Problems in the Initial Diagnosis of Renal Infarction.

Iga, Kanji; Izumi, Chisato; Nakano, Atsushi; Sakanoue, Yuji; Kitaguchi, Shouji; Himura, Yoshihiro; Gen, Hiromitsu; Konishi, Takashi

doi:10.2169/internalmedicine.36.330

Cited by 21 publications

(18 citation statements)

References 6 publications

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“…19,20 Renal infarction is often a difficult diagnosis to establish based on the rarity of the condition and the nonspecific clinical presentation and laboratory findings. 21,22 Patients typically present with sudden flank pain with or without fever, nausea, and vomiting. 23 Anuria is frequent in patients with bilateral involvement.…”

Section: Discussionmentioning

confidence: 99%

“…21 Typical lab findings in renal infarction include markedly elevated levels of serum LDH (95% of cases) and urinary LDH, as well as tubular proteinuria (80% of cases) and hematuria (X71% of cases). [22][23][24][25] LDH is a large molecule which is unlikely to pass through an intact glomerular basement membrane. As a result, urinary LDH is thought to originate directly from infarcted renal tissue.…”

Section: Discussionmentioning

confidence: 99%

“…[26][27][28] Other lab findings associated with renal infarction include leukocytosis and mild elevations of aspartate aminotransferase and alanine aminotransferase. 22,23,26,29 Literature review reveals 11 cases of cocaine-induced renal infarction (Table 3). 24,[30][31][32][33][34][35][36][37][38] Previous reports reveal unilateral involvement in all 10 of 11 cases, with involvement of the right kidney in 8 of 9 cases.…”

Section: Discussionmentioning

confidence: 99%

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Acute bilateral renal infarction secondary to cocaine-induced vasospasm

Madhrira

Mohan

Markowitz

et al. 2009

Kidney International

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A 47-year-old African-American male with a history of hypertension for 1 year and cocaine use presented to the emergency department with acute onset of bilateral flank pain, nausea, vomiting, and diarrhea. Physical examination was unremarkable. Laboratory evaluation revealed a white blood count of 15.1 K/ml (normal 4.5-11.5 K/ml) and a serum creatinine of 2.4 mg/100 ml. A non-contrast CT scan of the abdomen was unremarkable. The patient was treated with morphine (for pain) and i.v. fluids, felt better, and was discharged for out-patient follow-up.The patient saw his primary care physician 2 days later (day 3) and reported persistence of the bilateral flank pain. The patient also reported a transient inability to urinate for 36 h before the visit. An abdominal ultrasound and blood chemistry were obtained. On day 5, he was referred by his physician to the emergency department for a serum creatinine of 9.2 mg/100 ml from day 3. At the time of admission, the patient reported using 5-6 g/day of ibuprofen for the previous 4 days and admitted to sniffing cocaine a few hours before the initial onset of flank pain.On physical examination, the patient was a well-built African-American male with a temperature of 99.2 1F, pulse rate of 60/min, blood pressure of 150/85 mm Hg and weight of 85 kg (BMI 27.7 kg/m 2 ). There was no orthostasis, pallor, or skin rash. The heart and lung examinations were unremarkable. The abdomen was soft, with no suprapubic dullness. There was no costovertebral angle tenderness or pitting edema. The extremity pulses were symmetric and equal.Laboratory results are presented in Table 1. Serologic tests for hepatitis B and C viruses, human immunodeficiency virus, antinuclear antibody, and rheumatoid factor were negative. Serum complements, including C3, C4, and CH50, were within the normal range. Hemoglobin electrophoresis, chest X-ray, electrocardiogram, and echocardiogram were unremarkable. Renal ultrasound revealed normal-sized kidneys with mildly increased echogenecity and no hydronephrosis. A 99m Tc-MAG3 (mercaptoacetyltriglycine) radionuclide renogram showed multiple wedge-shaped photopenic areas in both kidneys (Figure 1a). Owing to the absence of a clear explanation for the patient's acute renal failure, renal biopsy was performed 12 days after the onset of symptoms.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Acute bilateral renal infarction secondary to cocaine-induced vasospasm

Madhrira

Mohan

Markowitz

et al. 2009

Kidney International

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“…Other causes include trauma, polycythemia vera, fibromuscular dysplasia, extra-adrenal pheochromocytoma, dissection of artery, aneurysm or renal artery dissection, marijuana and cocaine abuse [1]. Renal infarctions have been reported in patients with connective tissue disease, e.g., systemic lupus erythematosus (SLE), primary antiphospholipid syndrome, either with or without evidence of SLE, polyarteritis nodosa, mixed connective tissue disease, and Behcet disease [2].…”

Section: Introductionmentioning

confidence: 99%

Renal infarction in a child with systemic lupus erythematosus

Kuzmanovska¹,

Sahpazova

Grujovska

et al. 2004

Pediatric Nephrology

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Although patients with systemic lupus erythematosus (SLE), especially those with antiphospholipid antibodies, have a high incidence of arterial and venous thrombotic manifestations, renal infarction has been rarely reported in these patients and is probably underestimated. A 9-year-old boy with renal infarction, diagnosed by computed tomography and scintigraphy, is described. Initially he complained of severe flank pain; he had no urinary abnormalities and his blood pressure was normal. No evidence of systemic disease was found. He responded well to antibiotic treatment without the need for immunosuppressive therapy. In subsequent years he presented a spectrum of clinical symptoms, including fever, malaise, arterial hypertension headache, and mononeuritis multiplex, accompanied by an increased erythrocyte sedimentation rate and transitory proteinuria. This suggested vasculitis involving peripheral vessels as well as the central nervous system. Treatment with oral prednisone and azathioprine led to remission. Four years after the renal infarction, the child presented with recurrence of systemic disease. The diagnosis of SLE was established, with positive antiphospholipid antibodies. The sudden appearance of severe unexplained flank pain should alert the clinician to a possible underlying renal vessel thrombosis. Renal venous thrombosis is probably much more common; however, renal arterial thrombosis and infarction in association with SLE with positive antiphospholipid antibodies should be added to the differential diagnosis.

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“…Furthermore, SDVI may be underdiagnosed in patients with stroke because it may be asymptomatic or the symptoms and complaints may be more difficult to identify in the context of stroke. 4,5 Hence, the actual prevalence of SDVI in ischemic stroke is unknown. Improvements in CT imaging have resulted in a marked improvement in the diagnosis of SDVI and of related vascular occlusion.…”

mentioning

confidence: 99%

Prevalence and Determinants of Subdiaphragmatic Visceral Infarction in Patients With Fatal Stroke

Abboud

Labreuche

Gongora-Riverra

et al. 2007

Stroke

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Background and Purpose-Arterial thromboembolism is a common cause of both visceral and brain infarctions. Because the cause of brain infarction is unknown in up to 39% of patients, the discovery of subdiaphragmatic visceral infarction (SDVI) in this context is important, but its frequency is unknown. We therefore investigated the prevalence of SDVI in subjects who died from stroke. We also evaluated the yield of SDVI diagnosis for stroke subtyping. Methods-We performed a case-control study using a series of 815 consecutive autopsies of patients who had died from a neurological disease, including 350 with stroke (260 infarcts and 90 hemorrhages). We systematically assessed the presence of renal, splenic, and mesenteric infarction (no case of spinal cord was recorded) and analyzed their determinants in patients with stroke. Patients with other neurological diseases served as the control group. Results-Renal infarction was the most frequent SDVI (10.2%), whereas mesenteric infarction was rare (1.1%). At least one SDVI was found in 16.9% of patients with stroke (38.7% of patients with a cardioembolic stroke) and in 5.1% of patients with other neurological diseases (adjusted ORϭ2.12; 95% CIϭ1.08 to 4.16). Among patients with stroke, a significant heterogeneity in the prevalence of SDVI was found across etiological stroke subgroups with only three patients (3.3%) with hemorrhagic stroke having an SDVI (2 mesenteric and one renal infarction) compared with 56 patients (21.5%) with ischemic stroke (PϽ0.0001). Among patients with brain infarction and a SDVI, 76.8% had a definite cardiac source of embolism. Conclusions-In patients with fatal brain infarction, the prevalence of SDVI is higher than previously thought, especially in those with stroke attributed to cardiac emboli. Seeking SDVI may assist in the etiologic diagnosis of brain infarction

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Problems in the Initial Diagnosis of Renal Infarction.

Cited by 21 publications

References 6 publications

Acute bilateral renal infarction secondary to cocaine-induced vasospasm

Acute bilateral renal infarction secondary to cocaine-induced vasospasm

Renal infarction in a child with systemic lupus erythematosus

Prevalence and Determinants of Subdiaphragmatic Visceral Infarction in Patients With Fatal Stroke

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