Internal medicineWhy staging comes after diagnosis, what SDMA actually tells you, and how the proteinuria and blood pressure substages change what you treat.
Chronic kidney disease is among the most common internal medicine conditions in older cats, and its prevalence rises steeply past fifteen years of age. The diagnosis is usually not the difficult part; the skill lies in defining where the patient sits and fitting treatment to that point. The International Renal Interest Society (IRIS) staging system exists for exactly this.
One frequent error is misunderstanding what the system is: IRIS is not a diagnostic tool. It classifies a stable patient in whom chronic kidney disease has already been diagnosed. Staging an acute case, or a dehydrated cat, produces the wrong answer.
The diagnosis does not rest on a single value. It emerges from a combination:
Azotaemia alone is not enough. Creatinine rises in a dehydrated cat and may return to normal after fluids. For that reason staging is done after the patient is rehydrated and on at least two measurements.
Symmetric dimethylarginine reflects a falling glomerular filtration rate earlier than creatinine does, and it is less affected by muscle mass. In an old cat that has lost muscle, creatinine can look misleadingly normal while SDMA is already raised.
But SDMA does not make the diagnosis on its own either. A raised SDMA says: look more closely at renal function. Confirming it requires a repeat measurement and interpretation alongside urine specific gravity.
IRIS defines four stages based on a stable, fasted creatinine (and SDMA):
Stage 1 — No azotaemia, but some other evidence of renal disease: impaired concentrating ability, proteinuria, a structural abnormality on imaging, or a raised SDMA. The patient usually looks well at this stage.
Stage 2 — Mild azotaemia. Clinical signs are absent or subtle. This is the stage where early detection is worth the most.
Stage 3 — Moderate azotaemia. Systemic signs appear: weight loss, inappetence, vomiting, lethargy.
Stage 4 — Advanced azotaemia. Uraemic signs are prominent and quality of life comes to the foreground.
The numerical cut-offs between stages are revised periodically; when staging a patient, consult the current IRIS table rather than working from a remembered figure.
This is where the clinical value sits. The stage alone does not tell you what to do; the substages do.
The urine protein-to-creatinine ratio is measured and the patient classified as proteinuric, borderline, or non-proteinuric. Urinary infection and inflammation must be excluded first; otherwise what you are measuring is inflammation rather than renal damage.
Proteinuria both accelerates progression and is associated with shorter survival. Persistent proteinuria is the principal indication for treatment aimed at the renin-angiotensin system.
Blood pressure is classified by the risk of target organ damage. In cats, the most severe consequence of hypertension is sudden blindness through retinal detachment and intraocular haemorrhage. This is potentially reversible, and yet it is usually recognised late.
Every cat with chronic kidney disease therefore has its blood pressure measured and its fundus examined. The white-coat effect is real; take measurements once the patient has settled, repeated with a consistent technique.
The backbone of treatment is the same three headings at every stage, with the weighting shifting:
Diet. A renal diet is one of the few interventions shown to extend survival in feline chronic kidney disease. Phosphorus restriction sits at the centre of the effect. Transition slowly; forcing a new food on an inappetent cat creates food aversion, and you lose that diet permanently.
Water. Chronic dehydration both makes the patient feel unwell and places further strain on the kidney. Wet food, several water bowls, a running water source. In advanced disease, owners can be taught to give subcutaneous fluids at home.
Phosphorus. If serum phosphorus stays above target despite diet, a binder is added. Targets vary by stage.
Alongside these: treatment directed at proteinuria where present, antihypertensives where indicated, support for erythropoiesis if anaemia is marked, and symptomatic treatment for nausea and inappetence. Do not overlook hypokalaemia — it is common in cats, produces muscle weakness and inappetence, and correcting it makes the patient feel better quickly.
A stable patient is usually seen every three to six months; the interval shortens for a newly diagnosed cat or after a change in treatment. At each visit: body weight and body condition score, creatinine/SDMA, phosphorus, potassium, PCV, urine specific gravity and UPC, blood pressure.
Weight tracking is underrated, and it is among the earliest warnings available. Loss of muscle mass begins before the laboratory values move.
This article is for general education and does not replace clinical examination in the management of an individual patient.
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