A review of renal tubular acidosis.

OBJECTIVE: To review the current scientific literature on renal tubular acidosis (RTA) in people and small animals, focusing on diseases in veterinary medicine that result in secondary RTA. DATA SOURCES: Scientific reviews and original research publications on people and small animals focusing on RTA. SUMMARY: RTA is characterized by defective renal acid-base regulation that results in normal anion gap hyperchloremic metabolic acidosis. Renal acid-base regulation includes the reabsorption and regeneration of bicarbonate in the renal proximal tubule and collecting ducts and the process of ammoniagenesis. RTA occurs as a primary genetic disorder or secondary to disease conditions. Based on pathophysiology, RTA is classified as distal or type 1 RTA, proximal or type 2 RTA, type 3 RTA or carbonic anhydrase II mutation, and type 4 or hyperkalemic RTA. Fanconi syndrome comprises proximal RTA with additional defects in proximal tubular function. Extensive research elucidating the genetic basis of RTA in people exists. RTA is a genetic disorder in the Basenji breed of dogs, where the mutation is known. Secondary RTA in human and veterinary medicine is the sequela of diseases that include immune-mediated, toxic, and infectious causes. Diagnosis and characterization of RTA include the measurement of urine pH and the evaluation of renal handling of substances that should affect acid or bicarbonate excretion. CONCLUSIONS: Commonality exists between human and veterinary medicine among the types of RTA. Many genetic defects causing primary RTA are identified in people, but those in companion animals other than in the Basenji are unknown. Critically ill veterinary patients are often admitted to the ICU for diseases associated with secondary RTA, or they may develop RTA while hospitalized. Recognition and treatment of RTA may reverse tubular dysfunction and promote recovery by correcting metabolic acidosis.

Efficacy of telmisartan for the treatment of persistent renal proteinuria in dogs: A double-masked, randomized clinical trial.

BACKGROUND: Information regarding efficacy of the angiotensin II receptor blocker, telmisartan, for treatment of proteinuria in dogs is limited. OBJECTIVE: To evaluate the antiproteinuric efficacy of telmisartan, as compared to enalapril, in dogs with chronic kidney disease and persistent, renal proteinuria. ANIMALS: Thirty-nine client-owned dogs with chronic kidney disease and urinary protein-to-creatinine ratio (UPC) > 0.5 (if azotemic) or ≥ 1.0 (if nonazotemic). METHODS: In this prospective, randomized, double-masked clinical trial, dogs were block randomized, according to presence or absence of azotemia and systemic arterial hypertension, to receive telmisartan (1.0 mg/kg PO q24h), or enalapril (0.5 mg/kg PO q12h), and followed for 120 days. Up-titration of study drug dosage on days 30 and 60, and addition of the other study drug at day 90, were performed if UPC > 0.5 was noted at these visits. Percentage change in UPC relative to baseline was calculated for all time points. Data are presented as median (range). RESULTS: Thirty-nine (20 telmisartan-treated, 19 enalapril-treated) dogs were included. At day 30, percentage change in UPC was greater for telmisartan-treated (-65% [-95% to 104%]) vs enalapril-treated (-35% [-74% to 87%]) dogs (P = .002). Among dogs persistently proteinuric at earlier visits, telmisartan remained superior to enalapril at days 60 (P = .02) and 90 (P = .02). No difference in percentage change in UPC between study groups was observed at day 120, when combination therapy was allowed. Combination therapy resulted in relevant azotemia in 4/13 (31%) dogs. CONCLUSIONS AND CLINICAL IMPORTANCE: Telmisartan might be a suitable first-line therapy for dogs with renal proteinuria.

Long-term survival of dogs treated for gallbladder mucocele by cholecystectomy, medical management, or both.

BACKGROUND: Gallbladder mucoceles (GBM) typically are treated by cholecystectomy. Medical management rarely has been reported and medical and surgical management have not been compared. HYPOTHESIS/OBJECTIVES: To compare survival of dogs treated for GBM by medical management or cholecystectomy or both. ANIMALS: Eighty-nine client-owned dogs diagnosed with GBM that received cholecystectomy or medical treatment or both from 2011 to 2017. METHODS: Potential cases were identified by searching the medical records database. Data collected included signalment, clinicopathologic results, treatments, and ultrasonographic images and reports. Dogs were grouped according to the treatment received (medical management, surgical treatment, or both) that was chosen at the discretion of the attending veterinarian. Survival analysis was performed and prognostic variables identified and compared between treatment groups. RESULTS: Of dogs surviving at least 14 days after diagnosis, median survival times were 1802 (95% confidence interval [CI], 855-not reached) days, 1340 (95% CI, 444-1340) days, and 203 (95% CI, 18-525) days, for the surgical, medical, and medical then surgical treatment groups, respectively, and differed significantly (P < .0001). Gallbladder mucocele type (P = .05), serum alkaline phosphatase activity (P = .0001), and serum creatinine (P = .002) and phosphorus (P = .04) concentrations were associated with decreased survival across groups. Suspicion of biliary rupture on abdominal ultrasound (AUS) examination was correlated with increased survival in the surgical group (P = .02). CONCLUSIONS AND CLINICAL IMPORTANCE: Cholecystectomy for the treatment of GBM results in the best long-term survival in dogs surviving the immediate postoperative period (14 days) compared to medical management. Although medical management is associated with shorter survival compared to surgical treatment, it is a reasonable alternative when surgery cannot be pursued.