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.

BackgroundAcyclovir is one of the most common prescribed antiviral drugs. Acyclovir nephrotoxicity occurs in approximately 12–48% of cases. It can present in clinical practice as acute kidney injury (AKI), crystal-induced nephropathy, acute tubulointerstitial nephritis, and rarely, as tubular dysfunction. Electrolytes abnormalities like hypokalemia, were previously described only when given intravenously.Case presentationA 54 year-old female presented with weakness and lower extremities paresis, nausea and vomiting after receiving oral acyclovir. Physical examination disclosed a decrease in the patellar osteotendinous reflexes (++ / ++++). Laboratory data showed a serum creatinine level of 2.1 mg/dL; serum potassium 2.1 mmol/L. Kidney biopsy was obtained; histological findings were consistent with acute tubular necrosis and acute tubulointerstitial nephritis. The patient was advised to stop the medications and to start with oral and intravenous potassium supplement, symptoms improved and continued until serum potassium levels were > 3.5 meq/L.ConclusionsThe case reported in this vignette is unique since it is the first one to describe hypokalemia associated to acute tubular necrosis induced by oral acyclovir.

Background. There is no treatment for septic acute kidney injury (sAKI). The anti-inflammatory activity of prolonged-release pirfenidone (PR-PFD) could be beneficial in this clinical setting. Methods. This study was a double-blind randomized clinical trial in sAKI patients with nephrology consultation at the Civil Hospital of Guadalajara, in addition to the usual treatment of AKI associated with sepsis; patients were randomized to receive either PR-PFD at 1,200 mg/day (group A) or 600 mg/day (group B) or a matched placebo for 7 consecutive days. The primary objective was the decrease in serum creatinine (sCr) and increase in urinary volume (UV); the secondary objectives were changes in serum electrolytes, acid-base status, and mortality. Results. Between August 2016 and August 2017, 88 patients were randomized. The mean age was 54 (17 ± SD) years, and 47% were male. The main site of infection was the lung (39.8%), septic shock was present in 39.1% of the cases, and the mean SOFA score was 8.8 points. 28 patients received PFD 1,200 mg, 30 patients received PFD 600 mg, and 30 patients received placebo. During the study, sCr did not differ among the groups. The reversion rate of sCr, UV, and mortality was not different among the groups ( p = 0.70 , p = 0.47 , and p = 0.38 , respectively). Mild adverse events were not different among the groups. Conclusion. PR-PFD did not improve the clinical course of sAKI and seemed to be safe in terms of adverse events. This trial is registered with NCT02530359.

<b><i>Background:</i></b> Based on the pathophysiology of acute kidney injury (AKI), it is plausible that certain early interventions by the nephrologist could influence its trajectory. In this study, we investigated the impact of 5 early nephrology interventions on starting kidney replacement therapy (KRT), AKI progression, and death. <b><i>Methods:</i></b> In a prospective cohort at the Hospital Civil of Guadalajara, we followed up for 10 days AKI patients in whom a nephrology consultation was requested. We analyzed 5 early interventions of the nephrology team (fluid adjustment, nephrotoxic withdrawal, antibiotic dose adjustment, nutritional adjustment, and removal of hyperchloremic solutions) after the propensity score and multivariate analysis for the risk of starting KRT (primary objective), AKI progression to stage 3, and death (secondary objectives). <b><i>Results:</i></b> From 2017 to 2020, we analyzed 288 AKI patients. The mean age was 55.3 years, 60.7% were male, AKI KDIGO stage 3 was present in 50.5% of them, sepsis was the main etiology 50.3%, and 72 (25%) patients started KRT. The overall survival was 84.4%. Fluid adjustment was the only intervention associated with a decreased risk for starting KRT (odds ratio [OR]: 0.58, 95% confidence interval [CI]: 0.48–0.70, and <i>p</i> ≤ 0.001) and AKI progression to stage 3 (OR: 0.59, 95% CI: 0.49–0.71, and <i>p</i> ≤ 0.001). Receiving vasopressors and KRT were associated with mortality. None of the interventions studied was associated with reducing the risk of death. <b><i>Conclusions:</i></b> In this prospective cohort study of AKI patients, we found for the first time that early nephrologist intervention and fluid prescription adjustment were associated with lower risk of starting KRT and progression to AKI stage 3.