A 43-year-old man was admitted to the emergency room due to sudden, continuous and disabling low back pain, with no analgesic position or aggravating factors, without irradiation, with approximately 23 hours of evolution.
No nausea or vomiting, no macroscopic haematuria or discomfort in the lower urinary tract.
No precordial pain.
Hypertensive crisis with verdict
suffered an episode, interpreted as a transient ischaemic attack approximately eight weeks earlier (not confirmed).
No history of cardiac arrhythmia or heart valve disease.
No other previous thromboembolic events.
No known history of urinary lithiasis.
No osteoarticular or respiratory discomfort.
She denied cocaine abuse.
She denied a history of hepatitis B or C. She was treated with 160 mg/day of verapa.
The physical examination showed diaphoretic, TA 150 / 110 mmHg, 80 pulses per minute, rales and wides.
Ta 37.8 oC.
Painful abdomen due to deep iliac fossa and left flank, with defense, without signs of peritoneal irritation.
Decreased AHR.
No abdominal murmurs.
Bilateral renal Murphy was negative.
Existence of symmetrical arterial pulses.
No limb perfusion deficit.
Neurological examination showed no abnormalities.
Renal ultrasound showed no abnormalities, especially dilatation of the urinary tract.
Analytical data: Hb15.6 g/dL, Leuc 13.800/μL, Neut parameters of Creat 1.4 mg/dL, GDT 104 IU/L, GPT 74 IU/L, LDH 1.8.
The ECG showed sinus rhythm, with no alterations compatible with acute myocardial ischemia.
Abdominal and pelvic CT was requested, which showed the presence of multiple areas without contrast uptake in the left kidney, without morphostructural changes, compatible with multifocal areas of ischemia, with multisegmental distribution probably of embolic etiology.
No aortic dilatation or renal artery aneurysm.
No intraperitoneal alterations were observed.
Considering the multisegmental distribution of the ischemic process and the duration of discomfort, we conclude that there was no indication for invasive maneuvers.
The patient underwent systemic hypocoagulation with heparin in an attempt to avoid future embolic episodes and appropriate analgesia.
1.
Subsequently, he underwent multiple examinations in an attempt to identify an embolic focus and the etiological process.
Echocardiography eliminated pathology of the cardiac valvular apparatus or the existence of valve vegetations.
Absence of areas of myocardial dyskinesia.
Arteriography showed perfusion deficit in the lower pole of the left kidney with multiple less prominent areas that also present perfusion deficit.
No other changes were detected such as the presence of macro/ microaneurysms or changes in the main renal artery or aorta.
The study to rule out a prothrombotic and vascular disease (anti-lopic complement), ac. anti-cardiolipin, ANCA's, detection of cryoglobulins, ANA's resulted in immunoglobulin determination.
After 15 months of follow-up, we have no etiologic diagnosis.
The patient remains asymptomatic, with no new episodes of embolism or manifestations of systemic disease.
Anticoagulation was discontinued.
Keeps high blood pressure controlled with the same dose as usual.
The last analytical control had a serum creatinine of 1.2 mg/dL and a GFR of 93 ml/min. The follow-up scintigraphy showed a functional deficit of the affected renal unit (differential function 41%).
