Diagnosis and management of acute kidney injury (AKI) require diligent attention to detail by the small animal clinician. The stepwise pathophysiology of AKI is often predictable. Common etiologies are categorized as prerenal, intrinsic, and postrenal. Diagnostic tools include palpation of the abdomen, kidneys, and urinary bladder; assessing hydration; monitoring blood pressure; urinalysis; and abdominal imaging and\/or ultrasonography. Treatment involves fluid therapy, acid\u2013base and electrolyte management, urine output and blood pressure optimization, nutritional support, and administration of medications as needed. Early use of extracorporeal therapy can improve outcomes. Prognosis varies according to the underlying causes, comorbidities, and prescribed treatments.<\/p>\n
Take-Home Points<\/strong><\/p>\n <\/div><\/div><\/p>\n A<\/span>cute kidney injury (AKI) is frequently recognized in veterinary practice, defined as an abrupt decrease in renal function with a corresponding decline in glomerular filtration rate (GFR).1<\/sup> Patients with community-acquired AKI (decreased kidney function occurring outside of a hospital setting, typically due to such issues as dehydration and urinary obstruction) usually present for evaluation days after the initial insult. As a result of increased monitoring and awareness, hospital-acquired AKI (decreased renal function during the course of hospitalization) is becoming more frequently recognized.2 <\/sup><\/p>\n The general types of injury leading to AKI have been categorized as prerenal, intrinsic (renal), or postrenal changes.<\/p>\n Prerenal azotemia is typically volume responsive. It involves decreased renal perfusion secondary to hypovolemia, intrarenal vasoconstriction, and decreased perfusion (secondary to shock).2<\/sup><\/p>\n Tubular damage is thought to occur via 1 of 2\u00a0mechanisms: hypoxic injury or direct nephrotoxic injury (following exposure to numerous drugs and toxins).3,4 <\/sup>Intrinsic renal azotemia is subcategorized according to the type of injury.<\/p>\n Postrenal azotemia involves obstruction to flow within the urinary tract (e.g., obstructive [ureteral, urethral]) or other mechanisms that prevent effective excretion of urine (e.g., urinary tract rupture).<\/p>\n Additionally, AKI encompasses 4\u00a0phases: initiation, extension, maintenance, and recovery.<\/p>\n After some level of hypoxic insult, the initiation phase occurs immediately and is characterized by sublethal injury to tubular cells. The changes are secondary to breakdown of adenosine triphosphate (ATP), leading to cytoskeletal changes, loss of apical microvilli, loss of tight junctions between tubular cells, loss of attachment to the basement membrane, and redistribution of sodium\u2013potassium adenosine triphosphatase (Na-K-ATPase) pumps from the basolateral membrane to the apical membrane. These changes promote leakage of fluid and solute back into the interstitium, ultimately preventing normal function of the tubular cells.3,4<\/sup> Sloughed tubular cells can accumulate in the tubules and are recognized as casts on urinalysis; their presence can cause an occlusive effect, further worsening GFR. During the initiation stage, biochemical and clinical abnormalities may not be appreciated.3<\/sup><\/p>\n The extension phase is characterized by ongoing hypoxia combined with an inflammatory response. Necrotic and apoptotic tubular cells incite an inflammatory response in which neutrophils infiltrate first, followed by macrophages.3<\/sup> Neutrophils will adhere to endothelial cells and migrate to the interstitium, plugging capillaries and altering renal tubular integrity. Continued ischemic injury and tubular cell death are perpetuated by blood stasis as well as release of cytokines, chemokines, and reactive oxygen species.3-5<\/sup><\/p>\n During the maintenance phase, tubular cells undergo differentiation, migration, and proliferation4<\/sup>; azotemia and uremia are often present, and urine output may be excessively high or low. The maintenance stage can last days to weeks.<\/p>\n During the recovery phase, redifferentiation continues and cells regain their polarity, allowing for normal cellular function. Trends toward polyuria during this phase result from retained solutes causing diuresis, and the kidney adapts to its new level of functionality.3,4<\/sup> The recovery phase lasts weeks to months.<\/p>\n Potential causes of AKI are innumerable. Historical categorization into prerenal (volume responsive), intrinsic renal, and postrenal kidney injury remains useful when developing differential diagnoses. Unfortunately, even with diligent diagnostic testing, the ultimate underlying cause of an AKI may not be found (up to 24% of patients in 1 study).6<\/sup> Cardiorenal and hepatorenal syndromes are included among the different types of AKI etiologies in Box 1<\/b><\/span>; however, discussion of these syndromes is beyond the scope of this article.<\/p>\n Prerenal injury secondary to poor renal perfusion (hypovolemia) can be addressed by correcting intravascular volume deficits. Other causes, such as thromboses or poor perfusion secondary to systemic disease (e.g., heatstroke, disseminated intravascular coagulation) may be more difficult to detect and correct.<\/p>\n Intrinsic renal injuries include inflammatory, infectious, toxic, autoimmune, neoplastic, and various other general categories of insult (Box 1<\/b><\/span>).<\/p>\n Postrenal injury affects the urinary tract distal to the kidney; causes include ureteral obstructions, urethral obstructions, and uroabdomen.<\/p>\n Prerenal <\/strong><\/p>\n Intrinsic renal<\/strong><\/p>\n Postrenal <\/strong><\/p>\n <\/div><\/div>\n Clinical signs of AKI in cats and dogs are often nonspecific. The clinical signs reported in the literature are usually anorexia, lethargy, tachypnea, weight loss, diarrhea, and vomiting.1,9,10<\/sup><\/p>\n Polyuria and polydipsia may be noticed, or they may go unnoticed if urinary habits are not strictly supervised. Oligura and anuria are of concern in the presence of appropriate hydration. Renomegaly and pain may be noted during palpation of the kidneys but may not be noted for patients with preexisting chronic renal insufficiency (acute-on-chronic kidney injury).<\/p>\n Oral ulcerations can be encountered and may contribute to hyporexia. Tongue tip necrosis has been reported for uremic patients secondary to thrombosis. Coagulation profiles vary widely and include hypocoagulability; hypercoagulability (especially in patients with glomerular disease); or a mix of normal, hypercoagulable, or hypocoagulable states.11,12<\/sup><\/p>\n Other organ systems can be affected in patients with AKI. One study reported that 79% of dogs with International Renal Interest Society (IRIS) grade III or higher AKI had documented ventricular premature contractions,13<\/sup> likely secondary to myocardial injury as evidenced by cardiac troponin measurements. With respect to acute pancreatitis, more than 71% of dogs with AKI may exhibit increased lipase levels during hospitalization14<\/sup>; however, acute pancreatitis was subsequently confirmed for up to only 8.8% of dogs at admission and 14.9% during hospitalization.15<\/sup> Uremic gastropathy reported in humans, for whom gastric ulceration is common, seems to be less common among dogs (in which mucosal edema and mineralization predominate)16<\/sup>; the same seems to be true for cats, in which gastric fibrosis and mineralization have been noted during histopathologic examination.17,18<\/sup> Uremic encephalopathy may compound the clinical signs of lethargy and altered mental status via direct damage to white matter and astrocytes.19<\/sup> Neurologic abnormalities and retinopathies have been reported with concurrent systemic hypertension; 16% of dogs with AKI at a referral hospital had evidence of retinal damage.20<\/sup> Specific diseases may also result in specific clinical signs (e.g., pulmonary hemorrhage induced by leptospirosis).<\/p>\n Research models are finding more evidence of \u201crenal crosstalk\u201d and subsequent injury to distant organs secondary to the inflammation in patients with AKI.21<\/sup> Future therapeutic targets have been suggested by documented hepatic, intestinal, pulmonary, brain, and cardiac involvement.21<\/sup><\/p>\n Thorough physical examination should include abdominal and renal palpation, urinary bladder palpation, and hydration assessment (xerostomia\u2014that is, excessively dry mucous membranes despite appropriate hydration\u2014may hinder hydration assessment). Blood pressure evaluation is imperative as a large number of patients are hypertensive at presentation or during hospitalization.20,22,23<\/sup><\/p>\n Establishing a standard minimum database is indicated for all AKI patients and should include a CBC, biochemical profile, and urinalysis (BOX 2<\/b><\/span>). Venous blood gas analysis may help with further evaluation of acid\u2013base status. If referral for extracorporeal therapy (e.g., dialysis) is a possibility, jugular venipuncture should be avoided.<\/p>\n Minimum database <\/strong><\/p>\n Other considerations <\/strong><\/p>\n <\/div><\/div>\n Urinalysis should ideally be performed via cystocentesis unless there are contraindications, such as coagulopathy. Despite the necessity of routine urinalysis, a study of dogs with AKI detected cylindruria and glucosuria (with normoglycemia) in only 31% and 23% of dog urine samples, respectively.24<\/sup> Urine should be submitted for culture and a urine protein:creatinine (UPC) ratio. Note that some studies have shown that an active sediment may confound the results of the UPC ratio, although the potential for proteinuria should not be ignored.25<\/sup><\/p>\n Abdominal radiographs (FIGURE 1<\/b><\/span>) may be used to identify urolithiasis or other abnormalities in the lower or upper urinary tracts. Contrast cystourethrography or intravenous pyelography may help identify rupture or blockage of the lower and upper urinary tracts, although these procedures have been supplanted by more sophisticated techniques (e.g., computed tomography, fluoroscopy).<\/p>\n\n
Pathophysiology<\/span><\/h2>\n
Prerenal<\/h3>\n
Intrinsic<\/h3>\n
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Postrenal<\/h3>\n
Initiation<\/h3>\n
Extension<\/h3>\n
Maintenance<\/h3>\n
Recovery<\/h3>\n
Etiologies<\/span><\/h2>\n
Prerenal<\/h3>\n
Intrinsic Renal<\/h3>\n
Postrenal<\/h3>\n
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Clinical Signs<\/span><\/h2>\n
Diagnosis <\/span><\/h2>\n
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