Primary intrarenal azotemia
Pathogenesis. Intrarenal azotemic renal failure may be caused by many disease processes that destroy about three-fourths or more of the
parenchyma of both kidneys. Depending on the disease's biologic behavior, primary renal failure associated with intrarenal
azotemia may be reversible or irreversible and acute or chronic. Chronic irreversible azotemic renal failure is usually slowly
Diagnosis. In dogs, at least two-thirds of the nephron mass must be impaired if a dehydrated patient has impaired ability to concentrate
urine. Total loss of ability to concentrate and dilute urine does not always occur as a sudden event but often develops gradually.
Thus, a urine specific gravity between 1.007 to 1.029 in dogs or 1.007 to 1.039 in cats associated with clinical dehydration
or azotemia is indicative of intrarenal azotemia. Total inability of the nephrons to concentrate or dilute urine (so-called
fixation of specific gravity or isosthenuria) results in the formation of urine that is similar to that of glomerular filtrate (approximately 1.008 to 1.012).
If a hydrated patient has elevated BUN and creatinine concentrations and an impaired ability to concentrate or dilute urine,
likely at least three-fourths of the functional capacity of the nephron mass has become impaired.
More definitive studies (e.g., ultrasonography, radiography, biopsy, exploratory surgery) are required to establish the underlying
cause of primary azotemic renal failure. When formulating a prognosis and therapy, recall that the uremic signs are not directly
caused by renal lesions but are related to varying degrees of fluid, acid-base, electrolyte and nutrient imbalances; vitamin
and endocrine alterations; and retention of waste products of protein catabolism that develop as a result of nephron dysfunction
caused by an underlying disease (Table 1).
Azotemia associated with glomerulotubular imbalance. In some patients with primary renal failure caused by generalized glomerular disease, abnormally elevated BUN or creatinine
concentrations may occur in association with varying degrees of urine concentration. Be sure not to overinterpret the absolute
value of the urine specific gravity in such patients, since it may be slightly elevated by the effect of protein. Adding 40
mg protein/100 ml of urine will increase the urine specific gravity by about 0.001.
The renal lesion must be characterized by glomerular damage that is sufficiently severe to impair renal clearance of urea
and creatinine but that has not yet induced enough ischemic atrophy and necrosis or renal tubular cells to prevent varying
degrees of urine concentration. Thus, glomerular filtrate that is formed may be concentrated to such a degree that prerenal
azotemia is initially considered. However, this group of patients may be differentiated from patients with prerenal azotemia
by failure of a search for one of the extrarenal causes of poor perfusion, by persistent proteinuria and by persistent azotemia
despite restoration of vascular volume and perfusion with appropriate therapy.