P. 451

R. Jepson1
1Royal Veterinary College, London, United Kingdom
Dr Rosanne E. Jepson BVSc MVetMed PhD DipACVIM DipECVIM FHEA MRCVS
Royal Veterinary College, London (UK)
The kidney has many important functions including excretion of toxic wastes, water, electrolyte and acid base homeostasis and hormonal synthesis. At its simplest, kidney disease can therefore be de ned as any condition that alters one or more of these functions of the kidney. In canine and feline medicine we most often consider conditions affecting the kidney as being either tubular or glomerular in origin, relating to the primary site of altered function although conditions that affect both tubules and the glomeruli are possible. It is common for kidney disease to be classi ed as either acute or chronic depending on the duration of changes being present
in the kidney although it is certainly also possible for patients to experience an acute kidney injury (AKI) on
top of a pre-existing chronic kidney disease (CKD), often termed ‘acute on chronic’. Differentiation of acute from chronic disease is important in terms of differences in
the likely underlying aetiology, diagnostic and therapeutic management planning and prognostic information. Chronic disease usually implies that there has been an alteration in structure or function of the kidney present for at least 2-3 months. Recent studies have also begun to explore the potential relationship between AKI insults and the development of CKD, hypothesizing that serial small AKI episodes may be stimuli for the cascade of pro-in ammatory and pro- brotic events that mediate the development of tubulointerstitial nephritis.
Diagnosis of kidney disease is usually a multifactorial process requiring integration of clinical signs, historical information,  ndings on physical examination and assessment of renal function and structure. The clinical presentation of patients with kidney disease and indeed the results of diagnostic investigations will be dependent on the location of disease within the kidney e.g. tubular versus glomerular disease. It must be remembered that the clinical presentation of patients with kidney disease may range from those that are clinically asymptomatic (e.g. a cat with IRIS stage 1 CKD or dog with primary
glomerular disease that is detected due to identi cation of hypoalbuminaemia and proteinuria on a biochemical pro le) to those with more typical clinical signs referable to loss of the functional nephrons (e.g. polyuria, polydipsia, decreased appetite, nausea, vomiting) or glomerular disease (e.g. peripheral oedema, pleural
or abdominal effusions). Physical examination  ndings can elude to the duration of disease with  ndings such as poor body condition and small irregular kidneys supporting chronic disease whilst good body condition and palpably normal to enlarged kidneys may support an acute disease process. However, an unremakble physical examination does not preclude the presence of kidney disease.
Ultimately the diagnosis of kidney disease and localization of the disease process will be made on
the basis of the diagnostic investigation, including assessment of renal function, urinalysis, assessment
of proteinuria and potentially diagnostic imaging.
The gold standard for assessing renal function is
direct assessment of glomerular  ltration rate (GFR). Although GFR measurements using techniques such as iohexol clearance are not dif cult to perform, it is more common for surrogate markers of GFR to be used in clinical practice (e.g. urea, creatinine and symmetric dimethylargine (SDMA)). Interpretation of results of
these surrogate markers requires an understanding of the potential biological and laboratory variability and in particular factors that are likely to in uence results such as recent feeding for urea and body or muscle condition for creatinine. A key advantages of the novel GFR marker, SDMA, is that it is not in uenced by body muscle mass, meaning that it may provide a more accurate representation of renal function particularly in patients with appreciable muscle loss e.g. geriatric cat with CKD. Assessment of routine biochemistry for parameters that may in uence management e.g. phosphorus, potassium, calcium and for patients with proteinuria, albumin concentration is also important. A minimum of a packed cell volume and total solids is of use for identi cation of anaemia and where this occurs, a complete blood count may be considered.
In any patient where azoatemia is identi ed it is fundamental to establish whether the azotaemia is pre-renal, renal or post-renal in origin. The latter is often easily excluded on the basis of clinical presentation (i.e. obstructive urinary tract disease). However, establishing the presence of a pre-renal component involves assessment of hydration status of the patient and interpretation of renal function (i.e. creatinine) together with urine concentrating ability. In the dog azotaemia combined with a urine speci c gravity (USG) of >1.030 may be indicative of a pre-renal azotaemia whilst for the
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