1. Renal foundations and classification
   • Renal physiology, azotaemia versus uraemia, prerenal/renal/postrenal causes
   • AKI versus CKD versus acute-on-chronic kidney disease
   • IRIS staging and substaging for dogs and cats
2. AKI in dogs and cats
   • Triage, differentials, diagnostic work-up, fluid strategy, oliguria/anuria, toxin and infectious causes, ICU monitoring
3. CKD in dogs and cats
   • Staging, proteinuria and hypertension, renal diet, phosphate control, nausea/appetite management, anaemia, follow-up planning
4. Diagnostics and interpretation
   • CBC, biochemistry, SDMA, electrolytes, urinalysis, UPC, urine culture, blood pressure, radiography and ultrasound
   • Interpretation of difficult patterns, including dehydration masking CKD and AKI-on-CKD
5. Therapeutics and calculations
   • Evidence-based drug choices, renal dose cautions, fluid calculations, nutrition, antiemetics, antihypertensives, antiproteinuric therapy, phosphate binders, potassium management and antibiotic stewardship
6. Complications, referral decisions and case simulations
   • Hyperkalaemia, hypertension, pulmonary oedema, severe acidosis, oliguria/anuria, urolith obstruction, dialysis indications, prognosis, monitoring, and practical case reasoning

1. Renal foundations and classification
   • Renal physiology, azotaemia versus uraemia, prerenal/renal/postrenal causes
   • AKI versus CKD versus acute-on-chronic kidney disease
   • IRIS staging and substaging for dogs and cats
2. AKI in dogs and cats
   • Triage, differentials, diagnostic work-up, fluid strategy, oliguria/anuria, toxin and infectious causes, ICU monitoring
3. CKD in dogs and cats
   • Staging, proteinuria and hypertension, renal diet, phosphate control, nausea/appetite management, anaemia, follow-up planning
4. Diagnostics and interpretation
   • CBC, biochemistry, SDMA, electrolytes, urinalysis, UPC, urine culture, blood pressure, radiography and ultrasound
   • Interpretation of difficult patterns, including dehydration masking CKD and AKI-on-CKD
5. Therapeutics and calculations
   • Evidence-based drug choices, renal dose cautions, fluid calculations, nutrition, antiemetics, antihypertensives, antiproteinuric therapy, phosphate binders, potassium management and antibiotic stewardship
6. Complications, referral decisions and case simulations
   • Hyperkalaemia, hypertension, pulmonary oedema, severe acidosis, oliguria/anuria, urolith obstruction, dialysis indications, prognosis, monitoring, and practical case reasoning

1. AKI emergency care - triage, oliguria/anuria, hyperkalaemia, toxins, ICU fluids
2. CKD practical management - IRIS staging, diet, proteinuria, hypertension, phosphate, anaemia
3. Diagnostics interpretation - CBC, biochemistry, SDMA, urinalysis, UPC, BP, imaging
4. Renal therapeutics - drugs, doses, fluid calculations, contraindications, monitoring
5. Complications and case simulation - acute-on-chronic disease, obstruction, referral/dialysis, clinical case

Acute Kidney Injury in Dogs and Cats: Emergency-Care Module

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1. BASIC UNDERSTANDING

Definition

• Prerenal: reduced renal perfusion, kidneys initially structurally intact.
• Intrinsic renal: direct nephron injury.
• Postrenal: impaired urine outflow, urine leakage, or obstruction.
• Acute-on-chronic kidney disease: an acute insult in a patient with pre-existing CKD.

Species affected

• Cats: ureteral obstruction, ureterolithiasis, lily toxicity, and pyelonephritis are particularly important.
• Dogs: leptospirosis, ethylene glycol toxicity where relevant geographically, severe heat injury, infectious/inflammatory disease, and drug/toxin exposure are common concerns.

Predisposition

Epidemiology and major causes

• Vomiting, diarrhoea, poor intake
• Haemorrhage
• Shock, sepsis, anaphylaxis
• Severe dehydration
• Reduced effective circulating volume: severe cardiac disease, third spacing
• Hypotension under anaesthesia

• Ischaemic acute tubular injury
• Nephrotoxins: NSAIDs, aminoglycosides, radiographic contrast in at-risk patients, grapes/raisins in dogs, lilies in cats, ethylene glycol, vitamin D/cholecalciferol products
• Infectious: leptospirosis, pyelonephritis, bacterial sepsis
• Pigment nephropathy: haemoglobinuria/myoglobinuria
• Glomerular, vascular, interstitial, infiltrative, or immune-mediated disease
• Hypercalcaemia

• Urethral obstruction
• Bilateral ureteral obstruction, or unilateral obstruction in a solitary functioning kidney
• Uroabdomen
• Urolithiasis, strictures, neoplasia, blood clots
• Iatrogenic ureteral ligation or trauma

Pathogenesis: step-by-step

1. Initial insult reduces perfusion, directly injures tubular cells, or prevents urine leaving the urinary tract.
2. GFR falls because renal perfusion falls, intratubular pressure rises, or nephrons are damaged.
3. Tubular dysfunction develops. Tubules cannot reabsorb water, sodium, bicarbonate, and nutrients normally, or excrete potassium, acids, phosphorus, and waste products.
4. Azotaemia and uraemia develop. Urea and creatinine rise, but creatinine may lag 24-48 hours behind injury.
5. Electrolyte and acid-base abnormalities develop. Hyperkalaemia, hyperphosphataemia, metabolic acidosis, and sometimes hypocalcaemia are common in severe low-output AKI.
6. Systemic consequences follow: nausea, vomiting, anorexia, GI mucosal injury, weakness, hypertension or hypotension, arrhythmias, pulmonary oedema if fluid overloaded, and neurologic signs in severe uraemia.
7. Recovery is possible if surviving nephrons regain function. Recovery is often polyuric, so dehydration and hypokalaemia may then become major risks.

Why the signs occur

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2. HISTORY TAKING: CLINIC CHECKLIST

Immediate triage questions

• Is the patient producing urine? When was the last normal urination?
• Is there repeated straining with little or no urine?
• Has there been sudden collapse, profound weakness, slow heart rate, or dyspnoea?
• Could the cat have accessed lilies?
• Could the dog have eaten grapes/raisins, antifreeze, rodenticide, human medication, or unknown chemicals?
• Has there been NSAID, aminoglycoside, chemotherapy, contrast, or anaesthetic exposure?
• Is leptospirosis possible? Rodents, stagnant water, wildlife, farm exposure, local outbreaks?

Ready-to-use owner history checklist

Presenting complaint and time course

• What changed first: vomiting, anorexia, reduced urine, increased drinking, lethargy, collapse?
• Exact onset and rate of progression?
• Sudden onset or chronic weight loss/PU-PD before this illness?
• Any previous abnormal renal values or diagnosis of CKD?

Appetite, water, urine, faeces

• Appetite: reduced, absent, selective, painful swallowing?
• Water intake: increased, reduced, or unable to keep water down?
• Urination: frequency, volume, straining, dysuria, haematuria, inappropriate urination, last confirmed urine?
• Defecation: diarrhoea, melaena, constipation?
• Vomiting: frequency, blood/coffee-ground material, relation to food?
• Estimate fluid loss: vomiting/diarrhoea frequency and volume.

Systemic signs

• Lethargy, weakness, collapse, tremors, seizures?
• Cough, tachypnoea, or exercise intolerance?
• Fever, pain, lameness, jaundice?
• Weight loss, chronic PU/PD, poor coat?

Exposure history

• Any access to:
  • Lilies, grapes/raisins, antifreeze, vitamin D products?
  • Human painkillers, especially NSAIDs?
  • Rat poisons, pesticides, chemicals?
  • Contaminated water, rodents, wildlife, farms?
• Tick/flea exposure and travel?
• Boarding, shelter, new pets, dog parks?
• Trauma, pelvic injury, recent surgery?

Previous medical and medication history

• CKD, heart disease, diabetes, hyperthyroidism, pancreatitis, pyometra, urinary stones, FLUTD?
• Recent hospitalisation or anaesthesia?
• Medication name, strength, dose, frequency, last dose:
  • NSAIDs
  • ACE inhibitors/ARBs
  • Diuretics
  • Aminoglycosides
  • Chemotherapy
  • Steroids
  • Supplements/herbals
• Vaccination status, especially Leptospira vaccination in dogs.
• Deworming and parasite control.
• Reproductive history if relevant: intact female with possible pyometra; pregnancy/lactation.

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3. CLINICAL EXAMINATION

Triage first: ABC

• Airway: patency, mentation, vomiting/aspiration risk.
• Breathing: respiratory rate/effort, crackles, oxygen saturation, pulmonary oedema.
• Circulation: heart rate/rhythm, pulses, blood pressure, mucous membranes, CRT, temperature.

Specific examination findings

Pain assessment

• Renal palpation pain
• Abdominal guarding
• Tense posture
• Hunched stance
• Vocalisation
• Hypertension/tachycardia from pain

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4. DIFFERENTIAL DIAGNOSIS

The emergency rule

1. Hypovolaemia/shock
2. Urinary obstruction
3. Uroabdomen
4. Hyperkalaemia
5. Sepsis/leptospirosis
6. Toxin exposure

Azotaemia comparison

Important and life-threatening differentials

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5. CBC INTERPRETATION

Pattern recognition

• Regenerative anaemia: reticulocytosis, polychromasia, anisocytosis. Think bleeding or haemolysis.
• Non-regenerative anaemia: inadequate reticulocyte response. CKD, chronic inflammation, marrow disease.
• Left shift: increased immature neutrophils. Indicates high tissue demand/inflammation.
• Toxic neutrophils: accelerated marrow release, commonly severe inflammation/sepsis.
• Neutrophilia: stress, inflammation, steroid effect, infection.
• Neutropenia with toxic change: potentially overwhelming sepsis.
• Thrombocytopenia: verify manually, then consider leptospirosis, DIC, sepsis, immune destruction.

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6. SERUM BIOCHEMISTRY AND BLOOD GAS INTERPRETATION

Core AKI pattern

Hyperkalaemia: immediate interpretation

• Tall tented T waves
• Shortened QT
• Prolonged PR
• QRS widening
• Loss of P waves
• Ventricular arrhythmias or sine-wave pattern

Blood gas and lactate

• Venous blood gas: pH, bicarbonate, base excess, potassium, ionised calcium.
• Lactate: perfusion marker, not a direct renal marker.
• Severe metabolic acidaemia requires cause-directed treatment. Bicarbonate is not routine for every AKI patient.

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7. URINALYSIS

Important clinical cautions

• USG cannot by itself distinguish AKI from CKD.
• Collect urine for culture and susceptibility when pyelonephritis is possible.
• UPC is best deferred until haematuria, pyuria, bacteriuria, and marked postrenal protein contamination are controlled.
• A normal urine sediment does not exclude AKI.

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8. PRACTICAL DIAGNOSTIC PLAN

First 5-15 minutes

1. ABC assessment.
2. Place IV catheter, obtain blood and urine samples if this does not delay stabilization.
3. Check:
   • Bedside glucose
   • PCV/TS
   • Electrolytes, especially potassium
   • Blood gas/acid-base if available
   • Blood pressure
   • ECG if hyperkalaemia/bradycardia
4. Palpate bladder and kidneys.
5. POCUS: bladder size, free abdominal fluid, renal pelvis dilation, lung B-lines/effusion.

Minimum database

• CBC with smear review
• Serum biochemistry: BUN, creatinine, phosphorus, electrolytes, calcium, albumin, glucose, liver values
• Blood gas and lactate in ill patients
• Urinalysis with sediment and USG
• Blood pressure
• Accurate body weight
• Urine output measurement
• ECG if hyperkalaemic, bradycardic, or unstable

Recommended tests

• Urine culture and susceptibility, ideally cystocentesis sample
• Abdominal ultrasound
• Abdominal radiographs
• Serial creatinine, BUN, phosphorus, potassium, acid-base values
• UPC after sediment is inactive if proteinuria persists
• Leptospira PCR/serology as appropriate
• Spec cPL/fPL when pancreatitis is plausible
• Toxicology testing when it changes management
• Coagulation testing if bleeding/DIC is possible

Severe/emergency tests

• ECG and continuous rhythm monitoring
• Serial blood gases/electrolytes
• Thoracic radiographs or lung ultrasound if fluid overload is suspected
• Abdominocentesis if free fluid is present:
  • Compare abdominal-fluid creatinine and potassium with serum for uroabdomen
• Crossmatch/type if transfusion could be required
• Blood cultures when bacteraemia/sepsis is a credible concern, ideally before antibiotics

Confirmatory approach

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9. IMAGING

Radiography

Recommended views

• Abdominal right lateral
• Abdominal left lateral
• Ventrodorsal or dorsoventral view

Look for

• Renal size and shape
• Radiopaque uroliths
• Bladder distension
• Loss of abdominal serosal detail suggesting effusion
• Prostatic enlargement, masses, trauma
• Mineralized ureteral calculi, though many are not visible

Ultrasound

• Renomegaly
• Increased cortical echogenicity
• Medullary rim sign, nonspecific
• Pyelectasia/hydronephrosis
• Hydroureter
• Renal/ureteral calculi
• Perirenal fluid
• Irregular renal contour or small kidneys, supporting chronic disease
• Renal pelvic debris in pyelonephritis, but not diagnostic alone

CT

• Suspected ureteral obstruction not fully characterized by ultrasound/radiographs
• Complex stone mapping
• Surgical/interventional planning
• Renal/ureteral anomalies or masses

Echocardiography

• Fluid intolerance is suspected
• Cardiac disease complicates resuscitation
• Hypertension, pulmonary oedema, or shock is present

MRI

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10. DIAGNOSIS

Presumptive AKI

• Rising creatinine and/or SDMA
• Reduced urine production or tubular dysfunction
• Inappropriate urine concentration in an azotaemic patient
• Supportive urine sediment/imaging
• Compatible exposure or systemic disease

Definitive cause-based diagnosis

• Urethral obstruction: clinical exam plus catheterization/imaging.
• Uroabdomen: abdominal fluid creatinine and potassium exceed serum values.
• Pyelonephritis: compatible illness plus urine culture, ideally with imaging support.
• Leptospirosis: appropriate PCR/serology plus clinical context.
• Toxin exposure: credible exposure history, compatible findings, or assay.
• Ureteral obstruction: ultrasound/CT/interventional findings.

IRIS AKI grading

• Grade I: non-azotaemic AKI with documented renal injury or a relevant rising creatinine trend.
• Grades II-V: increasing severity of azotaemia.
• Subcategorize as oliguric, non-oliguric, or anuric, and identify need for renal replacement therapy.

Conflicting results

• High creatinine plus dehydration: may be prerenal, AKI, CKD, or mixed. Reassess after controlled rehydration.
• Normal creatinine with poor urine output: early AKI, low muscle mass, or obstruction remains possible.
• Concentrated urine: does not exclude early intrinsic AKI.
• Dilute urine: may result from fluids, diuretics, endocrine disease, CKD, or AKI.
• Small kidneys plus abrupt deterioration: acute-on-CKD is likely.
• Azotaemia improves after unblocking: postrenal component was present, but renal injury can persist.

Common diagnostic mistakes

• Calling all azotaemia “kidney failure.”
• Missing ureteral obstruction in a cat with a small bladder.
• Diagnosing UTI from pyuria without urine culture.
• Assuming normal creatinine excludes early AKI.
• Mistaking fluid-induced haemodilution for renal recovery.
• Missing hypertension and retinal injury.
• Ignoring medication and toxin history.
• Giving nephrotoxic drugs before collecting essential samples or assessing renal status.

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11. TREATMENT PROTOCOL

Treatment priorities

1. Stabilize ABCs.
2. Correct hypovolaemia and hypotension.
3. Stop nephrotoxins.
4. Relieve obstruction or repair urine leakage.
5. Treat hyperkalaemia, dangerous acidosis, and fluid overload.
6. Identify and treat the cause.
7. Provide antiemesis, nutrition, analgesia, and intensive monitoring.
8. Refer early for ureteral intervention or renal replacement therapy when indicated.

A. Mild AKI

• Hospitalize or closely supervise depending on cause and trend.
• Stop nephrotoxins.
• Address dehydration with individualized balanced isotonic crystalloid therapy.
• Monitor creatinine, electrolytes, body weight, urine output, and BP.
• Treat nausea/pain.
• Investigate cause: culture, imaging, infectious/toxin testing as indicated.
• Ensure enteral nutrition as soon as vomiting is controlled.

B. Moderate AKI

• Hospitalize with strict input-output charting.
• IV fluid plan tailored to deficit, ongoing losses, urine output, and cardiovascular tolerance.
• Urinary catheter if necessary for accurate output, using aseptic technique and removing as soon as practical.
• Urine culture before antibiotics when feasible.
• Serial electrolyte, acid-base, BP, body weight assessments.
• Early referral discussion if creatinine rises despite correction of perfusion, oliguria develops, or ureteral disease is suspected.

C. Severe/critical AKI

• ICU-level care.
• ECG and frequent blood gas/electrolyte monitoring.
• Treat hyperkalaemic cardiotoxicity immediately when ECG changes/bradyarrhythmia are present.
• Avoid blind high-rate fluid administration.
• Relieve postrenal obstruction urgently.
• Consult/referral for intermittent haemodialysis, continuous renal replacement therapy, or peritoneal dialysis early rather than after prolonged deterioration.

D. Emergency/ICU management: first-hour checklist

• Oxygen if hypoxaemic or in respiratory distress.
• IV access, blood pressure, ECG if indicated.
• Bedside electrolytes/blood gas/glucose.
• Palpate bladder, POCUS abdomen and lungs.
• Controlled isotonic crystalloid boluses only if hypovolaemic.
• Hyperkalaemia protocol if indicated.
• Urinary catheter/decompression if urethral obstruction.
• Abdominocentesis if uroabdomen suspected.
• Analgesia and antiemetic therapy.
• Infection control precautions when leptospirosis is possible.

Drug table: standard reference-style doses

Drugs usually avoided or used only with strong justification

• NSAIDs: avoid in suspected AKI.
• Aminoglycosides: avoid unless no safer option and use therapeutic drug monitoring.
• ACE inhibitors/ARBs: do not start during unstable AKI/hypotension.
• Mannitol: not routine; can worsen fluid overload and is inappropriate in anuric/fluid-overloaded patients.
• Dopamine “renal-dose”: do not use simply to “improve renal perfusion.” It has not shown reliable renal-protective benefit.
• Empirical antibiotics: do not prescribe merely because AKI is severe.

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12. FLUID THERAPY

The principle

1. Restore intravascular volume if hypovolaemic.
2. Correct interstitial dehydration deficit.
3. Replace maintenance needs plus measured ongoing losses.

Fluid selection

• Balanced isotonic crystalloids are appropriate in many AKI patients.
• 0.9% saline may be selected when clinically indicated, but excessive chloride exposure can worsen hyperchloraemic acidosis.
• Choice should be based on sodium, chloride, acid-base status, concurrent disease, and availability.
• Do not avoid balanced crystalloid solely because it contains a small amount of potassium. The potassium concentration in common balanced fluids is usually far lower than the patient’s plasma potassium and does not generally drive emergency hyperkalaemia management.
• Add potassium only after documented need and careful calculation. Never add potassium to fluids in a hyperkalaemic or anuric patient.

Shock resuscitation: titrated, not blind

• Dog: 10-15 mL/kg isotonic crystalloid over 10-15 minutes.
• Cat: 5 mL/kg over 10-15 minutes.

• HR/rhythm and pulse quality
• Mentation
• BP/MAP
• CRT and mucous membranes
• Lung sounds/POCUS B-lines
• Respiratory effort/SpO₂
• Body weight
• Urine output

Deficit calculation

Maintenance

Example maintenance estimates

Ongoing loss replacement

• Urine output: 0.8 mL/kg/hr = 8 mL/hr
• Estimated maintenance: 20 mL/hr
• Vomiting: 20 mL over 4 hours = 5 mL/hr

Urine output targets

• Expected normal urine output in hospitalized patients is often roughly 1-2 mL/kg/hr.
• Persistent oliguria is concerning. Confirm catheter patency, bladder emptying, hydration, BP, obstruction status, and measurement accuracy before adding drugs.
• Persistent anuria or very low urine output despite appropriate optimization requires urgent reassessment and often referral.

Stop or reduce fluids when

• Deficits are corrected.
• BP/perfusion is adequate.
• Urine output is low and body weight is increasing.
• New tachypnoea, crackles, pleural effusion, pulmonary oedema, or increased B-lines develop.
• Peripheral oedema, chemosis, serous nasal discharge, or worsening hypertension occurs.
• PCV/TS falls from dilution without clinical improvement.

Fluid overload signs

• Rapid weight gain
• Increased RR/effort
• Crackles, B-lines, pulmonary oedema
• Pleural effusion
• Chemosis, peripheral oedema
• Worsening hypertension
• Serous nasal discharge
• New oxygen requirement

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13. DOSE CALCULATIONS

Formula

Worked example: maropitant 1 mg/kg

Worked example: buprenorphine 0.02 mg/kg

Converting mg to mL

• Required dose: 10 mg
• Label concentration: ___ mg/mL
• Volume: 10 ÷ ___ = ___ mL

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14. SUPPORTIVE CARE

Nutrition

• Do not prolong starvation because of nausea alone.
• Control vomiting/nausea first, then start early enteral nutrition if safe.
• In acute critical illness, prioritize adequate calories and protein rather than automatically imposing severe protein restriction.
• Use feeding tubes when the GI tract is usable and voluntary intake is absent.
• In cats, avoid prolonged anorexia because hepatic lipidosis can develop.
• Renal therapeutic diets may be useful later, especially if CKD persists, but acute nutritional decisions must be individualized.

Antiemetics

Analgesia

• Prefer opioids titrated to effect.
• Avoid NSAIDs in AKI.
• Treat renal/ureteral pain, abdominal pain, and catheter-associated discomfort.

Gastroprotection

• Do not give acid suppressants automatically to every uraemic patient.
• Consider gastroprotective treatment for documented or strongly suspected GI ulceration, haematemesis, melaena, severe reflux, or other specific indication.
• Sucralfate can interfere with absorption of other drugs, so separate administration times.

Antibiotics

• Pyelonephritis/UTI supported by culture or strong clinical evidence
• Leptospirosis or credible bacterial infectious cause
• Sepsis/bacteraemia
• An infected urinary obstruction or urinary tract instrumentation complication

Electrolytes/vitamins

• Correct potassium, magnesium, phosphate, sodium, calcium, and acid-base abnormalities based on measured values.
• Do not add potassium “routinely.”
• Phosphate binders are more relevant once enteral feeding occurs and hyperphosphataemia persists; they do not replace treating severe AKI or dialysis.
• B vitamins may be considered in prolonged polyuric losses, but are not an AKI cure.

Oxygen

Blood products

Nursing care

• Accurate intake-output chart
• Closed urine collection if catheterized
• Catheter asepsis and daily need assessment
• Turn recumbent patients regularly
• Oral care for uraemic ulcers
• Anti-nausea feeding plan
• Daily weight, sometimes 2-4 times daily in unstable cases
• Barrier nursing/PPE for suspected leptospirosis

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15. ANTIBIOTIC STEWARDSHIP

When antibiotics are truly indicated

• Positive urine culture with compatible pyelonephritis/UTI signs
• Septic patient
• Leptospirosis
• Infected obstruction
• Bacterial focus outside the urinary tract causing AKI

Best practice

1. Obtain urine by cystocentesis for culture before antibiotics when patient stability allows.
2. Choose empirical therapy based on illness severity, likely site, local resistance, and renal safety.
3. Modify treatment promptly using culture/susceptibility results.
4. Use the narrowest effective drug.
5. Review renal dose adjustment and avoid nephrotoxic choices when alternatives exist.
6. Do not diagnose pyelonephritis from pyuria alone.
7. Repeat culture when clinically indicated, especially if response is poor or infection is complicated.

Avoid

• “Preventive” antibiotics for sterile AKI.
• Prolonged antibiotics without culture reassessment.
• Aminoglycosides in unstable AKI unless there is no viable alternative and specialist-level monitoring is available.

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16. PROGNOSIS

Better prognostic indicators

• Rapid correction of a prerenal cause
• Relief of obstruction before severe prolonged injury
• Improving creatinine trend
• Return of appropriate urine output
• Stable BP and electrolytes
• Controlled infection/toxin exposure
• Ability to eat and tolerate enteral nutrition
• No severe comorbidity

Poor prognostic indicators

• Persistent anuria/oliguria
• Worsening azotaemia despite corrected perfusion
• Refractory hyperkalaemia, acidosis, fluid overload, or hypertension
• Severe systemic sepsis/MODS
• Severe nephrotoxic injury
• Advanced acute-on-CKD
• Delayed presentation after lily or ethylene glycol exposure
• Inability to access obstruction relief or renal replacement therapy when indicated

Refer urgently when

• Suspected ureteral obstruction
• Persistent oliguria/anuria
• Refractory hyperkalaemia/acidosis
• Fluid overload
• Creatinine is rising in an appropriately hydrated patient
• Need for haemodialysis/CRRT/peritoneal dialysis
• Severe hypertension, pulmonary oedema, or neurological uraemia

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17. MONITORING SHEET

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18. COMMON CLINICAL MISTAKES

1. Giving large-volume fluids to every azotaemic patient.
2. Failing to document urine output.
3. Mistaking oliguria from obstruction for intrinsic renal failure.
4. Not palpating the bladder or using POCUS.
5. Missing ureteral obstruction in cats because the bladder is small.
6. Treating hyperkalaemia without ECG assessment when available.
7. Giving calcium gluconate and assuming potassium has been corrected.
8. Using furosemide repeatedly instead of reassessing perfusion, obstruction, and referral needs.
9. Starting antibiotics without obtaining culture in a stable patient.
10. Missing leptospirosis and exposing staff or other animals.
11. Assuming a single normal creatinine excludes AKI.
12. Failing to stop NSAIDs, aminoglycosides, and other nephrotoxins.
13. Ignoring blood pressure and fundic examination.
14. Underfeeding anorectic cats.
15. Calling a patient “recovered” because creatinine briefly falls after haemodilution.

What you may miss if you focus only on AKI

• Addisonian crisis
• Uroabdomen
• Pancreatitis/sepsis causing renal hypoperfusion
• Hypertensive emergency
• Cardiac disease limiting fluids
• Acute-on-CKD
• Pyometra
• Hypercalcaemia
• Severe toxic exposure needing antidotal therapy or decontamination
• Obstructive uropathy requiring intervention, not more medical therapy

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19. RED FLAGS

Immediate hospitalization

• Persistent vomiting/anorexia with azotaemia
• Oliguria or uncertain urine production
• AKI with dehydration, pain, fever, or toxin exposure
• Suspected pyelonephritis or leptospirosis
• Progressive creatinine or phosphorus increase

Emergency stabilization

• Bradycardia, weakness, or ECG changes with hyperkalaemia
• Hypotension/shock
• Urethral obstruction
• Suspected uroabdomen
• Any cat with possible lily ingestion
• Severe acidosis
• Dyspnoea or suspected fluid overload
• Seizures, coma, severe uraemic encephalopathy

ICU/referral

• Persistent urine output below approximately 0.3 mL/kg/hr for over 6 hours despite appropriate medical optimization
• Anuria
• Uncontrolled hyperkalaemia/acidosis
• Refractory fluid overload
• Rising creatinine despite corrected hydration/perfusion
• Suspected bilateral ureteral obstruction
• Need for dialysis or advanced interventional urology

Blood transfusion

• Active significant haemorrhage
• Severe symptomatic anaemia with poor oxygen delivery
• Not solely because a patient has AKI or mild non-regenerative anaemia

Surgery/interventional procedure

• Urethral obstruction not medically relieved
• Uroabdomen
• Ureteral obstruction requiring stent or subcutaneous ureteral bypass
• Selected stones, strictures, masses, trauma

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20. CASE SIMULATION

Case: do not scroll for an answer because none is provided yet

Signalment

History

Clinical examination

• Quiet but responsive
• Temperature: 37.4°C
• HR: 156 bpm, regular
• RR: 34/min, mildly increased but unlaboured
• BP: 178 mmHg systolic, repeated after acclimation
• Mucous membranes: tacky, pink; CRT 2 sec
• Estimated dehydration: 6%
• Kidneys palpably uncomfortable; left kidney seems enlarged
• Bladder: small to moderately sized, non-turgid
• Mild oral halitosis, no ulcers
• No heart murmur; lung sounds clear

CBC

Biochemistry and blood gas

Urinalysis

• USG: 1.018
• Protein: 2+
• Blood: 1+
• Glucose: negative
• Ketones: negative
• Sediment: 10-15 WBC/hpf, 5-10 RBC/hpf, rare granular casts, no visible bacteria
• Urine submitted for culture and susceptibility

Imaging

• Left renal pelvis: 8 mm dilation
• Proximal left ureter mildly dilated
• 2 mm hyperechoic focus with distal acoustic shadowing near proximal ureter
• Right renal pelvis: 2 mm dilation
• Both kidneys mildly irregular; left kidney enlarged
• Urinary bladder small, no obvious urolith
• No free abdominal fluid

Your tasks

1. Identify the major problem list.
2. List and prioritize differentials.
3. Interpret the CBC.
4. Interpret the biochemistry and blood gas.
5. Select further tests and explain why.
6. Give your presumptive diagnosis.
7. Create an emergency and ongoing treatment plan.
8. Calculate doses for antiemetic, analgesic, and any indicated hyperkalaemia treatment.
9. Create a monitoring plan for the first 24 hours.
10. Give prognosis and referral recommendation.

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21. QUICK CLINICAL ALGORITHM

AZOTAEMIC / VOMITING / OLIGURIC DOG OR CAT
                |
                v
1. TRIAGE ABCs
   - BP, ECG if K high/bradycardia, glucose, blood gas, oxygen if needed
                |
                v
2. IS THERE AN IMMEDIATE POSTRENAL EMERGENCY?
   - Palpate bladder, POCUS, assess for uroabdomen
   - Obstruction or urine leak -> decompress/repair/referral
                |
                v
3. IS THE PATIENT HYPOVOLAEMIC OR HYPOTENSIVE?
   - Small crystalloid bolus, reassess after each aliquot
   - Correct deficit carefully
                |
                v
4. MINIMUM DATABASE
   - CBC, chemistry, electrolytes, phosphorus, UA/culture, BP
   - Urine output, imaging, serial creatinine/SDMA
                |
                v
5. CLASSIFY
   - Prerenal, intrinsic renal, postrenal, or mixed
   - Identify cause: toxin, infection, ischaemia, obstruction, acute-on-CKD
                |
                v
6. TREAT COMPLICATIONS
   - Hyperkalaemia/ECG changes
   - Acidosis
   - Nausea, pain, hypertension, fluid overload
                |
                v
7. TARGETED THERAPY
   - Antidote/decontamination, antimicrobials only if indicated,
     relieve obstruction, treat sepsis or leptospirosis
                |
                v
8. MONITOR HOURLY IF CRITICAL
   - Urine output, inputs, BW, BP, ECG, RR/lung status, electrolytes
                |
                v
9. REFER EARLY
   - Anuria/oliguria, ureteral obstruction, rising creatinine,
     refractory K/acidosis/overload, dialysis need
                |
                v
10. DISCHARGE ONLY WHEN
    - Stable hydration, controlled vomiting, safe urine output,
      cause addressed, owner can monitor, recheck plan in place

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22. MEMORY TOOL

Ten key points

1. AKI is sudden renal dysfunction, not simply increased creatinine.
2. Always consider prerenal, intrinsic renal, and postrenal causes.
3. A normal creatinine does not exclude early AKI.
4. Urine output is a core vital parameter.
5. Correct hypovolaemia, but do not force fluids in oliguria/anuria.
6. Urethral and ureteral obstruction are time-sensitive emergencies.
7. Hyperkalaemia can kill by arrhythmia.
8. Cats with suspected lily exposure require immediate action.
9. Culture urine before antibiotics when practical.
10. Early referral can change outcome when dialysis or ureteral intervention is needed.

Ten important drug facts

1. NSAIDs are generally contraindicated in suspected AKI.
2. Calcium gluconate stabilizes myocardium but does not lower potassium.
3. Insulin plus dextrose lowers serum potassium temporarily by intracellular shifting.
4. Furosemide does not cure AKI and should not replace reassessment/referral.
5. “Renal-dose dopamine” is not a renal-protective treatment.
6. Maropitant controls vomiting but may not fully control nausea.
7. Ondansetron is useful for persistent nausea but consider QT risk.
8. Opioids are preferred analgesics over NSAIDs in AKI.
9. Avoid aminoglycosides where safer alternatives exist.
10. Antibiotics require a bacterial indication, culture plan, and renal dosing review.

Ten diagnostic clues

1. Large painful bladder plus hyperkalaemia: think urethral obstruction.
2. Small bladder plus azotaemia in a cat: do not miss ureteral obstruction.
3. Abdominal fluid creatinine/potassium above serum: think uroabdomen.
4. Fever, renal pain, pyuria: consider pyelonephritis.
5. AKI plus hepatic/pulmonary signs in a dog: consider leptospirosis.
6. Severe acidosis with compatible exposure: consider ethylene glycol.
7. Azotaemia resolving after rehydration: prerenal component likely.
8. Small irregular kidneys with anaemia: CKD or acute-on-CKD likely.
9. Rising weight and tachypnoea during fluids: fluid overload until proven otherwise.
10. Hyperkalaemia plus bradycardia: ECG immediately.

Ten common mistakes

1. Not measuring urine output.
2. Giving maintenance fluids automatically to anuric patients.
3. Missing a postrenal cause.
4. Delaying ultrasound in a possible ureteral obstruction.
5. Treating pyuria without culture.
6. Failing to ask about toxins and medications.
7. Ignoring blood pressure.
8. Using nephrotoxic drugs in a high-risk patient.
9. Waiting too long to discuss dialysis/referral.
10. Interpreting one lab value rather than serial trends.

Ten high-yield MCQs

1. In an AKI patient with bradycardia and ECG changes from hyperkalaemia, which treatment stabilizes cardiac membranes?
   Answer: Calcium gluconate.
2. Does calcium gluconate lower serum potassium?
   Answer: No.
3. What is the first major diagnostic category to exclude in an azotaemic cat with a small bladder?
   Answer: Ureteral obstruction.
4. What is the most useful routine measurement for guiding fluids in hospitalized AKI?
   Answer: Accurate urine output plus body weight and input-output balance.
5. Which drug class is generally avoided in AKI?
   Answer: NSAIDs.
6. Which sample should ideally be collected before starting antibiotics for suspected pyelonephritis?
   Answer: Urine culture, preferably cystocentesis sample.
7. Can a patient have early AKI with normal creatinine?
   Answer: Yes.
8. What is the key treatment for postrenal azotaemia from obstruction?
   Answer: Urgent relief of obstruction.
9. What is a classic serious toxin exposure causing AKI in cats?
   Answer: Lilies.
10. What is the fluid goal after deficits have been corrected?
    Answer: Approximately zero fluid balance, matching input to measured/estimated output.

Five clinical pearls

1. “No urine” is a diagnosis problem before it is a diuretic problem. Confirm catheter patency, obstruction, volume status, BP, and renal perfusion first.
2. Fluid overload is an iatrogenic emergency. Daily or frequent body weight is often more informative than skin turgor.
3. Ureteral obstruction can be subtle in cats. A small bladder does not make obstruction unlikely.
4. Treat the ECG and perfusion, not just numbers. Severe hyperkalaemia can be fatal before a full diagnostic work-up is complete.
5. Creatinine is delayed and muscle-dependent. Serial trends, USG, urine output, SDMA, and context are stronger than one isolated result.