The interpretation of urine specific gravity (SG) and serum urea and creatinine requires an understanding of renal physiology and the mechanisms that control these parameters. Too often a patient with low urine SG and azotaemia is diagnosed as having renal failure--this is of course a very possible diagnosis especially in cats, but there are other disorders that impair both urine concentration and cause azotaemia that the practitioner must always consider.

Urine Specific Gravity

If a patient has been confirmed as being polyuric and polydipsic and/or azotaemia has been identified, the initial and most important diagnostic step is to determine the urine specific gravity (SG)--without this information, appropriate interpretation of other pathology results can be difficult.

 Urine with an SG of < 1.008, (1.006 in cats) has been actively diluted

 Urine with an SG of 1.008-1.012 has neither been diluted or concentrated

 Urine with an SG of >1.012 has been concentrated to some degree--however whether the degree of concentration is appropriate must now be determined for the patient

Normal animals may have a urine SG of any value depending on the physiological circumstances. Always interpret urine SG in relation to the hydration status of the patient.

Although urine with a SG greater than 1.012 has been concentrated, the degree of concentration may not be appropriate.

If an animal is dehydrated or hypovolaemic, the appropriate renal response is to produce urine that is concentrated to at least a SG of 1.030 (dogs) or 1.035 (cats).

If a dehydrated animal has a urine SG less than these values it has by definition inappropriate urine concentration and it must have some degree of renal dysfunction (primary structural renal dysfunction or extra-renal dysfunction).

If an azotaemic animal has a urine SG less than these values then the patient must have impaired urine concentrating ability, because if the azotaemia was due to pre-renal factors only and the patient had normal renal concentrating ability, the urine SG would be >1.030 (dogs) or 1.035 (cats). Note that most dehydrated cats with normally functioning kidneys will have a urine SG > 1.045.

Structural vs. Functional Renal Disease

Persistent polyuria (primary or secondary to polydipsia) or failure to concentrate urine appropriately in the presence of dehydration or azotaemia may be the result of a structural renal abnormality (i.e., primary-renal disease) or a functional renal abnormality (extra-renal disease).

A functional (extra-renal) abnormality occurs when the kidney is structurally normal but urine concentration is impaired as a result of alterations in, for example, medullary hypertonicity (e.g., hyponatraemia) or ADH function (ADH deficiency, impaired ADH function secondary to hypercalcaemia).

If the urine is very dilute (hyposthenuria) there are a limited number of diagnostic possibilities and differentiation of the possible causes is relatively simple.

If the urine SG is between 1.008 and 1.030 the first consideration is whether the urine is inappropriately dilute. If the patient is dehydrated and renal function is normal, the urine SG should be greater than 1.030 (dog) or 1.035 (cat). If it is not, then renal dysfunction must be present--this can either be due to a structural or functional renal abnormality.

If the urine is concentrated the patient is either not polyuric or if it is definitely polyuric then there must be an osmotic solute in the urine that is creating polyuria--the most common of these would be glucose.

Interpreting Serum Urea and Creatinine Levels

Azotaemia is the laboratory finding of increased concentrations of non-protein nitrogenous wastes, measured as blood urea or serum creatinine. Azotaemia can result from primary renal disease or from prerenal or postrenal processes

Extensive renal lesions result in azotaemia when there is a loss of 75% or greater of functioning nephrons.

Prerenal Azotaemia

Prerenal processes include hypovolaemia and severe dehydration. Mild azotaemia may also occur after a large meat meal and when there is GI bleeding.

Urine SG?

A dehydrated animal with normal renal function should have highly concentrated urine (>1.030-1.035 in dogs - > 1.035 in cats) and if it does not it is possible that it may have renal azotaemia i.e., impaired renal function. However, if an animal with a polyuric disorder such as pyometra, hyperadrenocorticism or liver disease becomes dehydrated it may become azotaemic entirely due to the prerenal factor of dehydration but it may still have inappropriately dilute urine (because of the factors that interfere with urine concentration). Thus while a high urine SG in a dehydrated patient confirms that prerenal factors are responsible for the azotaemia, an inappropriately low SG does not necessarily rule out prerenal azotaemia if that patient has a polyuric disorder causing impaired urine concentration.

Renal Azotaemia

If the Patient is Dehydrated

If azotaemia is found in association with inappropriately dilute urine it is usually defined as renal azotaemia. The question then becomes 'Does the animal have structural renal disease or a functional problem?' As discussed above, dehydrated patients which have an impaired ability to concentrate urine may become azotaemic due to pre-renal factors. They thus have renal dysfunction at that time but do not have structural renal disease.

If the Patient is Not Dehydrated

If non-renal sources of increased urea or creatinine (e.g., GI bleeding, large meal) can be ruled out, the only disorders other than primary renal disease that can cause azotaemia in a non-dehydrated, normovolaemic patient are:

 Hyponatraemia--due to hypovolaemia--sodium is the osmotic backbone of the plasma, thus loss of sodium reduces total body water and blood volume which in turn reduces GFR and therefore results in azotaemia. Low sodium also impairs the natural osmotic stimuli for ADH secretion (low serum osmolality) and so promotes dilute urine despite the dehydration which exacerbates fluid loss and therefore pre-renal azotaemia.

 Hypercalcaemia--calcium causes constriction of the afferent arteriole in the glomerulus thus decreasing GFR and hence causing azotaemia.

It is therefore imperative that, before a diagnosis of primary structural renal disease is made, sodium and calcium levels are checked in any azotaemic patient with inappropriately dilute urine, especially if they are not dehydrated and there is no evidence for other polyuric disorders such as liver disease, pyometra and hyperadrenocorticism. This is particularly so in dogs where the prevalence of disorders of sodium and calcium metabolism (e.g., hypoadrenocorticism, profound sodium loss due to gut disease, hypercalcaemia of malignancy) are similar if not greater than the prevalence of primary structural renal disease.

Postrenal Azotaemia

Postrenal azotaemia results from either obstruction to urine flow or traumatic rupture of the excretory pathway resulting in accumulation of urine in the body.

Table. Interpretation of laboratory data relevant to renal disease

*This may include transient renal tubular dysfunction secondary to severe toxaemia as in pyometra or ketoacidosis