Decreased kidney function can be documented by

·       an increase in serum creatinine concentration of 0.3 mg/dL (26.5 µmol/L), even within the reference interval, from a known baseline over 48 hours.

·       change in urine production may range from polyuria (>2 mL/kg/h) to anuria (no urine production).

·       urinalysis findings that support AKI include casts, bacteriuria, renal glycosuria, and proteinuria.

Azotaemia or increasing serum creatinine may be volume responsive, renal in origin, post-renal, or due to a combination of factors.

Kidney aspirate or biopsy evaluation is not commonly indicated in patients with AKI unless there is concern for infiltrative disease, such as lymphoma or FIP. Coagulation status should be assessed before sampling any veterinary patient with AKI.

Specific testing for infectious disease may be required, including leptospirosis, leishmaniosis, Lyme disease (Borrelia burgdorferi), and Rocky Mountain spotted fever (Rickettsia rickettsii).

Hospitalised veterinary patients with recognised risk factors for AKI, such as pre-existing kidney disease, heart disease, sepsis, or administration of nephrotoxic drugs, should be actively monitored at least once daily.

Animals diagnosed with non-azotaemic AKI (IRIS Grade I) do not necessarily need to be hospitalised, but diagnostic work-up is recommended to identify the underlying aetiology. Nephrotoxic medications should be discontinued and animals should be closely monitored daily at first. Animals progressing to IRIS Grades II–V should be hospitalised.

Hypovolaemia should be corrected within 1–2 hours of detection using balanced isotonic crystalloid boluses: 10–20 mL/kg in dogs and 5–10 mL/kg in cats. Dehydration should be corrected within 6 hours of detection unless contraindicated; if cardiac disease is a concern, correction over 12–24 hours may be more appropriate. Sodium chloride 0.9% and synthetic colloids should be avoided. In animals with refractory hypotension after fluid resuscitation, early initiation of vasopressors is recommended. Once animals are euhydrated, the fluid administration rate should equal ongoing losses, including urine production, gastrointestinal losses, and insensible losses. Fluids may need to be discontinued in anuric patients. Forced diuresis with high fluid rates does not improve outcomes in AKI and increases the risk of volume overload.  Animals with AKI may be unable to excrete excess fluid, leading to life-threatening volume overload (≥10% body weight) with consequences such as pulmonary oedema, hypertension, delayed kidney recovery, and worsened organ function. Once an animal is consuming enough fluids, either voluntarily or via an enteral feeding tube, to maintain hydration and serum creatinine is trending down, intravenous fluid therapy can be tapered slowly while monitoring hydration status. Fluid balance should be monitored at least twice daily by physical examination, body weight monitoring, and assessment of urine production.

There is no evidence that diuretics, low-dose dopamine, or fenoldopam improve outcomes in AKI.

Metabolic acidosis is common in severe AKI and should be monitored at least once daily in hospitalised AKI patients. Electrolyte disorders are common at presentation and during hospitalisation, especially in oliguric and anuric animals. Electrolytes should initially be monitored at least twice daily. Dialysis is indicated if conventional treatment fails to maintain potassium below 6.5 mmol/L. Hypokalaemia may develop, especially during the polyuric phase. Where ionised hypomagnesaemia is identified, intravenous magnesium supplementation should be considered at concentrations ≤ 20%. Hypocalcaemia is common in dogs and cats with AKI. In patients with compatible clinical signs, or severe ionised hypocalcaemia (<0.75 mmol/L), intravenous calcium supplementation should be administered even in the face of hyperphosphatemia. The main treatment goal is to eliminate clinical signs rather than normalise the calcium concentration. Hypercalcaemia can contribute to perpetuation of AKI, although it is often mild and may not require specific treatment unless it is contributing to the primary pathogenesis.

Gastrointestinal disturbances induced by uraemia are common in severe AKI and should be treated supportively. Pancreatitis and AKI often coexist and can exacerbate each other; high-fat diets should be avoided in dogs with AKI and concurrent pancreatitis.

Arrhythmias are common in uraemic patients and should be treated when caused by severe hyperkalaemia or when causing cardiovascular compromise.

Coagulation and anaemia: Veterinary patients with AKI may be hypo- or hypercoagulable, or have a combination of both. At minimum, all patients with AKI should have a complete blood count, including a reliable platelet count. If there is progressive, ongoing non-regenerative anaemia, prophylactic treatment with darbepoetin should be considered.

Systemic hypertension is a severe and common complication of AKI. Iatrogenic fluid overload is a key contributor and should be avoided. Common manifestations include seizures, encephalopathy, and retinal detachment. Blood pressure should be measured at least 2–4 times per day, with frequency adjusted to clinical progression. Systolic blood pressure should be maintained below 160 mmHg. Amlodipine is recommended as first-line therapy, and hydralazine may be used as a second-line option or in more severe hypertension. Antihypertensives should be used cautiously in dehydrated animals because GFR may decrease precipitously.

Medication adjustment: Non-steroidal anti-inflammatory drugs, aminoglycosides, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and intravenous contrast agents should be avoided in veterinary patients with AKI. All medications should be reviewed for nephrotoxicity, renal elimination, and margin of safety. Where possible, use drugs with wider safety margins or predominant hepatic metabolism/excretion.

Nutrition: Nutritional support is indicated when anorexia or inappetence has persisted, or is expected to persist, for more than 48 hours. General anaesthesia can usually be provided safely in dogs and cats with AKI if renal perfusion and cardiovascular stability are maintained. Caloric requirements should exceed 1.5 times resting energy requirements. Enteral nutrition volumes must be included in fluid volume calculations, especially in oligoanuric animals. In the acute hospital phase, neither protein restriction nor phosphate binders are indicated.escription

Discharge can be considered when serum creatinine has stabilised and clinical signs are controlled without the need for intravenous medication or fluid therapy. The expected hospitalisation period for dogs and cats with severe AKI is approximately one week, although some patients require longer hospitalisation.

The inciting cause is a major determinant of prognosis. The severity of azotaemia, or IRIS AKI grade, are not accurate or consistent indicators of reversibility and should not be used alone to determine prognosis.

The recovery phase from AKI can take days to months. Lack of improvement in kidney function parameters within the first few days of treatment does not indicate an inability to recover. Even with apparent complete renal recovery, dogs and cats should be considered IRIS stage 1 CKD.

The first follow-up recheck should usually occur within a few days of discharge. Long-term monitoring should include regular rechecks of kidney function at least every 3 months initially for 1 year, and subsequently based on IRIS CKD stage.