ABSTRACT
Acute kidney injury (AKI) is a frequent finding in acutely ill and hospitalized patients arising from various etiologies. Anuric AKI, a more pronounced form of AKI in which less than 100 cc of urine is produced per day, is most frequently encountered in hospitalized, septic, and post-surgical patients, often secondary to shock or bilateral urinary tract obstruction. The development of anuric AKI in previously healthy patients after outpatient urological procedures presents a unique challenge to physicians, as many outpatient procedures require the routine perioperative administration of multiple nephrotoxic medications. Further complicating this clinical scenario, some surgical procedures that intrinsically involve iatrogenic injury to the kidney, ureter, bladder, or nearby organ can rarely lead to a phenomenon known as reflex anuria, an anuric state typically associated with AKI. Here, we report an unusual case of a previously healthy 56-year-old male who developed anuric AKI two days after direct visual internal urethrotomy (DVIU) for the treatment of a bulbar stricture. Non-contrast CT revealed no signs of an obstructive process, and laboratory findings supported an intrarenal cause of AKI. Consideration was given to non-steroidal anti-inflammatory drugs (NSAID)-induced nephrotoxicity, gentamicin-associated acute tubular necrosis, and propofol infusion syndrome, in addition to their potential synergistic effects. We also explore this as the first reported case of reflex anuria occurring at the level of the bulbar urethra, as most cases have involved direct injury to the kidney or ureter. Over the course of 10 days, our patient responded well to treatment with supportive measures and dialysis, with his vomiting, electrolyte abnormalities, renal state, and anuria eventually improving.
ABSTRACT
BACKGROUND: A few studies have shown aldosterone antagonists (AA) to be effective therapy in patients with resistant hypertension (RH). We performed a meta-analysis of randomized and nonrandomized studies of AA in patients with RH. METHODS: We searched PUBMED, EMBASE, and CENTRAL for studies on the use of AA in patients with RH. Meta-analysis was performed using random-effects model. The change in office and ambulatory blood pressures (BP), effects on biochemical profile, change in the number of antihypertensive agents, and adverse events were main outcomes. RESULTS: We included 15 studies (3 randomized controlled trials, 1 nonrandomized comparative study, and 11 single-arm studies) with 1,204 total patients in the meta-analysis. In comparative studies, AA reduced systolic BP (SBP) by 24.26 mm Hg (95% CI: 8.65-39.87, P = 0.002) and diastolic BP (DBP) by 7.79 mm Hg (3.79-11.79, P = 0.0001). Similarly, AA reduced SBP by 22.74 mm Hg (18.21-27.27, P < 0.00001) and DBP by 10.49 mm Hg (8.85-12.13, P < 0.00001) in single-arm studies. AA resulted in significant change in serum electrolytes in single-arm studies but not in comparative studies. Significantly more adverse events were noted in single-arm studies but not in comparative studies. CONCLUSIONS: On the basis of the current meta-analysis, we conclude that AA is safe and effective therapy in patients with RH.
