Acute kidney injury secondary to obstructive nephropathy is a frequent event that accounts for 5 to 10% of all acute kidney injury cases and has a great impact on the morbidity and mortality in those affected. The obstruction in the urinary tract has a profound impact on kidney function due to damage produced by ischemic and inflammatory factors that have been associated with intense fibrosis. This pathology is characterized by its effects on the management of fluids, electrolytes, and the acid-base mechanisms by the renal tubule; consequently, metabolic acidosis, hyperkalemia, uremia, and anuria are seen during acute kidney injury due to obstructive nephropathy, and after drainage, polyuria may occur. Acute urine retention is the typical presentation. The diagnosis consists of a complete medical history and should include changes in urinary voiding and urgency and enuresis, history of urinary tract infections, hematuria, renal lithiasis, prior urinary interventions, and constipation. Imaging studies included tomography or ultrasound in which hydronephrosis can be seen. Management includes, in addition to drainage of the obstructed urinary tract system, providing supportive treatment, correcting all the metabolic abnormalities, and initiating renal replacement therapy when required. Although its recovery is in most cases favorable, it seems to be an undervalued event in nephrology and urology. This is because it is mistakenly believed that the resolution and recovery of kidney function is complete once the urinary tract is unobstructed. It can have serious kidney sequelae. In this review, we report the epidemiology, incidence, pathophysiological mechanisms, diagnosis, and treatment of acute kidney injury due to obstructive nephropathy.

Introduction: In cardiorenal syndrome type 1 (CRS1), vascular congestion is central to the pathophysiology of heart failure and thus a key target for management. The venous evaluation by ultrasound (VExUS) system could guide decongestion effectively and thereby improve outcomes. Methods: In this randomized clinical trial, patients with CRS1 (i.e., increase in creatinine ≥0.3 mg/dL) were randomized to guide decongestion with VExUS compared to usual clinical evaluation. The primary endpoint was to assess kidney function recovery (KFR), and the key secondary endpoint was decongestion evaluated by physical examination and changes in brain natriuretic peptide (BNP) and CA-125. Exploratory endpoints included days of hospitalization and mortality. Results: From March 2022 to February 2023, a total of 140 patients were randomized 1:1 (70 in the VExUS and 70 in the control group). KFR was not statistically different between groups. However, VExUS improved more than twice the odds to achieve decongestion (odds ratio [OR]: 2.6, 95% CI: 1.9–3.0, p = 0.01) and the odds to reach a decrease of BNP >30% (OR: 2.4, 95% CI: 1.3–4.1, p = 0.01). The survival at 90 days, recongestion, and CA-125 were similar between groups. Conclusion: In patients with CRS1, we observed that VExUS-guided decongestion did not improve the probability of KFR but improved the odds to achieve decongestion.

During acute kidney injury (AKI) due to sepsis, the intestinal microbiota changes to dysbiosis, which affects the kidney function recovery (KFR) and amplifies the injury. Therefore, the administration of probiotics could improve dysbiosis and thereby increase the probability of KFR. In this double-blind clinical trial, patients with AKI associated with sepsis were randomized (1:1) to receive probiotics or placebo for 7 consecutive days, with the objectives of evaluate the effect on KFR, mortality, kidney replacement therapy (KRT), urea, urine volume, serum electrolytes and adverse events at day 7. From February 2019 to March 2022, a total of 92 patients were randomized, 48 to the Probiotic and 44 to Placebo group. When comparing with placebo, those in the Probiotics did not observe a higher KFR (HR 0.93, 0.52-1.68, p = 0.81), nor was there a benefit in mortality at 6 months (95% CI 0.32-1.04, p = 0.06). With probiotics, urea values decreased significantly, an event not observed with placebo (from 154 to 80 mg/dl, p = 0.04 and from 130 to 109 mg/dl, p = 0.09, respectively). Urinary volume, need for KRT, electrolyte abnormalities, and adverse events were similar between groups. (ClinicalTrial.gov NCT03877081) (registered 03/15/2019). In AKI related to sepsis, probiotics for 7 consecutive days did not increase the probability of KFR, nor did other variables related to clinical improvement, although they were safe.