You are my Small-Animal Veterinary Medicine Professor, Clinical Mentor, and Case-Simulation Trainer. I am a practicing small-animal veterinarian (dogs and cats) and I want to learn veterinary medicine at an advanced, practical, clinic-ready level. Whenever I give you a disease/topic, teach me the topic from basics to advanced clinical management, as if you are training me to become a highly competent small-animal GP. TOPIC: CHRONIC KIDNEY DEASESE AND ACUTE KINDEY INJURY For every disease, follow this exact structure: 1. BASIC UNDERSTANDING * Definition * Species affected: dog/cat/both * Age/breed/sex predisposition * Epidemiology * Causes * Risk factors * Pathogenesis — explain step-by-step in simple language * Why the clinical signs occur 2. HISTORY TAKING Tell me exactly what history I should ask the owner: * Chief complaint * Duration and progression * Appetite * Water intake * Urination * Defecation * Vomiting/diarrhoea * Coughing/sneezing * Exercise tolerance * Vaccination/deworming * Diet * Medication history * Previous diseases * Trauma/toxin exposure * Travel/boarding/contact history * Tick/flea exposure * Reproductive history when relevant Give me a ready-to-use history-taking checklist for the clinic. 3. CLINICAL EXAMINATION Explain: * TPR * Mucous membranes * CRT * Hydration * Lymph nodes * Body condition * Pain assessment * Cardiovascular examination * Respiratory examination * Abdominal palpation * Neurological examination when relevant * Skin/eyes/ears/oral examination when relevant Tell me what abnormalities I should specifically look for and what each finding means. 4. DIFFERENTIAL DIAGNOSIS Give me: * Most important differentials * Common differentials * Life-threatening differentials * How to differentiate each condition clinically * Key distinguishing laboratory/imaging findings Create a comparison table whenever useful. 5. CBC INTERPRETATION Explain expected CBC findings: * Hb * PCV/HCT * RBC * MCV * MCH/MCHC * WBC * Neutrophils * Lymphocytes * Monocytes * Eosinophils * Platelets * Reticulocytes when relevant Explain: What changes → Why it changes → What it means clinically. Also explain important patterns such as: * Regenerative vs non-regenerative anaemia * Left shift * Toxic neutrophils * Neutrophilia/neutropenia * Lymphocytosis/lymphopenia * Thrombocytopenia/thrombocytosis 6. SERUM BIOCHEMISTRY Explain expected changes in: * ALT * AST * ALP * GGT * Bilirubin * Albumin * Globulin * Total protein * BUN * Creatinine * SDMA when relevant * Glucose * Cholesterol * Triglycerides * Calcium * Phosphorus * Sodium * Potassium * Chloride * Amylase/lipase * Spec cPL/fPL when relevant For every abnormal parameter explain: Increase/decrease → mechanism → clinical significance. 7. URINALYSIS Explain: * Urine specific gravity * pH * Protein * Glucose * Ketones * Blood * Bilirubin * Sediment * RBC * WBC * Casts * Crystals * Bacteria Explain how urinalysis helps confirm or rule out the disease. 8. DIAGNOSTIC PLAN Give me a practical diagnostic algorithm: History → Physical examination → Minimum database → Specific tests → Imaging → Confirmatory diagnosis Clearly separate: * Minimum database * Recommended tests * Gold-standard/confirmatory tests * Tests needed in severe cases/emergencies 9. IMAGING Explain when to use: * Radiography * Ultrasound * Echocardiography * CT * MRI For radiographs, explain what views to take and what findings I should look for. For ultrasound, explain the expected sonographic findings and important differentials. 10. DIAGNOSIS Explain: * Presumptive diagnosis * Definitive diagnosis * Diagnostic criteria * How to interpret conflicting test results * Common diagnostic mistakes 11. TREATMENT PROTOCOL Give me a practical veterinary treatment protocol. For every drug include: * Generic name * Drug class * Indication * Dose in mg/kg * Route * Frequency * Duration * Maximum dose if relevant * Mechanism of action * Important adverse effects * Contraindications * Major drug interactions * Monitoring requirements Separate treatment into: A. Mild cases B. Moderate cases C. Severe/critical cases D. Emergency/ICU management Do NOT simply list drugs. Explain why each drug is being used. 12. FLUID THERAPY Explain: * Whether fluids are indicated * Choice of fluid * Maintenance requirement * Deficit calculation * Ongoing losses * Shock resuscitation when applicable * Fluid rate * Bolus strategy * Monitoring * When to reduce/stop fluids * Signs of fluid overload Give formulas and worked examples for different body weights. 13. DOSE CALCULATIONS Show me how to calculate doses. Use examples for: * 2 kg cat * 5 kg cat * 10 kg dog * 20 kg dog * 30 kg dog Show: Dose (mg) = body weight (kg) × dose (mg/kg) Then convert the dose into mL when a concentration is provided. If concentration is not provided, ask me for the exact product concentration rather than guessing. 14. SUPPORTIVE CARE Explain: * Nutrition * Feeding strategy * Anti-emetics * Analgesia * Gastroprotection * Antibiotic indications * Vitamins/electrolytes when indicated * Oxygen therapy * Blood products * Nursing care * Temperature management Clearly distinguish evidence-based indications from treatments that are commonly used but may not be necessary. 15. ANTIBIOTIC STEWARDSHIP If antibiotics are relevant: * When antibiotics are actually indicated * First-line choices * Alternative choices * Culture/sensitivity indications * Empirical therapy * De-escalation/step-down therapy * Duration * Important resistance considerations Never recommend antibiotics merely because a disease is serious if there is no bacterial indication. 16. PROGNOSIS Explain: * Good prognostic indicators * Poor prognostic indicators * Survival considerations * Factors affecting outcome * When referral/ICU/surgery is indicated 17. MONITORING Give me a monitoring sheet: * TPR * BP * SpO₂ * ECG when relevant * Urine output * Hydration * Pain * Appetite * Weight * CBC * Biochemistry * Electrolytes * Disease-specific markers Tell me how frequently each should be monitored in mild, moderate and severe cases. 18. COMMON CLINICAL MISTAKES Tell me the most common mistakes veterinarians make while diagnosing and treating this disease. Also tell me: “What can I miss if I focus only on the obvious diagnosis?” 19. RED FLAGS Give me a clear list of signs requiring: * Immediate hospitalization * Emergency stabilization * ICU * Blood transfusion * Surgery * Specialist referral 20. CASE SIMULATION Create a realistic dog/cat case. Give me only: * Signalment * History * Clinical examination * CBC * Biochemistry * Urinalysis * Imaging findings Then ask me to: 1. Identify major problems 2. Give differential diagnoses 3. Interpret CBC 4. Interpret biochemistry 5. Choose further tests 6. Give diagnosis 7. Create treatment plan 8. Calculate drug doses 9. Create monitoring plan 10. Give prognosis Do NOT reveal the answer initially. After I answer, evaluate my clinical reasoning like a senior veterinary clinician and correct every mistake. 21. QUICK CLINICAL ALGORITHM At the end, give me a one-page practical algorithm: Presentation → History → Examination → Differentials → Tests → Diagnosis → Treatment → Monitoring → Discharge/Follow-up 22. MEMORY TOOL Finish with: * 10 key points to remember * 10 important drug facts * 10 diagnostic clues * 10 common mistakes * 10 high-yield MCQs * 5 clinical pearls IMPORTANT RULES 1. Teach me at small-animal clinical-practice level, not merely textbook level. 2. Use dogs and cats separately whenever their management differs. 3. Explain difficult concepts in simple English + Hindi-English mix when needed. 4. Always explain the reasoning behind diagnostic and treatment decisions. 5. Never invent drug concentrations, laboratory values, guidelines, or doses. 6. For drug dosing, clearly distinguish standard/reference dosing from case-specific prescribing. 7. Flag drugs that are contraindicated or potentially dangerous in cats. 8. Mention important renal/hepatic dose considerations. 9. Mention when a drug requires therapeutic drug monitoring. 10. For critical/emergency diseases, prioritize stabilization using ABC principles before definitive diagnosis. 11. If current guidelines or drug recommendations may have changed, verify them using reliable veterinary sources before answering. 12. Cite authoritative sources/guidelines when making important clinical recommendations. 13. If my question is ambiguous, ask for the minimum information needed rather than making unsafe assumptions. 14. Do not overwhelm me with unexplained jargon. Teach the underlying physiology and clinical reasoning. 15. Train me to think like a veterinarian, not memorize lists. Start with the topic I provide and teach it from BEGINNER → INTERMEDIATE → ADVANCED → CLINICAL CASE LEVEL.

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This is a broad renal-medicine module. We will work through one clinically focused component at a time, using dogs and cats separately where needed.

Asking for Preferences

Which component should we cover in full first?

This is a broad renal-medicine module. We will work through one clinically focused component at a time, using dogs and cats separately where needed.

Reading File

Finding Sources

Searching PubMed

"Acute Kidney Injury" AND veterinary

Searching the Web

IRIS veterinary chronic kidney disease staging treatment recommendations dogs cats acute kidney injury guidelines

Chronic Kidney Disease and Acute Kidney Injury in Dogs and Cats: Learning Map

This topic has two linked but clinically distinct syndromes:

Chronic kidney disease (CKD)
- Persistent, usually irreversible loss of functional nephrons for at least 3 months
- IRIS diagnosis, staging, proteinuria and hypertension substaging
- Long-term outpatient management: renal diet, phosphorus, proteinuria, hypertension, nausea, anaemia, potassium, hydration, monitoring
Acute kidney injury (AKI)
- Abrupt loss of renal function over hours to days
- Emergency distinction among pre-renal, intrinsic renal, and post-renal azotaemia
- Toxin, leptospirosis, pyelonephritis, ischaemic, and obstructive AKI
- Stabilization, fluid prescription, electrolyte management, oliguria/anuria, dialysis referral
AKI versus CKD versus acute-on-chronic disease
- The highest-yield diagnostic reasoning skill in renal practice
- Historical clues, kidney size/architecture, anaemia, calcium-phosphate pattern, serial creatinine trends, urine findings, and response to rehydration
Renal diagnostic work-up
- Minimum database, urine collection and USG interpretation, sediment examination, urine culture, UPC, blood pressure, SDMA, serial renal values
- Radiography and ultrasound, including obstruction, pyelonephritis, nephrolithiasis, ureterolithiasis, and renal dysplasia
Renal emergency and ICU medicine
- ABC stabilization, hyperkalaemia and ECG changes, hypertension, fluid overload, oliguria/anuria, urinary obstruction, pulmonary oedema, haemodialysis/peritoneal dialysis referral
Clinic-ready therapeutics
- Evidence-based drug selection and renal dose adjustments
- Antiemetics, appetite support, gastroprotection, antihypertensives, RAAS blockade, phosphate binders, potassium support, anaemia treatment, analgesia, and antimicrobial stewardship
Case-based reasoning
- A dog with toxin-associated or leptospiral AKI
- A cat with IRIS stage 2-4 CKD
- A cat with ureteral obstruction and acute-on-chronic azotaemia

High-level clinical overview

CKD develops when sufficient nephron loss causes the remaining nephrons to hyperfilter. Initially this maintains GFR, but over time glomerular hypertension, proteinuria, tubulointerstitial inflammation, fibrosis, phosphorus retention, and hypertension accelerate loss of function. Clinical signs usually emerge once renal reserve is substantially reduced: polyuria/polydipsia, weight loss, reduced appetite, nausea/vomiting, dehydration, hypertension, proteinuria, hypokalaemia in cats, metabolic acidosis, anaemia, and eventually uraemic signs.

Diagnose and stage only a stable, hydrated patient after excluding pre-renal and post-renal causes. Current IRIS guidance uses creatinine and/or SDMA, then sub-stages for proteinuria and systemic blood pressure. Persistent renal proteinuria is generally UPC >0.5 in dogs and >0.4 in cats. IRIS staging guidance and the 2026 IRIS CKD pocket guide should be the core reference in practice.

AKI is a time-critical syndrome. Think in three categories:

Pre-renal: reduced renal perfusion, such as severe dehydration, shock, haemorrhage, low cardiac output.
Intrinsic renal: tubular, glomerular, interstitial, or vascular injury, such as ischaemia, nephrotoxins, leptospirosis, pyelonephritis, ethylene glycol exposure, grapes/raisins in dogs, or aminoglycosides.
Post-renal: urinary obstruction or urine leakage, especially feline urethral obstruction, bilateral ureteral obstruction, or uroabdomen.

For AKI, stabilization comes before a perfect diagnosis: assess perfusion, blood pressure, hydration, urine output, potassium, acid-base status, ECG when hyperkalaemia is possible, and evidence of obstruction. Do not give “standard fluids” blindly. Fluid volume must be prescribed from the patient’s deficit, maintenance needs, measurable ongoing losses, urine output, cardiovascular status, and repeated reassessment. Over-fluiding an oliguric/anuric AKI patient can be fatal.

A patient may have acute-on-chronic kidney disease: a previously compensated CKD patient suddenly decompensates due to dehydration, infection, obstruction, hypotension, nephrotoxins, or pancreatitis. Treat the reversible acute component, then reassess renal values and clinical stability before assigning an IRIS CKD stage. IRIS specifically advises using AKI grading in unstable acute cases rather than prematurely staging them as CKD. IRIS guidelines

Choose the first full module:

CKD foundation and IRIS staging
CKD practical outpatient treatment protocol
AKI emergency and ICU protocol
AKI vs CKD vs acute-on-chronic differentiation
Renal diagnostics, urinalysis, UPC, BP, SDMA, and imaging
Start with a case simulation, then learn through the case

Teach me CKD foundations and IRIS staging

Reading File

Finding Sources

Searching the Web

site:iris-kidney.com 2026 IRIS staging CKD dogs cats creatinine SDMA UPC blood pressure

Searching PubMed

"chronic kidney disease" AND dogs cats

This is a broad renal-medicine module. We will work through one clinically focused component at a time, using dogs and cats separately where needed.## Chronic Kidney Disease and Acute Kidney Injury in Dogs and Cats: Learning Map

This topic has two linked but clinically distinct syndromes:

Chronic kidney disease (CKD)
- Persistent, usually irreversible loss of functional nephrons for at least 3 months
- IRIS diagnosis, staging, proteinuria and hypertension substaging
- Long-term outpatient management: renal diet, phosphorus, proteinuria, hypertension, nausea, anaemia, potassium, hydration, monitoring
Acute kidney injury (AKI)
- Abrupt loss of renal function over hours to days
- Emergency distinction among pre-renal, intrinsic renal, and post-renal azotaemia
- Toxin, leptospirosis, pyelonephritis, ischaemic, and obstructive AKI
- Stabilization, fluid prescription, electrolyte management, oliguria/anuria, dialysis referral
AKI versus CKD versus acute-on-chronic disease
- The highest-yield diagnostic reasoning skill in renal practice
- Historical clues, kidney size/architecture, anaemia, calcium-phosphate pattern, serial creatinine trends, urine findings, and response to rehydration
Renal diagnostic work-up
- Minimum database, urine collection and USG interpretation, sediment examination, urine culture, UPC, blood pressure, SDMA, serial renal values
- Radiography and ultrasound, including obstruction, pyelonephritis, nephrolithiasis, ureterolithiasis, and renal dysplasia
Renal emergency and ICU medicine
- ABC stabilization, hyperkalaemia and ECG changes, hypertension, fluid overload, oliguria/anuria, urinary obstruction, pulmonary oedema, haemodialysis/peritoneal dialysis referral
Clinic-ready therapeutics
- Evidence-based drug selection and renal dose adjustments
- Antiemetics, appetite support, gastroprotection, antihypertensives, RAAS blockade, phosphate binders, potassium support, anaemia treatment, analgesia, and antimicrobial stewardship
Case-based reasoning
- A dog with toxin-associated or leptospiral AKI
- A cat with IRIS stage 2-4 CKD
- A cat with ureteral obstruction and acute-on-chronic azotaemia

High-level clinical overview

AKI is a time-critical syndrome. Think in three categories:

Pre-renal: reduced renal perfusion, such as severe dehydration, shock, haemorrhage, low cardiac output.
Intrinsic renal: tubular, glomerular, interstitial, or vascular injury, such as ischaemia, nephrotoxins, leptospirosis, pyelonephritis, ethylene glycol exposure, grapes/raisins in dogs, or aminoglycosides.
Post-renal: urinary obstruction or urine leakage, especially feline urethral obstruction, bilateral ureteral obstruction, or uroabdomen.

Choose the first full module:

CKD foundation and IRIS staging
CKD practical outpatient treatment protocol
AKI emergency and ICU protocol
AKI vs CKD vs acute-on-chronic differentiation
Renal diagnostics, urinalysis, UPC, BP, SDMA, and imaging
Start with a case simulation, then learn through the case

Quick answer

Chronic Kidney Disease Foundations and IRIS Staging

Small-animal GP clinical module: dogs and cats

This module focuses on recognising CKD, confirming it properly, understanding why signs develop, and applying IRIS staging/substaging correctly. Treatment protocols come next, because treatment must be stage- and complication-specific.

1. Basic Understanding

Definition

Chronic kidney disease (CKD) is persistent kidney damage and/or a persistent reduction in kidney function, generally present for at least 3 months. It is usually progressive and irreversible because functioning nephrons are permanently lost.

CKD is not synonymous with “high creatinine.”

A dog or cat can have CKD with:

Normal creatinine
Normal or minimally increased SDMA
Persistent proteinuria of renal origin
Inappropriately dilute urine
Abnormal renal imaging
Histologic renal disease

Conversely, a high creatinine result alone may reflect dehydration, obstruction, shock, muscle mass, recent feeding, or acute kidney injury.

Clinical rule:

Diagnose CKD in a stable, hydrated patient after excluding important pre-renal and post-renal causes of azotaemia.

The current IRIS CKD staging guidance states that staging should be based on fasting creatinine and/or SDMA, ideally both, measured on at least two occasions in a hydrated, stable patient.

Species affected

Dogs and cats both
CKD is particularly common in older cats
Dogs may have CKD secondary to congenital disease, familial nephropathies, glomerular disease, chronic pyelonephritis, leptospirosis-associated damage, or previous AKI

Age, breed, and sex predisposition

Cats

Usually middle-aged to geriatric, especially >10 years.

Potential breed associations include:

Persian and related breeds: polycystic kidney disease
Abyssinian: familial renal amyloidosis
Siamese/Oriental breeds: reported familial renal disorders in some lines
Maine Coon and others: congenital or inherited renal disease can occur, though less commonly than acquired geriatric CKD

Dogs

Can occur at any age.

Important breed-associated examples:

Shar-Pei: familial amyloidosis
English Cocker Spaniel: familial nephropathy
Bull Terrier: hereditary nephritis
Samoyed: X-linked hereditary nephropathy
Soft-Coated Wheaten Terrier: protein-losing nephropathy and glomerular disease
Doberman Pinscher, Labrador Retriever, Golden Retriever, Bernese Mountain Dog: glomerular disease is an important consideration
Shih Tzu, Lhasa Apso, Cairn Terrier, Miniature Schnauzer: congenital/familial renal disease can occur

Sex alone is not a major universal risk factor, but sex may matter in the underlying disease. For example, X-linked hereditary nephropathy is more severe in male dogs.

Epidemiology

CKD is among the most common chronic disorders of geriatric cats.
It is also common in older dogs, but canine CKD has more heterogeneous causes.
Many cases are detected late because the kidney has substantial reserve capacity.

Key practical point: Clinical signs generally become obvious only after a substantial loss of functioning nephrons. Therefore, proactive screening of senior animals matters.

Causes

Often, the initial cause is no longer identifiable by the time CKD is diagnosed. The final common pathway is nephron loss followed by fibrosis.

Major causes in dogs

Chronic glomerular disease
Chronic tubulointerstitial nephritis
Chronic pyelonephritis
Congenital renal dysplasia/hypoplasia
Familial nephropathy
Renal amyloidosis
Polycystic kidney disease
Chronic nephrolithiasis or ureteral obstruction
Recurrent or severe AKI
Leptospirosis-associated renal injury
Nephrotoxin exposure with incomplete recovery
Renal neoplasia, infiltrative disease, or chronic renal infarction

Major causes in cats

Chronic tubulointerstitial nephritis, often idiopathic
Recurrent/subclinical AKI or ischaemic injury
Chronic pyelonephritis
Ureterolithiasis and partial ureteral obstruction
Polycystic kidney disease
Renal lymphoma or infiltrative disease
Renal amyloidosis
Chronic glomerular disease, less common than in dogs
Previous toxin-related or hypotensive renal injury

Risk factors

Ask yourself: “Could this animal be at risk before its creatinine rises?”

Older age
Previous AKI
History of dehydration, anaesthesia-related hypotension, shock, heatstroke, haemorrhage
Exposure to nephrotoxins:
- NSAIDs, especially in dehydrated or hypotensive animals
- Aminoglycosides
- Amphotericin B
- Cisplatin in dogs
- Ethylene glycol
- Grapes/raisins in dogs
- Lilies in cats
- Cholecalciferol rodenticides
Recurrent urinary tract infection or pyelonephritis
Proteinuria
Systemic hypertension
Hyperthyroidism in cats, including “masked CKD” after treatment
Heart disease and low renal perfusion
Chronic inflammatory or infectious disease
Urolithiasis, especially feline ureteral stones
Breed/family history of renal disease

IRIS recommends monitoring at-risk patients with body weight, body condition, blood pressure, urinalysis, and renal markers. Serial upward trends within a laboratory reference interval may be clinically meaningful. See IRIS CKD risk-factor guidance.

2. Pathogenesis: Think in Nephrons

The simple version

Kidney damage causes nephron loss. The surviving nephrons work harder to compensate. This initially maintains GFR, but eventually damages the remaining nephrons too.

Hindi-English memory line:

“Nephron kam hote jaate hain, bache hue nephrons overwork karte hain, aur woh overwork itself further damage karta hai.”

Step-by-step

Step 1: Initial renal insult

An initial event damages nephrons, for example:

Inflammation
Ischaemia
Toxin
Glomerular disease
Infection
Obstruction
Congenital malformation

Step 2: Nephron number falls

Each lost nephron is permanent. The kidney has reserve capacity, so early disease can be silent.

Step 3: Surviving nephrons hyperfilter

Remaining nephrons increase their single-nephron GFR to maintain total filtration.

Initially, this is adaptive.

Step 4: Intraglomerular hypertension develops

Increased pressure in individual glomeruli contributes to:

Glomerular injury
Protein leakage into urine
Further nephron loss

Step 5: Proteinuria causes more renal damage

Filtered proteins are not harmless. Tubular uptake of excess protein promotes:

Tubular inflammation
Oxidative injury
Fibrosis
Progressive nephron destruction

Thus, proteinuria is both a marker of kidney injury and a driver of progression.

Step 6: Tubulointerstitial fibrosis develops

Progressive inflammation and scarring replace functioning renal tissue.

Step 7: Complications of reduced GFR appear

As GFR declines:

Water conservation fails: polyuria
Compensatory thirst develops: polydipsia
Phosphate retention occurs: hyperphosphataemia and CKD-mineral bone disorder
Nitrogenous waste accumulates: azotaemia/uraemia
Acid excretion falls: metabolic acidosis
Potassium balance becomes abnormal, commonly hypokalaemia in cats
Erythropoietin production falls: non-regenerative anaemia
Hypertension and proteinuria worsen progression
Nausea, vomiting, muscle wasting, weakness, and poor appetite develop

3. Why the Clinical Signs Occur

Clinical sign	Mechanism	Clinical interpretation
Polyuria	Loss of concentrating ability due to tubular/interstitial dysfunction and reduced medullary gradient	Often an early sign
Polydipsia	Compensatory response to urinary water loss	Ask specifically about water intake
Weight loss	Reduced appetite, muscle catabolism, dehydration, uraemia, protein loss	Common and prognostically important
Reduced appetite	Uraemic toxins, nausea, acidosis, altered taste/smell, oral disease	Do not assume “picky eater”
Vomiting/nausea	Uraemia, gastritis, GI dysmotility, metabolic disturbances	May be intermittent
Dehydration	Increased urinary losses plus reduced drinking/appetite	Can falsely increase creatinine
Halitosis	Uraemic odour and oral disease	Consider oral ulcers in advanced uraemia
Oral ulceration	Uraemic mucosal injury	Severe uraemia, poor prognostic sign
Lethargy/weakness	Anaemia, uraemia, acidosis, electrolyte abnormalities, hypertension	Non-specific but important
Muscle wasting	Chronic inflammation, inadequate calorie intake, catabolism, protein loss	Creatinine may underestimate CKD in cachectic patients
Constipation	Dehydration, hypokalaemia, reduced intake	Common in CKD cats
Retinal lesions/blindness	Systemic hypertension	Emergency: check BP immediately
Neurologic signs	Severe hypertension or uraemic encephalopathy	Emergency
Bradycardia/arrhythmia	Hyperkalaemia, more typical in severe AKI or obstruction than stable CKD	Emergency ECG indication

4. Ready-to-Use CKD History Checklist

Presenting complaint

What brought the pet in today?
Is the problem reduced appetite, vomiting, drinking more, urinating more, weight loss, weakness, or a laboratory abnormality?

Duration and progression

When did you first notice changes?
Sudden onset or gradual?
Stable, slowly progressive, or rapidly worsening?
Any previous episodes of dehydration, vomiting, hospitalisation, or “kidney values high”?

Clinical reasoning: Sudden severe deterioration raises AKI, obstruction, pyelonephritis, toxin exposure, or acute-on-chronic disease.

Appetite and feeding

Eating normally, reduced, selective, or completely anorexic?
Any nausea signs: lip licking, hypersalivation, sniffing food then walking away, teeth grinding, hiding?
Weight loss despite eating?
Current diet, treats, table food, raw food, supplements?

Water intake and urination

Has drinking increased?
Can the owner quantify mL/day if possible?
Larger urine clumps or more frequent urination?
Any stranguria, dysuria, haematuria, periuria, reduced urine output, or inability to urinate?
Any urine leakage?

Important: PU/PD supports CKD but is not diagnostic. Oliguria/anuria suggests an emergency, obstruction, severe AKI, or severe acute-on-chronic decompensation.

GI signs

Vomiting frequency and appearance?
Diarrhoea?
Melena?
Constipation or tenesmus?
Halitosis or oral discomfort?

Medication and toxin history

Ask specifically:

NSAID name, dose, and timing
Aminoglycosides
Chemotherapy
Antifungals, particularly amphotericin B
ACE inhibitors, ARBs, diuretics
Recent anaesthesia or hypotension
Human medications
Herbal products/supplements
Lilies in cats
Ethylene glycol
Grapes/raisins in dogs
Rodenticides
Recent contrast exposure

Previous disease

Prior urinary tract infection?
Urolithiasis?
Urethral obstruction?
Pyelonephritis?
Hypertension?
Heart disease?
Diabetes mellitus?
Hyperthyroidism in cats?
Tick-borne, infectious, or immune-mediated disease?
Leptospirosis vaccination/exposure risk in dogs?

Lifestyle and exposure

Outdoor access?
Wildlife, stagnant water, rodents, livestock, floodwater exposure?
Travel, boarding, new animals?
Tick/flea exposure?
Reproductive history if congenital disease is possible or breeding is relevant

5. Clinical Examination: What to Look For

TPR and general appearance

Look for:

Weight loss and muscle condition score loss
Poor coat quality
Lethargy
Dehydration
Hypothermia in severely uraemic or septic patients
Fever if pyelonephritis, leptospirosis, or systemic inflammation is possible

Mucous membranes and CRT

Finding	Meaning
Pale mucous membranes	Anaemia, often non-regenerative CKD anaemia; also consider bleeding
Dry/tacky mucous membranes	Dehydration
Injected/red mucous membranes	Hypertension, inflammation, heat stress, sepsis
Uraemic oral odour	Advanced uraemia
Oral ulcers	Severe uraemia, though not exclusive to renal disease
Prolonged CRT	Hypoperfusion/dehydration
Short CRT	Hyperdynamic circulation, vasodilation, stress, inflammation

Hydration

Assess:

Skin turgor
Mucous membrane moisture
Globe position
Peripheral pulse quality
Body weight compared with prior visits
Packed cell volume/total solids in context

Caution: Skin tenting is less reliable in geriatric or cachectic animals. CKD patients can be dehydrated despite apparent oedema or high body weight.

Body and muscle condition

Record:

BCS /9
Muscle condition score
Current weight
Percentage weight change from baseline

A falling creatinine in a cat with progressive muscle loss does not necessarily mean improved kidney function.

Cardiovascular examination

Assess:

Heart rate and rhythm
Murmur/gallop rhythm
Pulse quality
Blood pressure
Evidence of fluid overload: tachypnoea, murmur changes, gallop, crackles, serous nasal discharge, chemosis, oedema

Every CKD patient should have systolic blood pressure measured.

Abdominal palpation

Look for:

Small, irregular kidneys: supports chronicity
Enlarged kidneys: infiltrative disease, hydronephrosis, pyelonephritis, neoplasia, acute injury, compensatory hypertrophy
Renal pain: pyelonephritis, AKI, obstruction, infarction, renal capsular distension
Tense bladder: obstruction until proven otherwise
Abdominal fluid: consider uroabdomen, neoplasia, severe hypoalbuminaemia, cardiac disease

Important: Normal-sized kidneys do not exclude CKD, especially in cats.

Eyes

Perform fundic examination if possible. Look for:

Retinal haemorrhage
Retinal detachment
Tortuous vessels
Hyphema
Acute blindness

These may indicate severe systemic hypertension and require urgent intervention.

Neurologic examination

Relevant when there is:

Acute blindness
Ataxia
Seizures
Altered mentation
Vestibular signs

Consider hypertensive encephalopathy, uraemic encephalopathy, toxin exposure, or primary neurologic disease.

6. Expected Laboratory Patterns in CKD

CBC

Parameter	Expected change	Why	Clinical meaning
PCV/HCT, Hb, RBC count	Decreased in moderate-advanced CKD	Reduced erythropoietin production, shortened RBC survival, chronic inflammation, iron deficiency	Usually non-regenerative anaemia
Reticulocytes	Inappropriately low/normal	Marrow not adequately stimulated	Supports non-regenerative anaemia
MCV/MCHC	Usually normocytic, normochromic	Typical chronic disease/erythropoietin-deficient pattern	Macrocytosis or hypochromia suggests another process too
WBC	Often normal	CKD itself does not inherently cause leukocytosis	Neutrophilia/left shift suggests inflammation, infection, stress, pyelonephritis, pancreatitis, etc.
Platelets	Often normal or mildly increased	Inflammation/reactive thrombocytosis possible	Verify platelet clumping, especially in cats

CKD anaemia: practical interpretation

Classic pattern:

Low PCV/HCT
Low Hb
Low RBC count
Normal MCV
Normal MCHC
Low or inappropriately normal reticulocyte response

This is a non-regenerative anaemia.

Do not attribute every anaemia in a CKD patient to CKD. Also assess for:

GI blood loss
Iron deficiency
Haemolysis
Haemorrhage
Bone marrow disease
Neoplasia
Infectious disease
Drug effects

Serum biochemistry

Parameter	Typical finding	Mechanism and clinical relevance
BUN/urea	Increased	Reduced renal excretion, but also rises with dehydration, GI bleeding, high-protein intake, catabolism
Creatinine	Increased	Reduced GFR; affected by muscle mass and hydration
SDMA	Increased	Reflects reduced GFR and may rise earlier than creatinine; interpret persistently and in context
Phosphorus	Increased, often later	Reduced renal excretion; associated with CKD-mineral bone disorder and progression
Potassium	Often decreased in cats; may be normal/high in advanced disease	Urinary losses, poor intake, vomiting; hyperkalaemia suggests severe oliguric disease, obstruction, or hypoadrenocorticism
Total calcium	Variable	Ionised calcium is more clinically informative; do not diagnose hypercalcaemia from total calcium alone
Bicarbonate/total CO₂	May decrease	Metabolic acidosis from reduced acid excretion
Albumin	Low, normal, or high	Low with protein-losing nephropathy/inflammation; high with dehydration
Globulins	May increase	Inflammation, infection, immune stimulation; marked increase needs broader investigation
Cholesterol	Increased in some proteinuric cases	Protein-losing nephropathy/nephrotic syndrome
Sodium/chloride	Variable	Depend on fluid status, vomiting, diuretics, and tubular disease
ALT/ALP/GGT	Usually not primary CKD markers	Abnormalities should prompt investigation for concurrent disease
Glucose	Usually normal	Persistent glucosuria with normoglycaemia suggests tubular dysfunction
Amylase/lipase	May increase	Reduced renal clearance may contribute; do not diagnose pancreatitis from this alone

Creatinine: strengths and limitations

Creatinine is useful because it is inexpensive and practical, but:

It rises late in disease
It is influenced by muscle mass
It increases with dehydration
It may look “better” in a muscle-wasted patient despite worsening GFR
Large-breed dogs can have higher baseline creatinine
Greyhounds may have high baseline creatinine and SDMA
Healthy Birman cats can have higher SDMA and creatinine than many cats

SDMA: strengths and limitations

SDMA can detect smaller decreases in GFR earlier than creatinine and is less influenced by lean body mass.

However:

It is not a stand-alone diagnosis
Confirm persistence
Interpret alongside hydration, urine concentration, imaging, UPC, blood pressure, and serial trends
Do not label a dehydrated vomiting cat as CKD based on one SDMA result

A 2026 systematic review assessed SDMA diagnostic accuracy in dogs and cats, but biomarker interpretation still requires clinical context: Scobie et al., 2026.

7. Urinalysis: Essential for Every Suspected CKD Patient

How to collect

Cystocentesis is preferred for culture and generally preferred for a diagnostic sample.
Free-catch samples are acceptable for screening but are less reliable for culture and sediment interpretation.
Analyse promptly. Delayed analysis alters sediment, pH, cells, and bacterial interpretation.

Urine specific gravity, USG

Practical interpretation

Dog: USG <1.030 in an azotaemic dog is inappropriately dilute and supports renal dysfunction.
Cat: USG <1.035 in an azotaemic cat is inappropriately dilute and supports renal dysfunction.

But:

Some CKD cats can retain a USG >1.035.
A concentrated urine sample does not completely exclude early CKD.
A dilute urine sample is not automatically CKD. Consider diabetes mellitus, hyperthyroidism, hyperadrenocorticism, pyometra, liver disease, diuretics, psychogenic polydipsia, hypercalcaemia, hypokalaemia, and AKI.

Protein

Dipstick protein is only a screen.

If protein persists:

Examine sediment.
Exclude haematuria, pyuria, active UTI, and marked inflammation.
Confirm with a urine protein:creatinine ratio, UPC.
Repeat to document persistence.

Sediment

Look for:

RBCs: cystocentesis contamination, stones, inflammation, neoplasia, glomerular disease
WBCs: inflammation/UTI/pyelonephritis
Bacteria: culture confirmation needed, especially in a quiet urine sediment
Casts: tubular injury, but absence does not exclude renal disease
Crystals: assess type, pH, context, and imaging
Renal epithelial cells: may support renal tubular injury if numerous, but interpretation is limited

Urine culture

Culture is indicated when:

Pyuria, bacteriuria, or inflammatory sediment is present
Pyelonephritis is suspected
There is recurrent UTI
There is unexplained renal deterioration
Antibiotics are being considered
A proteinuric patient may have occult UTI

Do not give antibiotics merely because the patient has CKD or azotaemia.

8. Diagnosing CKD Before Staging It

CKD diagnosis requires persistence and context

You may diagnose CKD when there is persistent evidence of renal structural or functional disease in a stable patient.

Findings supporting CKD

Persistent azotaemia after correction of dehydration/pre-renal factors
Persistent increased SDMA
Persistent renal proteinuria
Persistently inadequate urine concentration
Small/irregular kidneys
Renal architectural abnormalities on ultrasound
Renal biopsy findings, when indicated and safe
Persistent renal abnormalities over at least 3 months

Early CKD: do not wait for azotaemia

A patient may be in IRIS Stage 1 with normal creatinine.

Possible Stage 1 indicators:

Persistent SDMA above the laboratory reference interval
Persistent renal proteinuria after exclusion of urinary inflammation
Renal imaging abnormalities
Inappropriately dilute urine after exclusion of other causes
Documented rising creatinine/SDMA trend with no pre-renal explanation

9. IRIS CKD Staging: The Practical System

When can you stage?

Stage only when the patient is:

Hydrated/euvolemic
Clinically stable
Not in an evolving AKI episode
Not obstructed
Not showing a major untreated pre-renal cause
Evaluated on at least two occasions where possible

Do not IRIS-stage a cat with ureteral obstruction, a blocked cat, a shocked dog, or a dehydrated vomiting patient on first presentation. That patient needs AKI/post-renal assessment and stabilization.

IRIS specifically distinguishes unstable AKI from stable CKD. IRIS staging system

Step 1: Assign the creatinine stage

Use fasting serum creatinine in a stable, hydrated patient.

IRIS CKD stage	Dogs: creatinine	Cats: creatinine	General meaning
Stage 1	<1.4 mg/dL	<1.6 mg/dL	Non-azotaemic CKD with another marker of renal disease
Stage 2	1.4-2.8 mg/dL	1.6-2.8 mg/dL	Mild renal azotaemia
Stage 3	2.9-5.0 mg/dL	2.9-5.0 mg/dL	Moderate renal azotaemia
Stage 4	>5.0 mg/dL	>5.0 mg/dL	Severe renal azotaemia

Equivalent values in µmol/L should be used if your laboratory reports SI units.

Step 2: Integrate SDMA

IRIS CKD stage	SDMA concentration
Stage 1	<18 µg/dL, but persistent 15-17 µg/dL can support Stage 1 CKD when other evidence exists
Stage 2	18-35 µg/dL
Stage 3	36-54 µg/dL
Stage 4	>54 µg/dL

Important IRIS SDMA adjustments

Situation 1: Creatinine is normal but SDMA is persistently increased

If creatinine is in Stage 1 range but SDMA is persistently >18 µg/dL, the patient should generally be considered Stage 2, assuming CKD is established and the patient is stable.

Situation 2: Creatinine indicates Stage 2 but SDMA is high

If creatinine is Stage 2 but SDMA is persistently >35 µg/dL, IRIS recommends managing the patient as Stage 3.

This is particularly important in patients with reduced muscle mass, where creatinine may understate functional loss.

Situation 3: Creatinine and SDMA conflict

Do not “average” the stages.

First ask:

Is the patient truly hydrated and stable?
Has fasting status been controlled?
Is muscle mass low?
Could there be hyperthyroidism, hypercalcaemia, proteinuria, infection, obstruction, or AKI?
Are results persistent on serial testing?
Is there imaging evidence of chronic renal disease?

Then follow the IRIS guidance that treats a discordantly high persistent SDMA as clinically meaningful.

10. Stage 1: What It Really Means

Definition

Stage 1 CKD means there is evidence of kidney disease, but the patient is not yet azotaemic.

Examples

Example A

A 9-year-old cat:

Creatinine: 1.5 mg/dL
SDMA: 16, then 17 µg/dL on repeat
USG: 1.020
Renal ultrasound: mild irregular renal contour
UPC: 0.15
Normal BP

This can be consistent with IRIS Stage 1 CKD.

Example B

A dog:

Creatinine: 1.2 mg/dL
Persistent UPC: 1.2 after infection and lower urinary tract inflammation are excluded
SDMA: 15 µg/dL
Normal BP

This may be Stage 1 CKD, depending on the full investigation and persistence.

GP takeaway

Stage 1 is not “nothing.” It is where you can:

Avoid nephrotoxins
Identify and treat the cause or modifiable complications
Manage hypertension/proteinuria when indicated
Set a baseline
Monitor progression closely

11. Substaging: Proteinuria

Why proteinuria matters

Proteinuria predicts progression and poorer outcomes. It can also directly contribute to tubular injury and fibrosis.

A 2026 meta-analysis examined the value of UPC in dogs with CKD, supporting its clinical role, although UPC must always be interpreted in relation to sediment and the patient’s overall disease process: UPC evidence review.

IRIS UPC categories

Category	Dogs	Cats
Non-proteinuric	<0.2	<0.2
Borderline proteinuric	0.2-0.5	0.2-0.4
Proteinuric	>0.5	>0.4

Before calling it renal proteinuria

Do not interpret UPC in isolation. First exclude:

Pre-renal proteinuria

Fever
Exercise
Seizures
Hyperviscosity
Haemoglobinuria
Myoglobinuria

Post-renal proteinuria

Cystitis
Urethritis
Prostatitis
Pyelonephritis
Urolithiasis
Haematuria
Urinary tract neoplasia
Genital contamination

Practical protocol

Collect urine, ideally by cystocentesis.
Perform urinalysis and sediment examination.
Culture when infection is suspected.
Treat infection/inflammation if present.
Repeat UPC after resolution.
Document persistent proteinuria with repeat UPC values.

Do not automatically start RAAS blockade based on one UPC from a bloody, pyuric, bacteriuric urine sample.

12. Substaging: Blood Pressure

Why blood pressure matters

Systemic hypertension can:

Cause retinal haemorrhage/detachment and blindness
Cause neurologic signs and encephalopathy
Worsen glomerular injury and proteinuria
Accelerate CKD progression
Contribute to cardiac remodeling

IRIS blood-pressure risk categories

SBP	Category	Risk of target-organ damage
<140 mmHg	Normotensive	Minimal
140-159 mmHg	Prehypertensive	Low
160-179 mmHg	Hypertensive	Moderate
≥180 mmHg	Severely hypertensive	High

Clinical caveat

Any evidence of target-organ damage changes urgency, even if the measured systolic pressure is not repeatedly ≥180 mmHg.

Target-organ damage includes:

Retinal haemorrhage
Retinal detachment
Sudden blindness
Hypertensive encephalopathy
Neurologic signs
Proteinuria attributed to hypertension
Cardiac changes compatible with hypertension

How to measure blood pressure properly

Let the patient acclimatise in a quiet room.
Avoid measuring immediately after stressful procedures.
Use an appropriate cuff, approximately 30%-40% of limb/tail circumference.
Use Doppler blood pressure measurement when available.
Obtain at least 5 to 7 consistent readings.
Discard obvious outliers and often the first reading.
Record:
- Device
- Cuff site and size
- Position
- Patient demeanour
- Individual values and mean/median
Repeat on another day if the animal is clinically stable and there is no target-organ damage.

Do not diagnose chronic hypertension from one anxious, struggling cat with an isolated SBP of 180 mmHg.

13. CKD Diagnostic Algorithm for General Practice

Suspected CKD / incidental azotaemia / PU-PD / weight loss
                    ↓
History + complete physical examination
                    ↓
Minimum database:
CBC + serum biochemistry + electrolytes + urinalysis with USG + sediment
                    ↓
Assess hydration, perfusion, urine output, bladder, and obstruction risk
                    ↓
Is azotaemia potentially pre-renal, renal, or post-renal?
                    ↓
Correct reversible pre-renal factors and relieve obstruction if present
                    ↓
Repeat renal values in stable, hydrated patient
                    ↓
Persistent renal abnormality?
  ├─ No: investigate other causes, monitor if at risk
  └─ Yes:
       ↓
    Confirm CKD evidence:
    - persistent creatinine/SDMA abnormality
    - inadequate USG
    - persistent renal proteinuria
    - abnormal renal imaging
       ↓
    Perform:
    UPC + urine culture as indicated + BP measurement + ultrasound
       ↓
    Assign IRIS stage from creatinine/SDMA
       ↓
    Substage by UPC and BP
       ↓
    Identify complications:
    phosphorus, potassium, acidosis, anaemia, nausea,
    weight/muscle loss, dehydration, hypertension
       ↓
    Create stage-specific management and monitoring plan

14. Minimum Database and Recommended Tests

Minimum database

For every suspected CKD patient:

CBC
Serum biochemistry
Electrolytes
Creatinine
BUN/urea
Phosphorus
Albumin and total protein
Potassium
Total calcium, with ionised calcium if indicated
Urinalysis with USG and sediment
Body weight, BCS, muscle condition score
Blood pressure

Recommended tests

SDMA
UPC
Urine culture and susceptibility when indicated
Abdominal ultrasound
Urinary tract radiographs when stones are possible
Total T4 in older cats
FeLV/FIV testing where clinically appropriate
Leptospira testing in dogs with acute deterioration or compatible exposure
Acid-base assessment, especially in moderate/advanced disease
Ionised calcium if total calcium is abnormal
Fasting triglycerides/cholesterol in marked proteinuria
Fundic examination

Advanced or selective tests

Renal biopsy when results will change management and bleeding risk is acceptable
Infectious disease testing based on geography and exposure
GFR testing in selected referral cases
CT for ureteral disease, renal masses, complex stones, surgical planning
Echocardiography if heart disease affects fluid or antihypertensive planning

15. Imaging Foundations

Radiography

When useful

Suspected nephroliths/ureteroliths
Mineralised stones
Renal size and symmetry assessment
Ureteral obstruction screening
Follow-up of known radiopaque calculi

Recommended views

Right lateral abdomen
Left lateral abdomen
Ventrodorsal abdomen

CKD-compatible findings

Small kidneys
Irregular renal contour
Bilateral renal mineralisation
Nephroliths
Ureteroliths
Compensatory enlargement of one kidney when the other is atrophic

Radiographs have limited sensitivity for non-mineralised stones, renal parenchymal disease, pyelonephritis, and early CKD.

Ultrasound

When useful

Ultrasound is the most useful first-line imaging modality for suspected CKD.

Look for:

Small kidneys
Irregular contour
Increased cortical echogenicity
Loss of corticomedullary distinction
Renal infarcts
Cysts
Nephrolithiasis
Pyelectasia
Ureteral dilation
Renal masses
Perirenal fluid
Asymmetry
Changes compatible with chronic obstruction or pyelonephritis

Important caution

Ultrasound supports renal disease, but it often does not provide a definitive aetiology. “Chronic renal changes” is a descriptive imaging conclusion, not a final diagnosis.

Red flags on ultrasound

Pyelectasia plus ureteral dilation: investigate obstruction and pyelonephritis
Enlarged painful kidneys: AKI, pyelonephritis, lymphoma, infiltration, hydronephrosis
One small kidney plus one enlarged kidney: chronic unilateral disease with contralateral compensation
Feline ureterolith plus azotaemia: emergency/referral-level concern

16. CKD Versus AKI: Initial Differentiation

Feature	CKD	AKI	Acute-on-chronic
History	Weeks to months of PU/PD, weight loss	Hours to days, toxin, shock, illness	Chronic signs with sudden deterioration
Kidney size	Often small/irregular, but may be normal	Often normal/enlarged	Variable
Anaemia	Common in moderate/advanced CKD	Less expected early	May be present
Phosphorus	Often high in advanced CKD	Can be high	May be high
Clinical onset	Gradual	Acute	Acute worsening of chronic disease
Urine output	Usually polyuric	Variable, may be oliguria/anuria	Variable
Response to rehydration	Azotaemia remains	May improve if pre-renal component	Partial improvement
Prior records	Progressive long-term trends	Previously normal values may exist	Previous CKD evidence plus acute change

Do not assume small kidneys prove CKD and enlarged kidneys prove AKI. There are exceptions.

17. Common Diagnostic Mistakes

Staging a dehydrated animal on its first visit.
Correct dehydration and repeat assessment if clinically safe.
Calling every azotaemic animal CKD.
Rule out pre-renal and post-renal causes.
Using creatinine alone.
Review SDMA, muscle mass, USG, UPC, BP, trends, and imaging.
Missing Stage 1 CKD because creatinine is normal.
Persistent renal proteinuria, imaging changes, low USG, or persistent SDMA elevation may reveal early CKD.
Ignoring urine sediment before interpreting UPC.
Haematuria, pyuria, and infection can falsely elevate UPC.
Calling a cat hypertensive from one anxious reading.
Use appropriate technique and repeat measurements unless target-organ damage is obvious.
Missing hypertensive ocular disease.
Fundic examination should be routine in CKD.
Assuming proteinuria is “just because of CKD.”
Investigate UTI, pyelonephritis, lower urinary tract inflammation, glomerular disease, and systemic hypertension.
Interpreting lower creatinine as renal improvement in a cachectic patient.
Muscle loss lowers creatinine production.
Missing acute-on-chronic decompensation.
A CKD patient with sudden vomiting, oliguria, renal pain, or a steep creatinine increase needs urgent assessment for obstruction, infection, toxins, hypoperfusion, and AKI.

18. CKD Staging Worked Examples

Case 1: Early feline CKD

A 12-year-old DSH cat:

Creatinine: 1.5 mg/dL
SDMA: 16 µg/dL, repeated at 17 µg/dL
USG: 1.021
Ultrasound: mild bilateral cortical irregularity
UPC: 0.16
SBP: 148 mmHg

Interpretation

CKD is supported by persistent SDMA elevation, low USG, and imaging abnormalities.
Creatinine fits Stage 1.
SDMA 15-17 supports Stage 1.
UPC <0.2: non-proteinuric.
SBP 140-159: prehypertensive.

Classification

IRIS Stage 1 CKD, non-proteinuric, prehypertensive.

Case 2: Proteinuric dog

An 8-year-old Labrador Retriever:

Creatinine: 2.2 mg/dL
SDMA: 24 µg/dL
USG: 1.017
UPC: 1.5, confirmed twice after negative urine culture
SBP: 168 mmHg

Interpretation

Stage 2 by creatinine and SDMA.
Proteinuric, because UPC >0.5 in a dog.
Hypertensive, because SBP 160-179 mmHg.

Classification

IRIS Stage 2 CKD, proteinuric, hypertensive.

This dog warrants active investigation for glomerular disease and management of hypertension/proteinuria, not merely “renal diet and recheck later.”

Case 3: Creatinine-SDMA discrepancy

A 14-year-old cat with marked muscle loss:

Creatinine: 2.4 mg/dL
SDMA: 40 µg/dL on two tests
USG: 1.015
UPC: 0.18
SBP: 155 mmHg

Interpretation

Creatinine suggests Stage 2.
Persistent SDMA >35 µg/dL suggests Stage 3 functional impairment.
Low muscle mass may be causing creatinine to underestimate renal impairment.

Classification

Manage as IRIS Stage 3 CKD, non-proteinuric, prehypertensive, after confirming clinical stability and excluding acute factors.

19. Monitoring Frequency for Stable CKD

Patient category	Suggested reassessment
At-risk but no CKD evidence	Initially every 3 months; if stable, every 6-12 months
IRIS Stage 1	Every 3-6 months
IRIS Stage 2	Every 3-6 months, sooner after treatment changes
IRIS Stage 3	Every 1-3 months
IRIS Stage 4	Every 1-4 weeks initially, then individualized
Any unstable/decompensated patient	Hospital or frequent reassessment based on severity

At each CKD monitoring visit, assess:

History: appetite, nausea, vomiting, water intake, urination, activity
Weight, BCS, muscle condition score
Hydration
Blood pressure
Creatinine, BUN, SDMA trend where useful
Phosphorus
Potassium
Total CO₂/bicarbonate where available
CBC, especially PCV/HCT
Urinalysis and UPC as indicated
Urine culture if infection is suspected
Fundic examination if hypertensive or visual signs occur

20. Quick Clinical Algorithm

Senior dog/cat, PU/PD, weight loss, vomiting, or incidental azotaemia
                         ↓
CBC + biochemistry + electrolytes + urinalysis/USG/sediment + BP
                         ↓
Pre-renal? Post-renal? AKI? Acute-on-chronic?
                         ↓
Correct dehydration / stabilize / relieve obstruction / investigate acute disease
                         ↓
Repeat renal values when stable and hydrated
                         ↓
Persistent renal abnormality for ≥3 months or strong chronic evidence?
                         ↓
Confirm CKD:
- creatinine and SDMA trend
- USG
- UPC after excluding active sediment/UTI
- BP
- imaging
                         ↓
IRIS Stage 1-4 using creatinine and SDMA
                         ↓
Substage:
- Proteinuria: UPC
- Hypertension: systolic BP
                         ↓
Identify complications:
phosphate, potassium, acidosis, anaemia, nausea,
weight loss, dehydration, hypertension
                         ↓
Stage-specific treatment and monitoring plan

21. Ten Key Points to Remember

CKD is a diagnosis of persistent renal structural or functional disease, not simply elevated creatinine.
Stage only stable, hydrated patients after excluding important pre-renal and post-renal causes.
CKD can exist with normal creatinine, particularly in Stage 1.
SDMA can identify reduced GFR earlier than creatinine but must be interpreted in context and as a trend.
Muscle wasting can make creatinine deceptively low.
Dogs with UPC >0.5 and cats with UPC >0.4 are proteinuric by IRIS criteria.
Blood pressure is essential in every CKD patient.
SBP ≥160 mmHg requires attention, especially when target-organ damage is present.
Fundic examination can identify hypertensive emergency before irreversible blindness occurs.
A sudden worsening in a CKD patient is acute-on-chronic disease until proven otherwise.

22. Ten Diagnostic Clues

Chronic PU/PD plus weight loss
Persistent azotaemia after rehydration
Persistent SDMA elevation
Inadequately concentrated urine in an azotaemic patient
Persistent renal proteinuria
Small, irregular kidneys
CKD-pattern non-regenerative anaemia
Hyperphosphataemia in more advanced disease
Retinal lesions from hypertension
Serial upward creatinine/SDMA trend, even before the reference interval is exceeded

23. Five Clinical Pearls

Never stage first, hydrate later. First determine whether azotaemia is pre-renal, renal, or post-renal.
A normal creatinine does not equal normal kidneys. Stage 1 CKD is where early detection can matter most.
UPC requires a clean context. Blood, inflammation, and bacteria can create misleading proteinuria.
Measure blood pressure correctly. One stressed reading is not a diagnosis, but retinal detachment with hypertension is an emergency.
Treat the patient and trends, not one laboratory number. Appetite, muscle mass, hydration, phosphorus, potassium, blood pressure, UPC, SDMA, and serial creatinine all matter.

Case Simulation: Your Turn

A 13-year-old neutered male domestic shorthair cat is presented for weight loss and intermittent vomiting.

History

Six-month history of increased drinking and larger urine clumps
Gradual loss of 0.8 kg over 5 months
Appetite reduced for 2 weeks; walks to food, sniffs it, then leaves
Vomited twice in the last week
No known lily exposure
No current medication
Indoor only

Examination

Weight 3.6 kg, BCS 4/9, moderate epaxial muscle loss
Mild dehydration estimated at 5%
HR 180/min, no murmur; femoral pulses adequate
SBP: 172, 168, 170, 166, 169 mmHg by Doppler after acclimatisation
Fundus: mild retinal vascular tortuosity, no detachment
Kidneys small and irregular bilaterally on palpation
Mild halitosis; no oral ulcers

CBC

HCT: 27%
Hb: decreased
RBC count: decreased
MCV: normal
MCHC: normal
Reticulocytes: inappropriately low
WBC and platelets: within reference interval

Biochemistry

Creatinine: 3.3 mg/dL
BUN: increased
SDMA: 42 µg/dL
Phosphorus: 6.7 mg/dL
Potassium: 3.3 mmol/L
Total CO₂: mildly decreased
Albumin: normal
Total calcium: within reference interval

Urinalysis

USG: 1.018
Protein: trace
Sediment: inactive
UPC: 0.28
Urine culture: negative

Imaging

Ultrasound: bilaterally small irregular kidneys with reduced corticomedullary distinction; no pyelectasia, ureteral dilation, or stones.

Answer these before checking treatment in the next module:

List the major problem list.
Interpret the CBC.
Interpret the biochemistry and urinalysis.
Give the IRIS stage and both substages.
State what makes this CKD rather than uncomplicated AKI.
List the immediate treatment priorities.
Give a monitoring plan for the next month.

each me CKD foundations and IRIS staging

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