ABSTRACT
BACKGROUND: Acute kidney injury (AKI) is common in the postoperative period and is associated with negative patient outcomes. The definition of perioperative hypotension is wide, but it is associated with various complications, including AKI. SUMMARY: Preclinical data suggest that sustained severe renal hypoperfusion per se does not cause persistent AKI. The evidence associating blood pressure levels and postoperative renal dysfunction is predominantly retrospective and observational, and therefore potentially misled by the complex interactions between exposures, confounders, and mediators. KEY MESSAGES: To better understand how perioperative hemodynamic management could affect the occurrence of kidney injury, it is pivotal to further investigate the association between hypotension and kidney dysfunction in the perioperative period and determine the degree to which hypotension is a causal factor.
Subject(s)
Acute Kidney Injury , Hypotension , Humans , Retrospective Studies , Postoperative Complications/epidemiology , Kidney , Hypotension/etiology , Risk FactorsABSTRACT
Inferior vena cava agenesis is a rare congenital vascular defect often diagnosed as an incidental finding in asymptomatic patients. When symptoms arise, it can present with chronic venous stasis or unprovoked deep vein thrombosis (DVT). A 42-year-old man with history of unprovoked right lower extremity (RLE) DVTs was admitted for swelling, pain and erythema to the RLE, concerning for new DVT. Venous Doppler ultrasound showed a chronic DVT of the right proximal femoral vein in addition to an acute DVT of the distal femoral vein. Extensive thrombophilia workup was negative and additional imaging with abdominal computed tomography scan revealed the absence of the infrarenal inferior vena cava. Patient was treated with oral anticoagulation and compression stockings and discharged with clinical improvement. At 3-month follow-up, patient was completely asymptomatic. Recurrent unprovoked DVTs in young patients require exhaustive work up including imaging studies to rule out vascular anomalies.
ABSTRACT
Due to multiple compensating mechanisms, the serum bicarbonate concentration is a relatively insensitive marker of acid-base status; especially in chronic kidney disease (CKD). This is a major drawback that impairs the ability to diagnose acid excess or monitor alkali therapy. We postulated that it is more logical to measure the compensatory defense mechanism(s) rather than the defended parameter, which remains normal if the compensation is successful. Therefore, a retrospective cross-sectional study was performed in 1733 stone formers along with a prospective cross-sectional study of 22 individuals with normal kidney function and 50 patients in different stages of CKD. While serum bicarbonate was flat and did not fall below the reference range until near CKD stage 5, citrate excretion (24-hour urinary citrate excretion rate; urinary citrate-to-creatinine ratio, in the retrospective analysis, and spot urinary citrate-to-creatinine ratio in the prospective study) progressively and significantly declined starting from CKD stage 2. Following an acute acid load in 25 participants with a wide range of estimated glomerular filtration rates, the urinary citrate-to-creatinine ratio inversely and significantly associated with acid accumulation, whereas serum bicarbonate did not. We compared changes in serum bicarbonate and urinary citrate-to-creatinine ratio in response to alkali therapy in patients with CKD stage 3 or 4 started on potassium citrate in our kidney stone database. With alkali therapy, there was no change in serum bicarbonate, but the urinary citrate-to-creatinine ratio rose consistently in all patients adherent to potassium citrate therapy. Thus, the urinary citrate-to-creatinine ratio (the defense mechanism) is a potential easily implementable, pragmatic, and a superior parameter to serum bicarbonate (the defended entity) to assess acid-base status, and monitor alkali therapy. Additional studies are needed before a clinical test can be devised.
