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Staging of Kidney Disease
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2. Staging of Kidney Disease
A comprehensive scheme for staging CKD in cats (and dogs) has been proposed by the International Renal Interest Society (IRIS) and endorsed by the American and European Societies for Veterinary Nephrology and Urology (ASVNU and ESVNU). The staging system should be applied after a diagnosis of CKD. It has been made on the basis of clinical and laboratory tests and only once a clinical case has been shown to be in a stable state rather than acutely deteriorating and requiring supportive therapy to avert a uremic crisis.
The basis for the staging system is the plasma creatinine concentration. The IRIS group is well aware of the limitations of this approach as plasma creatinine concentration is influenced by:
- Muscle mass
- Hydration status
- Diet composition
Plasma creatinine concentration is exponentially and inversely correlated to the gold standard measure of renal function and renal mass, namely the glomerular filtration rate (GFR). At the present time, practical methods that have been validated for use in the cat under primary care practice conditions for the measurement of GFR in the cat are not available. In the fullness of time, these methods will become available and then GFR will replace plasma creatinine concentration as the physiological measurement upon which staging of CKD will be based (Le Garreres et al, 2007) (Figure 4).
Figure 4. Plasma creatinine vs time curves in 2 cats after intravenous administration of exogenous creatinine (dose: 40 mg/kg BW). From B. Reynolds, National Veterinary School of Toulouse.
Table 1 defines the staging system based on plasma creatinine concentration. The main challenge to the veterinary profession is to identify kidney disease when it is in the non-azotemic stage (stage I and early stage II). The veterinary profession has traditionally identified CKD by the finding of chronically elevated plasma creatinine concentration in conjunction with relatively dilute urine (often inappropriately so for the hydration status of the animal). At this stage (late stage II to IV) the primary cause of the kidney disease is often not evident, even on renal biopsy, and so the opportunity to treat the underlying cause of the kidney disease has been lost. Routine screening of older cats (from 8 years on) for evidence of kidney dysfunction examining serial plasma creatinine concentrations on an annual basis (and eventually measuring GFR) will increase our ability to detect CKD at an earlier stage and perhaps address the primary disease process at a stage where we can treat the primary disease.
Table 1. The International Renal Interest Society (IRIS) Staging System Based on Plasma Creatinine | ||
Stage | Creatinine* | Comments |
I | < 140 μmol/L (< 1.6 mg/dL) | Non-azotemic Some other renal abnormality present e.g. inadequate concentrating ability without identifiable non-renal cause; abnormal renal palpation and/or abnormal renal imaging findings; proteinuria of renal origin; abnormal renal biopsy results; increasing plasma creatinine concentrations noted on serial samples |
II | 140 - 249 μmol/L (1.6 - 2.8 mg/dL) | Mild renal azotemia (lower end of the range lies within the reference range for many laboratories but the insensitivity of creatinine as a screening test means that animals with creatinine values close to the upper reference limit often have excretory failure) Clinical signs usually mild or absent |
III | 250 - 439 μmol/L (2.8 - 5.0 mg/dL) | Moderate renal azotemia Many extra-renal clinical signs may be present |
IV | > 440 μmol/L (> 5.0 mg/dL) | Severe renal azotemia Many extra-renal clinical signs are usually present |
*To convert μmol/L to mg/dL divide by 88.4 |
Progression is thought to occur through three basic mechanisms:
- Repeated episodes of the primary disease process leading to further damage and loss of functioning nephrons;
- Mal-adaptive mechanisms, intrinsic to the kidney leading to glomerular capillary hypertension, hyperfiltration and hypertrophy. This is thought to occur through local activation of the reninangiotensin system. The appearance of increasing amounts of protein in the urine may indicate that this process is occurring and there is some evidence that excess filtered protein may damage the tubules and contribute to progressive renal injury;
- Mal-adaptive responses occurring extrinsic to the kidney resulting from reduced renal function which may have detrimental effects on the remaining functioning nephrons:
- Hyperphosphatemia, hyperparathyroidism and nephrocalcinosis
- Systemic arterial hypertension due to an inability to regulate extracellular fluid volume. The diseased kidney’s ability to autoregulate and protect itself from systemic arterial hypertension is reduced and this can lead to hypertensive kidney damage.
Progression of CKD in cats, as alluded to above, occurs at different rates such that some cases remain stable in stage II/III CKD and later die of some other problem whereas others progress to stage IV and suffer a renal death. The pattern of progression seems to take at least two forms, namely:
- Stepwise progression with a sudden decrement of kidney function leading to a uremic crisis
- Gradual linear progression with increases in plasma creatinine occurring steadily over time
Stepwise decrement in kidney function is the more common pattern of progression seen in cats with naturally occurring CKD (Elliott et al, 2003b; Ross et al, 2006).
It is clear from evidence in other species that risk factors for rapid progression of chronic kidney disease include proteinuria and systemic arterial hypertension. Thus, the IRIS staging system requires that CKD is sub-staged based on the urine protein to creatinine (UPC) ratio and on the systemic arterial blood pressure. Recent evidence suggests that UPC is an independent risk factor for all cause mortality of cats with CKD (Syme et al, 2006) and in cats with systemic hypertension (Jepson et al, 2007b). Table 2 sets out the IRIS sub-staging system based on UPC. The substaging of cases based on UPC refers only to renal proteinuria. Pre-renal and post-renal causes should be ruled out if the substaging system recommended below is to be utilized (Lees et al, 2005). Thus, it is imperative to undertake a complete urinalysis and assess the microscopic sediment of a urine sample to ensure evidence of inflammation in the lower tract is absent before assessing the urine protein to creatinine ratio.
Table 2. Substaging on Urine Protein to Creatinine Ratio (UPC) | |
UPC* value | Interpretation |
< 0.2 | Non-proteinuric (NP) |
0.2 to 0.4 | Borderline proteinuric (BP) |
> 0.4 | Proteinuric (P) |
* Calculated using mass units |
Table 3 presents the IRIS sub-staging system based on systemic arterial blood pressure.
The IRIS group recognizes that there is no agreed standard for measuring feline blood pressure. The method used in our practice is the Doppler method which gives readings of systolic pressure only. Cases should not be classified based on measurements taken at a single clinic visit. At least two or more visits should be used to establish their blood pressure status unless significant signs of target organ damage are evident (see above) whereupon specific antihypertensive therapy may be indicated.
Table 3. Substaging on Blood Pressure | |||
Risk | Systolic (mm Hg) | Diastolic (mm Hg) | Classification according to evidence of extra-renal complications* |
Minimal [N] | < 150 | < 95 | - Minimal or no risk of end organ damage [N] - Highly unlikely to see evidence of extra-renal damage at this level |
Low [L] | 150-159 | 95-99 | - Low risk of end organ damage - If no extra-renal complication seen [Lnc] - If evidence of extra-renal complications seen [Lc] |
Moderate [M] | 160-179 | 100-119 | - Moderate risk of end organ damage - If no extra-renal complications seen [Mnc] - If evidence of extra-renal complications seen [Mc] |
High [H] | ≥ 180 | ≥ 120 | - High risk of end organ damage - If no extra-renal complications seen [Hnc] - If evidence of extra-renal complications seen [Hc] |
nc – no extra-renal complications present; c – extra-renal complications detected. *Extra-renal complications might include: - left ventricular concentric hypertrophy in the absence of structural/valvular heart problems identified - ocular abnormalities compatible with damage by high blood pressure such as hyphema or hypertensive retinopathy - neurological signs - dullness and lethargy, seizures |
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1. Adams LG, Polzin DJ, Osborne CA, et al. Comparison of fractional excretion and 24-hour urinary excretion of sodium and potassium in clinically normal cats and cats with induced renal failure. Am J Vet Res 1991; 52: 718-722.
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Affiliation of the authors at the time of publication
1Royal Veterinary College, London, United Kingdom. 2
Royal Canin USA, St Charles, MO, USA.
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