ADJ Watson, Sydney, Australia, HP Lefebvre, Toulouse, France and J Elliott, London, UK
USG measurement is used frequently in veterinary practice to help evaluate renal function by assessing whether water is being excreted or conserved appropriately, according to need. It is measured using a refractometer, and provides an approximate guide to urinary solute concentration that is sufficiently accurate for clinical purposes.
The USG can also help verify the presence of polyuria (USG is inversely related to 24 hour urine volume), assist evaluation of urinary losses of protein, bilirubin and glucose, and aid assessment of the patient's state of hydration.
A wide range of USGs can be encountered in healthy animals – 1.001 to >1.075 for dogs and 1.001 to >1.085 for cats – although values encountered typically for normally hydrated individuals are often closer to 1.015 to 1.045 for dogs, and 1.035 to 1.060 for cats. It is important to note that any USG value could be considered 'normal' in a patient, depending on certain other factors, including the patient's hydration status.
In healthy animals, urine concentration can change substantially over time, and 2 to 3 fold variations have been observed within 2 hours in some dogs. Cats typically produce more highly concentrated urine than dogs, but similar variation might be expected for normal cats.
Excretion of urine that is concentrated like this indicates that significant modification of glomerular filtrate (which has specific gravity of 1.008 to 1.012) has occurred by means of active resorptive processes in the renal tubules. A substantial number of functioning nephrons is needed to produce urine of this concentration, so the simultaneous presence of azotaemia suggests there is likely to be a large pre-renal component to the azotaemia; this conclusion can be confirmed by determining if the azotaemia reverses on rehydrating the animal. If the patient is not azotaemic, this finding is generally considered incompatible with a diagnosis of substantial kidney disease, although kidney disease, with loss of up to 2/3 of normal nephron function may still be present.* However, USG values in some cats with chronic kidney disease (CKD) and azotaemia may be as high as 1.040 or 1.045, so kidney disease could still be suspected in a cat if these values are accompanied by persistent azotaemia.
The production of very concentrated urine (USG >1.050) can be seen when reduced renal perfusion results from hypovolaemia, haemoconcentration or heart failure. However, it can also occur in healthy cats eating mainly dry food but not drinking much water.
Excretion of urine more dilute than glomerular filtrate requires the kidneys to perform metabolic work to produce hypotonic fluid in the distal tubules (reabsorbing solutes in excess of water), and this does not occur in patients that have lost nephron function sufficient to cause persistent azotaemia, as in CKD. But substantial kidney disease can still be present in animals producing dilute urine if at least 1/3 of normal nephron function is retained.
Possible causes of USG <1.008 include primary polydipsia, central diabetes insipidus and conditions causing tubular insensitivity to vasopressin (ADH). Tubular sensitivity to ADH is often impaired in pyelonephritis, pyometra, glucocorticoid excess, hypercalcaemia, hypokalaemia, hyponatraemia, liver failure, and erythrocytosis.
Note that USG <1.008 can occur in normal healthy animals that are excreting surplus fluid to maintain homeostasis, as in primary polydipsia. However, further investigation is warranted if urine is consistently dilute with repeated sampling; a water deprivation test and/or ADH response test might be considered here to investigate the underlying disorder.
Patients producing samples with USG within this range often have adequate renal function, but these values can also be associated with partial impairment of renal function due to kidney disease, or to some other factor inhibiting the ability to retain water, such as partial deficiency or inhibition of tubular responsiveness to ADH.
If dehydration is evident, moderately concentrated urine can be considered to be 'inappropriately dilute', warranting further investigation as indicated below.
If hydration is normal and there is no other evidence of kidney or other disease, it may be useful to reassess USG at intervals before undertaking additional studies. Only animals failing to produce concentrated urine (USG >1.030 for dog, >1.035 for cat) require further investigation: possible options include testing urine concentrating ability in response to water deprivation and/or ADH administration, determining glomerular filtration rate (GFR), renal ultrasound examination, and renal biopsy.
Algorithms derived by machine learning that effectively predict the onset of azotaemic CKD within 12 months of health screening of older apparently healthy cats have incorporated USG together with serum creatinine and urea (Biourge et al., 2020). Single measurements of USG alone can not be used in this way (Jepson et al., 2009).
Historically, it has been suggested that USG can be used as a marker for the cats that will develop azotaemia with treatment of hyperthyroidism, but studies that have objectively evaluated this have either not supported this view (Williams et al., 2010), or have found that it has worse sensitivity/specificity than blood biomarkers such as creatinine and SDMA (Peterson et al. 2018).
Failure to produce more concentrated urine in the presence of dehydration can indicate kidney disease. Alternatively, a partial deficiency in production, release or activity of ADH might be responsible (see section on Dilute urine: USG <1.008, above). Amongst possible contributing causes are: diuretic drugs, glucocorticoids, glucosuria, renal medullary washout, pyelonephritis, liver failure, and major electrolyte abnormalities (low K or Na, high Ca).
If azotaemia is also present, primary kidney disease and failure are even more likely. Another possibility, although less likely, is that the animal has prerenal azotaemia together with some other factor hindering water retention (e.g. hypercalcaemia).
Patients with inappropriately dilute urine should be investigated further for renal disease once other possible causes are excluded. This could involve testing urine concentrating ability in response to water deprivation and/or ADH administration, evaluating clearance of creatinine or another suitable marker to measure GFR, and/or performing renal imaging studies and/or a renal biopsy.
Urine is inappropriately concentrated if USG exceeds 1.007 when the patient is over-hydrated. The combination suggests substantial kidney disease because adequate renal function should lead to excretion of excess water and more dilute urine.
This situation is unusual and mostly encountered when using intravenous fluids to induce diuresis in a patient with oliguric or anuric acute kidney injury or end-stage chronic kidney disease.
USG values in this range occur from time to time in samples from healthy dogs and cats, but kidney disease and impaired function should be suspected if dehydration and/or azotaemia are present as well.
If isosthenuria persists in subsequent samplings, a concentrating defect should be suspected and investigated as indicated for 'inappropriately dilute urine'.
*Note: it is commonly said that urine concentrating ability will become compromised once approximately 2/3 of total nephron function has been lost, and that azotaemia reflects loss of at least 3/4 of overall nephron function. While these two fractions are useful conceptually, they should not be regarded as literally correct true in all circumstances. What they do reflect, however, are two fundamentally important aspects of kidney disease and dysfunction: firstly, that a large proportion of renal function must be compromised before functional changes become evident clinically, and, secondly, that chronic progressive kidney diseases can be expected to cause loss of urine concentrating (and diluting!) capacity before inability to excrete metabolic wastes becomes evident.
Biourge V, Delmotte S, Feugier A, Bradley R, McAllister M, Elliott J. An artificial neural network-based model to predict chronic kidney disease in aged cats. J Vet Intern Med. 2020 Sep;34(5):1920-1931.
Jepson RE (2017) Polyuria and polydipsia. In"BSAVA Manual of Canine and Feline Nephrology and Urology" 3rd edn, eds J Elliott, GF Grauer and JL Westropp pp 8-23.
Peterson, M. E., et al. (2018). "Evaluation of Serum Symmetric Dimethylarginine Concentration as a Marker for Masked Chronic Kidney Disease in Cats With Hyperthyroidism." Journal of Veterinary Internal Medicine 32(1): 295-304.
Wamsley H and Alleman R (2017) Complete Urinalysis. In"BSAVA Manual of Canine and Feline Nephrology and Urology" 3rd edn, eds J Elliott, GF Grauer and JL Westropp pp 60-83.
Williams, T. L. and J. Archer (2016). "Evaluation of urinary biomarkers for azotaemic chronic kidney disease in cats." J Small Anim Pract 57(3): 122-129.
Williams, T. L., et al. (2010). "Survival and the development of azotemia after treatment of hyperthyroid cats." J Vet Intern Med 24(4): 863-869.
