Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016199 (flank pain)
 2,189 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cocaine abuse is commonly associated with myocardial ischemia, mesenteric ischemia, and cerebrovascular accidents. Renal infarction is an uncommon complication of cocaine abuse. Various mechanisms have been postulated for this cocaine-related injury. There are only 15 cases reported on cocaine-induced renal infarction. Among the cases with available data, very few cases had left kidney involvement. We report a case of a 65-year-old African American man with history of cocaine abuse who presented with left flank pain and had left renal infarction.
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PMID:Cocaine: A Rare Cause of Left-Sided Renal Infarction. 2642 33

Renal infarction is a rare occurrence accounting for 0.007% of patients seen in the emergency department for renal insufficiency or hypertension. Dysfibrinogenemia is also rare, and the combination of renal artery infarct in the setting of congenital dysfibrinogenemia has not been described in the literature. Our patient, with a remote history of congenital dysfibrinogenemia with no known haemorrhagic or thrombotic complications, presented with acute flank pain and was subsequently diagnosed with an acute renal arterial infarction. He was treated with subcutaneous enoxaparin and then transitioned to lifelong anticoagulation with rivaroxaban therapy.
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PMID:Acute renal artery infarction secondary to dysfibrinogenemia. 3015 55

BACKGROUND This is a case report of a male patient who presented with a history of right flank pain based on renal infarction. Initially the symptoms were misdiagnosed as acute pyelonephritis. CASE REPORT A 47-year-old male with a history of familial hypercholesterolemia and cerebral infarction presented at the Emergency Department with a 3-day history of acute right-sided flank pain. Physical examination revealed hypertension, subfebrile temperature, and costovertebral angle tenderness. Blood tests were unremarkable except for renal impairment, a high C-reactive protein level of 215 mg/L (normal <8 mg/dL) and an elevated lactate dehydrogenase (LDH) of 1289 U/L (normal <248 U/L). Renal ultrasonography was normal. He was admitted with a presumed diagnosis of acute pyelonephritis and treated accordingly. However, 2 days later, we rejected this diagnosis as the urine culture was sterile. Based on the acute onset of symptoms and the initial high LDH, renal infarction was suspected. A computed tomography scan confirmed right-sided partial renal and splenic infarctions likely due to spreading emboli from atherosclerosis of the descending aorta. CONCLUSIONS Acute renal infarction is often missed or delayed as a diagnosis because patients often present with flank pain that can resemble more frequently encountered conditions such as pyelonephritis and nephrolithiasis. Renal infarction should be considered in cases with acute flank pain accompanied by (low-grade) fever, high LDH level, increased C-reactive protein level, hypertension, and renal impairment, especially in those patients with an increased risk of thromboembolism.
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PMID:Renal and Splenic Infarction in a Patient with Familial Hypercholesterolemia and Previous Cerebral Infarction. 3053 77


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