infarction. Fever and leukocytosis can also be founda Segmental re- nal infarction can be evaluated by excretory urogram, computerized tomography, renal scans, ultrasound, and angiography. With par- tial or segmental infarction the excretory uro- gram may be entirely normal, as was seen in this patient.
The renal scan is helpful, but not diagnostic of segmental renal arterial occlusion. This study will reveal a focal decrease in renal blood flow, but cannot distinguish segmental renal infarc- tion from other hypovascular focal lesions of the kidney. 4
The definitive diagnosis of renal infarction is made by renal angiography. Segmental renal infarction results in any of the following: (1) a nephrographic defect, sometimes wedge shaped, (2) occluded vessels, (3) delayed circu- lation throughout the involved segment, and (4) attenuated vessels.
Interestingly, this patient’s blood pressure had no response to hydralazine, which acts
directly to decrease arteriolar resistance, and did respond to captopril, which inhibits the en- zyme which converts angiotensin I to angioten- sin IIe5 This would be compatible with hyper- tension secondary to renovascular ischemia. It is noteworthy that in 1940 this diagnosis was made clinically in only 1.4 per cent of 14,100 autopsies.2 We believe that today, with present diagnostic techniques and a high index of suspi- cion, this diagnosis will be made more fre- quently.
3525 Prytania Street Suite 614
New Orleans, Louisiana 70115 (DR. BAUM)
References
1. Lang EK, Mertz JHO, and Nourse M: Renal arteriography in the assessment of renal infarction, J Urol 99: 506 (1968).
2. Hoxie HJ, and Coggin CB: Renal infarction. Statistical study of 205 cases and detailed report of an unusual case, Arch Intern Med 65: 587 (1940).
3. Mounger EJ: Hypertension resulting from segmental renal artery infarction, Urology 1: 189 (1973).
4. Parker MD: Acute segmental renal infarction. Difficulty in diagnosis despite multimodality approach, ibid 18: 523 (1973).
5. Ferguson RK, and Vlasses PH: Clinical pharmacology and therapeutic applications of the new oral angiotensin converting enzyme inhibitor, captopril, Am Heart J 101: 650 (1981).
UROLOCY .4UCUST 1985 \‘(>LU~IE SXVI. NCJMBER 2
FIGURE 1. (A) Intravenous pyelogram (ZVP) without obstructive uropathy. (B) Renal scan demonstrates wedge-shaped area of absent perfusion to lower and lateral aspect of right kidney. (C) ZVP with tomography demonstrating nonvisualization of lateral aspect of right kidney. (0) Subtraction aortogram revealing avas- cular segment of inferior and lateral aspect of Tight kidney.
Comment
Renal infarction is commonly caused by arte- rial occlusion. Frequent disease entities asso- ciated with renal infarction are cardiac ar- rhythmias, subacute bacterial endocarditis, prosthetic valves, rheumatic heart disease with fibrillation, atria1 or ventricular thrombi, arte- riosclerosis, polyarteritis nodosa, lupus erythe- matosus, and trauma.’ Hypertension caused by segmental renal artery infarction from segmen- tal arteriothrombosis is often overlooked and undiagnosed. In 1940 Hoxie and Coggin found 205 cases of renal infarction in 14,411 autop- sies, mostly from emboli, but only 2 were cor- rectly diagnosed antemortem. Hypertension caused by segmental renal infarction has been
reported from: (1) ligation of the accessory re- nal vessel causing obstruction at the uretero- pelvic junction and hydronephrosis; (2) segmental renal arterial thrombosis after renal artery surgery; (3) thrombosis of segmental ves- sels due to arteriosclerosis; (4) infarction due to arterial emboli; and (5) infarction due to traumas3
The signs and symptoms of renal infarction may be absent or, if present, nonspecific. In the largest study by Hoxie and Coggin the signs and symptoms were flank pain or tenderness in 7 per cent of the patients, and gross hematuria was noted in only 2 per cent of the patients. However, approximately one third of the pa- tients had microscopic hematuria. Albuminuria is more common than either microscopic or
UROLOGY 1 AUGUST 1985 / VOLUMEXXVLNUMBER2 165
