Page 911 - Small Animal Clinical Nutrition 5th Edition

Feline Lower Urinary Tract Diseases 943

Table 46-11. Potential factors associated with formation of uncommon feline uroliths.
VetBooks.ir Factors Causes Pathogenesis
Urate
Hyperuricosuria Portosystemic shunt or severe hepatic Decreased hepatic conversion of uric acid to allantoin,
disease which is more soluble in urine
Excessive purine intake Promotes hyperuricemia with subsequent hyperuricosuria
Hyperammonuria Excessive protein intake Additional urea and glutamine available for conversion to
ammonium (NH )
4
Metabolic acidosis Promotes metabolism of glutamine to NH 4
Acidic urine Ammonia (NH ) is converted to NH , which is excreted in urine
4
3
Hypokalemia Results in intracellular acidosis (potassium exchanged for
hydrogen) and subsequent excretion of NH 4
Urinary tract infection with urease- Converts urea in urine to NH and NH 4
3
producing organism
Aciduria Acidic urine Decreased solubility of uric acid in urine
Decreased urine volume Decreased water intake Increased urine concentration and saturation with uric acid
Decreased urination causes retention of crystals and uroliths
Calcium phosphate
Hypercalciuria Hypercalcemia Increased urinary calcium excretion
Excessive vitamin D Increased intestinal calcium absorption and suppressed
parathyroid hormone secretion, which promotes calcium
excretion
Hypophosphatemia Stimulates vitamin D production, which augments intestinal
absorption of calcium
Acidosis Promotes skeletal release of calcium and inhibits renal tubular
reabsorption of calcium
Excessive calcium intake Increases urinary calcium excretion
Excessive sodium intake Increases urinary calcium excretion
Hyperphosphaturia Excessive phosphorus intake Increased urinary phosphorus excretion
Alkaline urine Increases urine concentration and saturation of phosphate
Alkaline urine Alkaline urine Reduces solubility of calcium phosphates, especially brushite
Decreased urine volume Decreased water intake Increased urine concentration and saturation with calcium
phosphate
Decreased urination causes retention of crystals and uroliths

ated (Nakagawa et al, 1987; Hess, 1991; Asplin et al, 1991). cause was not obvious (Osborne et al, 1996a). Cystinuria, pre-
Although a cause-and-effect relationship remains to be sumably due to a defect in renal tubular transport of certain
established, feeding foods formulated to maintain an acidic uri- amino acids including cystine, has been identified in a small
nary pH (≤6.29 in one study and between 5.99 and 6.15 in number of cats with cystine uroliths (DiBartola et al, 1991;
another study) has been associated with calcium oxalate Osborne et al, 1996a).
uroliths in two epidemiologic studies of cats (Kirk et al, 1995;
Lekcharoensuk et al, 2001a). Acidosis may cause mobilization Urethral Plugs
of calcium from bone (along with buffers), resulting in It is likely that urethral plugs result from different pathogenic
increased urinary calcium excretion. In addition, metabolic aci- mechanisms than uroliths.In contrast to uroliths,urethral plugs
dosis is associated with decreased urinary citrate excretion and typically contain large amounts of matrix and tend to be soft,
increased citrate metabolism by renal tubular cells. compressible and friable (Figure 46-12). Although most plugs
contain crystalline minerals, some do not. On occasion, plugs
OTHER UROLITHS can be composed almost completely of matrix, blood cells,
Pathogenesis of less commonly diagnosed urolith types is not inflammatory cells and sloughed tissue (Table 46-5). Matrix is
well understood, although several factors may be involved in the nondialysable portion of urethral plugs that remains after
formation of uroliths composed of purine (e.g., ammonium mild solvents have dissolved crystalline components. Matrix
acid urate, uric acid) or calcium phosphate (Table 46-11). An may provide the “glue” for urolith and plug formation (Osborne
underlying metabolic disorder is likely in these patients; how- et al, 1996b). The exact composition of feline urethral plug
ever, often one is not identified. Detection of certain crystals matrix is unknown. It is possible that a major component of
(i.e., ammonium urate, cystine and xanthine), even in patients matrix is Tamm-Horsfall mucoprotein based on the observa-
without clinical signs, suggests an important underlying meta- tion that the urinary concentration of Tamm-Horsfall muco-
bolic defect, but not all cats with these crystals will develop protein is increased in cats with a history of forming uroliths
uroliths. UTI may be associated with uncommon urolith types, (Rhodes et al, 1992). Tamm-Horsfall mucoprotein may be a
but there is little evidence to support that UTI is the cause of local host defense against bacterial and viral UTIs. Excess
these uroliths. Xanthine uroliths have been reported to occur in mucus may be secreted by cells within the urinary bladder and
seven cats that had not received allopurinol; an underlying urethra in response to an irritant or inflammatory stimulus.