Acute bilateral renal vein thrombosis secondary to sepsis from pyelonephritis

Abstract

A 62-year-old obese female with no known chronic medical problems presented to the emergency department complaining of increasing fatigue and generalized weakness over several weeks duration. She appeared toxic with tachycardia, tachypnea, and hypotension. Initial laboratory tests revealed white blood cell count of 23,000/μL with a left shift, sodium of 151 mmol/L, potassium of 5.3 mmol/L, bicarbonate of 6 mmol/L, chloride of 121 mmol/L, creatinine of 1.8 mg/dL, glucose of 700 mg/dL, and positive serum ketones. Her urine was grossly bloody, and urinalysis revealed greater than 100 white blood cells and 100 bacteria per high-power field. Due to impending respiratory failure, she was intubated and transferred to the intensive care unit with a diagnosis of diabetic hyperosmolar non-ketotic acidosis and sepsis from pyelonephritis.On examination, the patient was noted to grimace with abdominal palpation. Bedside abdominal ultrasound was obtained and suggested a left renal mass, but imaging was suboptimal. After stabilization with intravenous (IV) fluids, insulin, and antibiotics, a computed tomography (CT) scan of abdomen and pelvis with IV contrast was ordered and showed bilateral RVTs and a 7.3 × 4 × 4 cm heterogeneously enhancing solid mass with cystic components of the left kidney (Figure-1).

Acute pyelonephritis with renal vein and inferior vena cava thrombosis and pulmonary emboli in poorly controlled type 2 diabetes and HHS

“…It is striking that previous case reports of renal vein thrombosis secondary to acute pyelonephritis have frequently documented newly diagnosed or poorly controlled diabetes mellitus . Our patient had severe hyperglycaemia and mild HHS on a background of poorly controlled diabetes and significant obesity.…”

“…It is likely therefore that this patient's acute severe hyperglycaemia and chronically poorly controlled diabetes were contributory factors to the development of renal vein thrombosis in the context of pyelonephritis. She also had sepsis with Gram‐negative bacteraemia, features which have been associated with renal vein thrombosis in pyelonephritis . Endotoxins released from Gram‐negative bacteria can cause disruption of the endothelial lining of blood cells predisposing to thrombosis.…”

“…Renal vein thrombosis as a complication of acute pyelonephritis is rare and poorly recognised . The literature is confined to a few case reports . Acute pyelonephritis and sepsis can cause a hypercoaguable state which may predispose to thrombosis of the renal vein .…”

Acute Pyelonephritis: The Clot Unfolds, Evidence than Supports Complex Nature of the Renal Vein Thrombosis; Therapeutical Implications

“…Considering that acute pyelonephritis is not contemplated as a common cause of renal RVT and inferior vena cava thrombosis (IVCT), but not an uncommon condition amongst patients with nephrotic syndrome (NS) and commonly seen in patients with membranous glomerulonephritis [4], requires that physicians take into consideration genetic causes and other risk factors that leads to thrombophilia. Previously, the association of RVT with acute pyelonephritis was reported in probands with sepsis plus trombotic risk factor as can be seen in hyperhomocysteinemia or diabetes mellitus [4][5][6][7]. In order to explain the physiopathology of RVT seen ocassionaly in patients with pyelonephritis it is important to explore the possibility of hyperhomocysteinemia in the case described by Talwar et al, who had diabetes but without sepsis.…”

“…Nevertheless that possibility was not studied. This is important, because, in addition to the well clinical and conservative management, carried out by the authors, they could be used supplements of B complex and folic acid in order to handle the possible hyperhomocysteinemia reported by Kumar et al This condition cannot be excluded from the evidence presented in the paper [1,5]. Detection of homocysteine, or preventive treatment with folic acid is crucial because it reduces the risk, by 10% to 20%, of venous thrombosis [8].…”