Cutaneous Small-Vessel Vasculitis Induced by Escitalopram: A Case-Based Brief Review of the Literature.

A 65-year-old male with multiple comorbidities and recently diagnosed with diabetic kidney disease developed upper and lower extremity rash following escitalopram initiation for his depressive mood. Clinical assessment and skin biopsy confirmed cutaneous small-vessel vasculitis (CSVV), prompting drug discontinuation and oral methylprednisolone therapy. The resolution of the rash was achieved within a week. This rare case of CSVV induced by escitalopram highlights the importance of timely recognition and management of drug-induced CSVV and adds to the limited literature on selective serotonin reuptake inhibitor-associated CSVV.

Abiraterone-Induced Secondary Hypertension: Two Wrongs Don't Make a Right.

Abiraterone, an inhibitor of both 17α-hydroxylase and 17,20-lyase, is considered a novel, state-of-the-art, life-prolonging therapy in the urologists' arsenal when treating prostate cancer. Despite its efficacy, it is linked with an increased risk of cardiovascular adverse effects. Herein, we report a case in which the administration of abiraterone resulted in a full-blown syndrome of apparent mineralocorticoid excess despite the concomitant administration of prednisolone; that is, secondary hypertension, hypokalemia, metabolic alkalosis, as well as elevated levels of adrenocorticotropic hormone (ACTH).

DNAJB9 Fibrillary Glomerulonephritis With Membranous-Like Pattern: A Case-Based Literature Review.

Fibrillary glomerulonephritis (FGN) is a rare immune-mediated glomerular disease traditionally characterized by the presence of amyloid-like, randomly aligned, fibrillary deposits in the capillary wall, measuring approximately 20 nm in diameter and composed of polyclonal IgG. FGN is usually a primary disease with no pathognomonic clinical or laboratory findings. More than that, on light microscopic evaluation, it can receive various histological patterns, rendering its diagnosis indistinguishable. However, the identification by immunohistochemistry of a novel biomarker, DNA-J heat-shock protein family member B9 (DNAJB9), has created a new era in FGN diagnosis even in the absence of electron microscopy. Typically, most patients manifest various degrees of renal insufficiency, hypertension, microscopic hematuria, proteinuria, and occasionally frank nephrotic syndrome. The prognosis is usually severe and progression to end-stage kidney disease (ESKD) is the rule, given that no specific treatment is available until now, despite the fact that in small studies rituximab-based therapy seems to alleviate the severity and improve the disease progression. Herein, we report the case of a 63-year-old Caucasian man presenting with uncontrolled hypertension, headache, shortness of breath, and lower limb edema. Diagnostic evaluation revealed mild deterioration of kidney function, nephrotic range proteinuria, and faint IgGκ monoclonal bands in serum and urine immunofixation. After negative meticulous investigation for secondary nephrotic syndrome causes, the patient underwent a kidney biopsy. Biopsy sample showed two glomeruli with mesangial expansion and thickened glomerular basement membrane (GBM) on light microscopy, a pattern masquerading as membranous nephropathy stage III-IV, while IgG and C3 were 1-2+ on GBM and mesangium in immunofluorescence. Thickened GBM with fibrils on electron microscopy were found, while DNAJB9 in immunohistochemistry was positive, confirming FGN. Once diagnosis of FGN was made, a combination of steroids with rituximab was initiated while the patient was receiving the standard anti-hypertensive therapy, simultaneously with a sodium-glucose cotransporter-2 (SGLT2) inhibitor. The 12-month follow-up showed approximately 85% decrease in proteinuria alongside stabilization of kidney function and blood pressure normalization. Hence, in this article, we aim to highlight that DNAJB9-associated FGN may mimic membranous glomerulopathy stage III-IV on light microscopy, especially when a small kidney sample with extensive involvement by fibrils of GBM is examined. Moreover, we underscore the fact that ultramicroscopic examination is of crucial importance in the differential diagnosis of glomerular deposition diseases and that DNAJB9 identification on immunohistochemistry consists of a revolutionary and robust biomarker in FGN diagnosis.

Antisynthetase Syndrome: The Classical Phenotype With a Twist.

Antisynthetase syndrome is a systemic autoimmune rheumatic disease characterized by multiple organ involvement, including interstitial lung disease, myositis, non-erosive arthritis, fever, Raynaud's phenomenon, "mechanic's hands," and the presence of autoantibodies against aminoacyl-tRNA synthetases, mainly anti-Jo1 (histidyl) antibodies. Patients with antisynthetase syndrome and active muscle inflammation are usually presented with elevated creatine phosphokinase levels, even in the range of acute rhabdomyolysis. Despite that, the presence of myoglobinuric acute kidney injury is rarely seen in patients with myositis-associated rhabdomyolysis. Herein, we report the case of a 64-year-old man who presented with acute kidney injury due to severe rhabdomyolysis in the setting of antisynthetase syndrome diagnosed by the classical clinical triad of (1) interstitial lung disease, (2) non-erosive arthritis, and (3) active myositis and the presence of anti-Jo1 antibodies. The diagnosis was confirmed by muscle biopsy histological findings as well as electromyography. In this case report, we also discuss the classical clinical manifestations of antisynthetase syndrome and a twist toward this unusual complication associated with active muscle inflammation.

Difficulties in the Differential Diagnosis of Thrombotic Microangiopathy.

No Abstract.  DOI: 10.52547/ijkd.6916.

Uremic Leontiasis Ossea: Theoretical Concepts and Practical Considerations.

Leontiasis ossea (LO) in chronic kidney disease patients, also known as Sagliker syndrome, is an exceptionally uncommon uremic complication of long-lasting and severe secondary hyperparathyroidism. The prominent features of uremic LO (ULO) encompass the characteristic clinical trial of massive thickening of maxillary and mandibular bones, widening of interdental spaces, and flattening of nasal bridges and nares. Moreover, during the transformation of craniofacial architecture, significant structural and functional consequences may appear, including upper airway patency, visual and hearing acuity, oral phase of swallowing as well as various neurological and psychiatric disorders. Only few cases of ULO have been reported in the literature until now, making challenging not only the traditional diagnostic procedures but also the optimal therapeutic approach. In this narrative review, we aim to explore the underlying pathophysiological mechanisms, summarize the evidence for adverse outcomes, and highlight the current therapeutic strategies for ULO prevention and treatment, given that precise genetic determinants remain elusive.

Rosuvastatin and Colchicine combined myotoxicity: lessons to be learnt.

Statins and colchicine co-administration consists of a potentially catastrophic drug-drug interaction since it provokes myotoxicity, myopathy and various degrees of rhabdomyolysis. Lipophilic statins and colchicine are biotransformed in the liver, primarily via CYP3A4 enzyme system leading to elevated blood levels of both agents and resulting in increased potential for combined myotoxicity. Hence, it would be of great clinical importance not only the awareness of this devastating complication but also the more advantageous type of statin that we should choose to achieve the recommended therapeutic goals regarding LDL levels with minimal myopathy risk. Therefore, once colchicine's use is commenced, a hydrophilic statin selection, such as rosuvastatin, seems favorable regarding the risk of myotoxicity. Herein, we aim to describe a patient with chronic kidney disease stage III and nephrotic syndrome that developed acute rhabdomyolysis soon after the administration of rosuvastatin while receiving colchicine. To the best of our knowledge, this is the first report of the combined effect of rosuvastatin and colchicine in the setting of chronic kidney disease leading to myotoxicity.

Acute Respiratory Distress Syndrome Induced by Parathyroid Storm.

Hypercalcemic crisis associated with the development of acute respiratory distress syndrome (ARDS) has been rarely documented in the literature. Most cases have been described in patients suffering from malignancies or renal failure with the presence of metastatic calcifications being a prominent feature. Only three cases of ARDS have been reported to date in patients with hypercalcemic crisis due to primary hyperparathyroidism (PHPT). Herein, we report a 72-year-old patient with PHPT that presented with severe hypercalcemic crisis and developed ARDS. He had mild chronic kidney disease and at presentation he had extremely high levels of serum calcium (22.5 mg/dl) and parathormone (3822 pg/ml). After receiving medical treatment for hypercalcemia and the initiation of hemodialysis, he developed ARDS with a fatal outcome, without the presence of pancreatitis, sepsis or heart failure. Although very rare, ARDS should be taken into account as a possible complication of parathyroid crisis, especially in patients with excessive calcium and parathormone levels.

Central Retinal Artery Occlusion Secondary to Patent Foramen Ovale: The Unexpected Journey of a Paradoxical Embolus.

Central retinal artery occlusion (CRAO) represents one of the most devastating ophthalmic emergencies, since the inner two-thirds of the retina lose their blood supply. The acute obstruction of the central retinal artery is characterized by severe, sudden and unilateral painless visual loss and usually occurs secondary to an embolus of cardiovascular origin. A paradoxical thromboembolic event of the central retinal artery through patent foramen ovale is an exceptionally unusual clinical entity as well as a great diagnostic challenge since the source of initial thrombus formation requires extensive investigation. Herein, we aim to describe a patient with no significant comorbidities who experienced a paradoxical thromboembolic episode of central retinal artery associated with patent foramen ovale.

Fondaparinux-Associated Rectus Sheath Hematoma: Skating on Thin Ice.

Rectus sheath hematoma (RSH), an exceptionally rare clinical entity, results from the rupture of epigastric arteries or tear of the rectus abdominis muscle itself. Spontaneous RSH represents a potentially life-threatening bleeding complication in anticoagulated patients with distinct characteristics. The non-specific nature of RSH clinical manifestations renders RSH a kaleidoscopic disease that may be misdiagnosed. The widespread use of anticoagulants for deep vein thrombosis (DVT) prophylaxis or therapy is among the most commonly documented risk factors. To the best of our knowledge, this is the first report of a fondaparinux-associated giant RSH in a 58-year-old Caucasian man who presented with severe pain at the right abdominal quadrant accompanied with a large ecchymosis secondary to violent cough due to a respiratory infection. The aim of our study is to broaden current knowledge regarding the predisposing factors, the pathophysiological mechanisms, and the management of this bleeding disorder.

Renal manifestations of human brucellosis: First report of minimal change disease.

Human brucellosis is considered a great example of the complexity of clinical manifestations possibly affecting multiple organs or systems. Renal manifestations of human brucellosis have been documented in few case reports and one case series. Herein, we present a case of Nephrotic syndrome (NS) due to minimal change disease in the course of acute brucellosis. A 53-year-old male farmer was admitted to our department with acute brucellosis and NS. Renal biopsy revealed minimal change disease. Combined treatment with prednisone (1 mg/kg), rifampicin (600 mg/day), and doxycycline (200 mg/day) was initiated. Complete remission of NS was achieved at the end of the fourth week. One year later, the patient remained in complete remission of NS without any sign of relapse of brucellosis.

Hypofibrinogenemia induced by tigecycline: a potentially life-threatening coagulation disorder.

A 74-year-old female patient with end-stage renal disease, undergoing periodic hemodialysis, was hospitalized due to infection by multidrug-resistant Acinetobacter baumannii after hip replacement surgery. She was treated with tigecycline, a glycylcycline agent. Subsequently she developed coagulation disorders as substantiated by increased international normalized ratio (INR), prolonged partial thromboplastin time (aPTT), and severe hypofibrinogenemia, followed by transaminasemia, cholestasis, and anemia. Ultrasonography and computed tomography revealed no underlying pathological entities. Tigecycline was discontinued and the patient underwent daily hemodialysis and received multiple fresh frozen plasma transfusions. Additionally, she was treated with colistin. Her clinical and laboratory status improved. We suggest that patients treated with tigecycline should be monitored for changes in INR, aPTT, and fibrinogen levels to avoid severe, life-threatening coagulation disturbances.

An Uncommon Presentation of Spontaneous Rectus Sheath Hematoma with Acute Kidney Injury due to Obstructive Uropathy and Prerenal Azotemia.

Rectus Sheath Hematoma (RSH) represents an unusual entity which is characterized by acute abdominal pain and tender palpable abdominal mass usually, among elderly patients receiving anticoagulant therapy. We report the case of an 81-year-old woman admitted to our department due to acute abdominal pain and oligoanuria. The patient had recently been hospitalized due to acute myocardial infarction (AMI) and atrial fibrillation (AF) and received both anticoagulant and antiplatelet therapies. The radiological assessments revealed an extended Rectus Sheath Hematoma and bilateral hydronephrosis. Treatment of the hematoma required cessation of anticoagulants and antiplatelet agents, immobilization, blood and fresh frozen plasma transfusion, and administration of vasopressors. The patient recovered gradually and was discharged home fifteen (15) days later.