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Renal infarction is a relatively infrequent condition, most commonly occurring in the presence of predisposing factors, including atherosclerosis, valvular or ischemic heart disease, atrial fibrillation, endocarditis, hypercoagulability, malignancy, vasculitis, and kidney trauma.1, 2 About 30% of renal infarctions, however, occur in the absence of these classic risk factors and are usually called “idiopathic.”1 In this noncategorized group, an emerging diagnosis is spontaneous renal artery dissection (SRAD), which may account for several, if not the majority of cases. The largest series so far published reports on 17 cases, mostly in males in their fourth or fifth decade of life, usually without any underlying disease.3, 4 Strenuous exercise may be a facilitating factor, and SRAD is associated with diseases and conditions affecting the vascular tunica media, including fibromuscular dysplasia, Marfan syndrome, Ehlers-Danlos syndrome, polyarteritis nodosa, and cystic medial necrosis.5 The clinical and laboratory presentation is shared with all other types of kidney infarction, with sudden-onset flank pain, which radiates to the epigastrium or groin, and high lactate dehydrogenase. Retroperitoneal hemorrhage may be a rare presentation of SRAD, whereas new onset, occasionally severe hypertension may suggest SRAD in the context of kidney infarction.3, 5 The case reported here highlights this emerging diagnosis as a cause of kidney infarction and suggests that it should be considered in the case of symptoms that appear suddenly after physically strenuous activities or sexual intercourse.6, 7

Coronavirus disease 2019 (COVID-19) is a contagious life-threatening infection caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Recent findings indicate an increased risk for acute kidney injury during COVID-19 infection. The pathophysiologic mechanisms leading to acute kidney injury in COVID-19 infection are unclear but may include direct cytopathic effects of the virus on kidney tubular and endothelial cells, indirect damage caused by virus-induced cytokine release, and kidney hypoperfusion due to a restrictive fluid strategy. In this report of 2 cases, we propose an additional pathophysiologic mechanism. We describe 2 cases in which patients with COVID-19 infection developed a decrease in kidney function due to kidney infarction. These patients did not have atrial fibrillation. One of these patients was treated with therapeutic doses of low-molecular-weight heparin, after which no further deterioration in kidney function was observed. Our findings implicate that the differential diagnosis of acute kidney injury in COVID-19–infected patients should include kidney infarction, which may have important preventive and therapeutic implications.

Kidney infarction is an uncommon thromboembolic complication of atrial fibrillation (AF). Diagnosis of this condition can be challenging due to its rarity and the fact that its presentation is associated with a multitude of other pathologies. No treatment guidelines have been established so far; however, multiple modalities have been employed, including systemic thrombolytics, intra-arterial thrombolytics and anticoagulants. In this article, we review acute renal infarction pathogenesis with a focus on AF as an important etiology. World J Nephrol Urol. 2016;5(1):11-15 doi: http://dx.doi.org/10.14740/wjnu242e

Native renal infarction is uncommon in patients with atrial fibrillation (AF)-related thromboembolism. Graft infarction is also rare, with such cases mostly occurring in the main graft artery postoperatively. To date, there have been no studies of AF-related graft kidney infarction. We herein describe the first case of AF-related graft kidney infarction. The clinical manifestations of this condition mimic and follow those of acute pyelonephritis; therefore, these diseases should be differentially diagnosed as early as possible using lactic dehydrogenase testing and computed tomography. Aggressive treatment with intravascular thrombolysis should be administered, even when the diagnosis is delayed, in order to restore a viable renal function.

G-CSF is a critical regulator of hematopoietic cell proliferation, differentiation and survival. It has been reported that G-CSF attenuates renal injury during acute ischemia-reperfusion. In this study we evaluated the effects of G-CSF on the renal and cardiovascular systems of 2K1C hypertensive mice.Male C57BL/6 mice were subjected to left renal artery clipping (2K1C) or sham operation and were then administered G-CSF (100 μg/kg/day) or vehicle for 14 days.Arterial pressure was higher in 2K1C + vehicle animals than in 2K1C + G-CSF (150±5 vs. 129±2 mmHg, p0.01, n=8). Plasma angiotensin I, II and 1-7 concentrations were significantly increased in 2K1C + Vehicle when compared to the normotensive Sham group. G-CSF prevented the increase of these vasoactive peptides. The clipped kidney/contralateral kidney weight ratio showed a less atrophy of the ischemic kidney in the treated group (0.50±0.02 vs. 0.66±0.01, p0.05). The infarction area in the clipped kidney was completely prevented in 7 out of 8 2K1C + G-CSF mice. Administration of G-CSF protected the clipped kidney from apoptosis.Our data indicate that G-CSF prevents kidney infarction and markedly attenuates the increases in plasma angiotensin levels and hypertension in 2K1C mice, reinforcing the protective effect of G-CSF on kidney ischemia.

Acute renal infarction is a well known, although relatively unfrequent, cause of flank pain resistant to administration of spasmolytic and nonsteroidal anti-inflammatory drugs. We present an original case of a 41-year-old man, complaining of acute severe left flank pain, resistant to common analgesic therapy, who was diagnosed of segmental renal infarction of a branch of left renal artery. Pathophysiology of renal damage in cocaine users is multifactorial, and it has been postulated that the right kidney was more prone to ischaemia. Left kidney represents an extremely unusual site of cocaine-related renal infarction.

A previously healthy 31-year-old man experienced a sudden onset of severe left loin pain radiating into the left lower abdomen during a side-movement, while performing a workout of the abdominal muscles in a fitness club. He collapsed and was immediately brought to our emergency department. Vital signs were blood pressure 130/75 mmHg, heart rate 64/min, height 185 cm and weight 85 kg. The clinical examination was unremarkable. Relevant laboratory parameters were a serum creatinine of 1.2 mg/dL, blood–urea nitrogen of 15 mg/dL, creatinine kinase of 24 IU/L (25◦C) and a normal urinalysis. Abdominal CT revealed the absence of perfusion of the lower and middle pole of the left kidney, corresponding to an 80% perfusion deficit (Figure 1A). Subsequent angiography demonstrated a dissection and thrombotic occlusion of the left renal artery (Figure 1B). Multi-step local lysis was performed within 6 h and on the following day, using 7 mg of recombinant tissue–plasminogen activator (rt-PA), respectively. As estimated by final angiography, perfusion could be essentially restored (Figure 1C). On Day 2, LDH rose to 1950 U/L (25◦C), demonstrating tissue damage, and serum creatinine was 1.5 mg/dL but reached a steady state at 1.3 mg/dL during the next days. Subsequently, blood pressure remained normal and the patient was discharged on oral phenprocoumon for 6 months without antihypertensive medication. At 6-month follow-up, blood pressure was 110/75 mmHg, serum creatinine was 1.0 mg/dl and creatinine clearance was 95 mL/min. Doppler ultrasonography showed a renal arterial resistive-index of 0.6 bilaterally, indicating the absence of re-occlusion or re-stenosis. The lysed kidney had shrunk by 2 cm in length but ∼50% of its function was

SummaryThree cases of renal infarcts in which clinical signs suggested an acute abdominal crisis are reportedIn two of these cases clinical diagnosis was possible; post-mortem examination was obtained in one case.75 cases of renal infarct have been collected from the files of the medical department of St.-Pierre Hospital. Clinical diagnosis was possible in 8,7 % of these cases. Clinical signs are described. These are clear enough when te renal infarct is large and when cardiac signs suggest the possibility of arterial embolisation.

IN previous experiments we have showrn that injection of plastic microspheres into a renal artery results in production of erythropoietin and reticulocytosis1 and development of hypertension2.