Association between dietary factors and calcium oxalate and magnesium ammonium phosphate urolithiasis in cats.

OBJECTIVE: To identify dietary factors associated with the increase in occurrence of calcium oxalate (CaOx) uroliths and the decrease in occurrence of magnesium ammonium phosphate (MAP) uroliths in cats. DESIGN: Case-control study. ANIMALS: 173 cats with CaOx uroliths, 290 cats with MAP uroliths, and 827 cats without any urinary tract diseases. PROCEDURE: Univariate and multivariate logistic regression were performed. RESULTS: Cats fed diets low in sodium or potassium or formulated to maximize urine acidity had an increased risk of developing CaOx uroliths but a decreased risk of developing MAP uroliths. Additionally, compared with the lowest contents, diets with the highest moisture or protein contents and with moderate magnesium, phosphorus, or calcium contents were associated with decreased risk of CaOx urolith formation. In contrast, diets with moderate fat or carbohydrate contents were associated with increased risk of CaOx urolith formation. Diets with the highest magnesium, phosphorus, calcium, chloride, or fiber contents and moderate protein content were associated with increased risk of MAP urolith formation. On the other hand, diets with the highest fat content were associated with decreased risk of MAP urolith formation. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that diets formulated to contain higher protein, sodium, potassium, moisture, calcium, phosphorus, and magnesium contents and with decreased urine acidifying potential may minimize formation of CaOx uroliths in cats. Diets formulated to contain higher fat content and lower protein and potassium contents and with increased urine acidifying potential may minimize formation of MAP uroliths.

Effects of dietary fat and L-carnitine on plasma and whole blood taurine concentrations and cardiac function in healthy dogs fed protein-restricted diets.

OBJECTIVE: To evaluate plasma taurine concentrations (PTC), whole blood taurine concentrations (WBTC), and echocardiographic findings in dogs fed 1 of 3 protein-restricted diets that varied in fat and L-carnitine content. ANIMALS: 17 healthy Beagles. DESIGN: Baseline PTC and WBTC were determined, and echocardiography was performed in all dogs consuming a maintenance diet. Dogs were then fed 1 of 3 protein-restricted diets for 48 months: a low-fat (LF) diet, a high-fat and L-carnitine supplemented (HF + C) diet, or a high-fat (HF) diet. All diets contained methionine and cystine concentrations at or above recommended Association of American Feed Control Officials (AAFCO) minimum requirements. Echocardiographic findings, PTC, and WBTC were evaluated every 6 months. RESULTS: The PTC and WBTC were not significantly different among the 3 groups after 12 months. All groups had significant decreases in WBTC from baseline concentrations, and the HF group also had a significant decrease in PTC. One dog with PT and WBT deficiency developed dilated cardiomyopathy (DCM). Taurine supplementation resulted in significant improvement in cardiac function. Another dog with decreased WBTC developed changes compatible with early DCM. CONCLUSIONS AND CLINICAL RELEVANCE: Results revealed that dogs fed protein-restricted diets can develop decreased taurine concentrations; therefore, protein-restricted diets should be supplemented with taurine. Dietary methionine and cystine concentrations at or above AAFCO recommended minimum requirements did not prevent decreased taurine concentrations. The possibility exists that AAFCO recommended minimum requirements are not adequate for dogs consuming protein-restricted diets. Our results also revealed that, similar to cats, dogs can develop DCM secondary to taurine deficiency, and taurine supplementation can result in substantial improvement in cardiac function.

Evaluation of urinary carnitine and taurine excretion in 5 cystinuric dogs with carnitine and taurine deficiency.

Five client owned dogs with cystinuria were diagnosed with carnitine and taurine deficiency while participating in a clinical trial that used dietary management of their urolithiasis. Stored 24-hour urine samples collected from the cystinuric dogs before enrollment in the clinical diet trial were quantitatively evaluated for carnitine and taurine. These results were compared to those obtained from 18 healthy Beagles. Both groups of dogs were fed the same maintenance diet for a minimum of 2 weeks before 24-hour urine collection. The protocol used for 24-hour urine collections was the same for cystinuric dogs and healthy Beagles except that cystinuric dogs were catheterized at baseline, 8 hours, 12 hours, and at the end of the collection, whereas Beagles were catheterized at baseline, 8 hours, and at the end of the collection. Three of 5 dogs with cystinuria had increased renal excretion of carnitine. None of the cystinuric dogs had increased renal excretion of taurine, but cystinuric dogs excreted significantly less (P < .05) taurine in their urine than the healthy Beagles. Carnitinuria has not been recognized previously in either humans or dogs with cystinuria, and it may be 1 risk factor for developing carnitine deficiency. Cystinuric dogs in this study were not taurinuric; however, cystine is a precursor amino acid for taurine synthesis. Therefore, cystinuria may be 1 risk factor for developing taurine deficiency in dogs. We suggest that dogs with cystinuria be monitored for carnitine and taurine deficiency or supplemented with carnitine and taurine.

Effects of dietary fat and carnitine on urine carnitine excretion in healthy dogs.

Turnover of carnitine in the body is primarily the result of renal excretion, and high-fat (HF) diets have been shown to increase urine carnitine excretion in healthy people. Recently, increased renal excretion of carnitine was observed in dogs diagnosed with cystinuria and carnitine deficiency. Carnitine deficiency has been linked to dilated cardiomyopathy and lipid storage myopathies in dogs and humans, and low-fat (LF) diets have been beneficial in some human patients with carnitine deficiency. In addition, HF, protein-restricted diets are often recommended for management of cystinuria in dogs. However, whether HF diets increase renal carnitine excretion in dogs or whether dogs with carnitine deficiency would benefit from LF diets remains unknown. Therefore, the purpose of this study was to determine the influence of dietary fat and carnitine on renal carnitine excretion in healthy dogs. Results from this study revealed that an HF diet increased urine carnitine excretion in dogs; however, carnitine excretion with the HF diet was not significantly different from that in dogs consuming an LF diet. Nonetheless, these results raise the possibility that increased renal carnitine excretion associated with HF diets could be one risk factor for development of carnitine deficiency in dogs with an underlying disorder in carnitine metabolism, and some dogs with carnitine deficiency may benefit from an LF diet. Another important observation in this study was that renal excretion of carnitine exceeded dietary intake in all diet groups, confirming previous reports that concluded that canine renal tubular cells reabsorb carnitine poorly when compared with those of humans.

Patient and environmental factors associated with calcium oxalate urolithiasis in dogs.

OBJECTIVE: To test the hypothesis that breed, age, sex, body condition, and environment are risk factors for development of calcium oxalate uroliths in dogs. DESIGN: Case-control study. ANIMALS: 1,074 dogs that formed calcium oxalate uroliths and 1,724 control dogs that did not have uroliths. PROCEDURE: A validated multiple-choice questionnaire was designed to collect information from veterinarians and owners within 1 year of the date of urolith detection concerning signalment and environment of the dogs. Univariate and multivariate analyses were performed to calculate odds ratios to assess whether breed, age, sex, body condition, and environment were risk factors for calcium oxalate urolith formation. RESULTS: Middle-aged (8- to 12-year-old) castrated male dogs had increased risk for formation of calcium oxalate uroliths. Urolith formation was also associated with increasing age. Dogs of certain breeds, including Miniature and Standard Schnauzer, Lhasa Apso, Yorkshire Terrier, Bichon Frise, Shih Tzu, and Miniature and Toy Poodle, had increased risk for developing calcium oxalate uroliths. Overweight dogs also had increased risk. CONCLUSIONS AND CLINICAL RELEVANCE: Knowledge of patient and environmental risk factors for development of calcium oxalate uroliths may facilitate development of surveillance strategies that result in earlier detection of this disease. Modification of environmental factors and body weight may minimize calcium oxalate urolith formation and recurrence.

Association between patient-related factors and risk of calcium oxalate and magnesium ammonium phosphate urolithiasis in cats.

OBJECTIVE: To determine whether breed, age, sex, or reproductive status (i.e., neutered versus sexually intact) was associated with the apparent increase in prevalence of calcium oxalate (CaOx) uroliths and the decrease in prevalence of magnesium ammonium phosphate (MAP) uroliths in cats over time. DESIGN: Case-control study. ANIMALS: Case cats consisted of cats with CaOx (n = 7,895) or MAP (7,334) uroliths evaluated at the Minnesota Urolith Center between 1981 and 1997. Control cats consisted of cats without urinary tract disease admitted to veterinary teaching hospitals in the United States and Canada during the same period (150,482). PROCEDURE: Univariate and multivariate logistic regression were performed. RESULTS: British Shorthair, Exotic Shorthair, Foreign Shorthair, Havana Brown, Himalayan, Persian, Ragdoll, and Scottish Fold cats had an increased risk of developing CaOx uroliths, as did male cats and neutered cats. Chartreux, domestic shorthair, Foreign Shorthair, Himalayan, Oriental Shorthair, and Ragdoll cats had an increased risk of developing MAP uroliths, as did female cats and neutered cats. Cats with CaOx uroliths were significantly older than cats with MAP uroliths. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that changes in breed, age, sex, or reproductive status did not contribute to the apparent reciprocal relationship between prevalences of CaOx and MAP uroliths in cats during a 17-year period. However, cats of particular breeds, ages, sex, and reproductive status had an increased risk of developing CaOx and MAP uroliths.

Analysis of 77,000 canine uroliths. Perspectives from the Minnesota Urolith Center.

Of the hundreds of minerals that are found in the earth, most canine uroliths are comprised of only six types: (1) magnesium ammonium phosphate, (2) calcium oxalate, (3) calcium phosphates, (4) ammonium urate and other salts or uric acid, (5) cystine, or (6) silica. Each type has characteristics that allow its identification. During the past two decades, the prevalence of calcium oxalate canine uroliths has dramatically increased, while struvite has decreased. The most effective treatment and prevention protocols are based on knowledge of the primary mineral type comprising the urolith.

Medical dissolution and prevention of canine struvite urolithiasis. Twenty years of experience.

Two types of canine struvite uroliths have been recognized: infection-induced struvite is the most common type; sterile struvite is uncommonly recognized. Infection-induced struvite is most commonly associated with urease-producing staphylococcal UTI. For dogs that qualify, medical dissolution is an effective method of treatment. Medical dissolution protocols encompass: (1) eradication or control of UTI; (2) use of calculolytic diets; and (3) administration of urease inhibitors to patients with persistent UTI caused by urease-producing microbes.

Epidemiology of canine calcium oxalate uroliths. Identifying risk factors.

Calcium oxalate uroliths are most commonly encountered in Miniature Schnauzers, Lhaso Apsos, Yorkshire Terriers, Bichons Frises, Shih Tzus, and Miniature Poodles. They are more common in males than females, and more common in older than young dogs. Dogs that form abnormal nephrocalcin are also predisposed to calcium oxalate uroliths. Dietary risk factors for calcium oxalate uroliths include excessive calcium supplementation or excessive calcium restriction, excessive oxalic acid, high protein, high sodium, restricted phosphorus, restricted potassium, and restricted moisture (dry formulations). Dogs with hyperadrenocorticism or hypercalcemia are predisposed to calcium oxalate urolith formation.

Canine cystine urolithiasis. Cause, detection, treatment, and prevention.

Cystine uroliths are a sequela to cystinuria, an inherited renal tubular defect in reabsorption of cystine and some other amino acids. At the Minnesota Urolith Center, 67 breeds of dogs were identified, including English Bulldogs, Dachshunds, Mastiffs, and Newfoundlands. In some dogs, the severity of cystinuria may decline with advancing age. Current recommendations for dissolution of cystine uroliths include various combinations of diet modification, diuresis administration of 2-MPG, and alkalinization of urine.

Canine silica urolithiasis. Risk factors, detection, treatment, and prevention.

Uroliths containing 70% or greater silica comprise approximately 1% of the canine uroliths submitted to the Minnesota Urolith Center. Male dogs are far more commonly affected than females. In our series, 84 different breeds were affected. Currently available data suggest dietary factors play a role in their formation. Diagnosis is facilitated by the characteristic jackstone configuration of silica uroliths, but must be confirmed by quantitative analysis. Voiding urohydropropulsion or surgery are currently the most practical methods of removal of silica uroliths.

Canine and feline nephrolithiasis. Epidemiology, detection, and management.

Calcium oxalate (39%) and struvite (33%) were the predominant mineral types in canine nephroliths submitted to the Minnesota Urolith Center. Urate salts (12%) and calcium phosphate (2%) occurred less frequently. Provided they are not causing obstruction, struvite nephroliths may be dissolved with medical protocols. Although there are no dissolution protocols for nephroliths containing calcium, risk-benefit ratios should be considered before proceeding with surgery.

Drug-induced urolithiasis.

Diagnostic and therapeutic drugs may enhance urolithiasis in one or a combination of ways, including: (1) alteration of urine pH in such fashion as to create an environment that increases the solubility of some lithogenic substances, (2) alteration of glomerular filtration rate, tubular reabsorption, and tubular secretion of drugs of endogenous substances so as to enhance promoters or impair inhibitors of urolithiasis, and (3) precipitation (e.g., drugs or their metabolites) to form a portion or all of a urolith.

Voiding urohydropropulsion. Lessons from 5 years of experience.

Voiding urohydropropulsion is a nonsurgical method of removing uroliths from the urinary bladder. Any urocystolith of sufficient size to pass through the distended urethral lumen can be safely and effectively removed by this technique. Compared to cystotomy, voiding urohydropropulsion offers several advantages: urolith removal can be performed in minutes, anesthetic period is shorter, postprocedural dysuria and hematuria are less severe, and it provides greater success for complete removal of small urocystoliths. This technique is not suitable for removal of large urocystoliths or uroliths that become lodged in the urethral lumen.

Diagnosis, medical treatment, and prognosis of feline urolithiasis.

Radiographic or ultrasonographic evaluation of the urinary tract is required to consistently detect feline uroliths. Evaluation of clinical, laboratory, and radiographic findings facilitate "guesstimation" of the mineral composition of uroliths. Therapy should not be initiated before appropriate samples have been collected for diagnosis. The objectives of medical management of uroliths are to arrest further growth and to promote urolith dissolution by correcting or controlling underlying abnormalities. For therapy to be effective, it must induce undersaturation of urine with calculogenic crystalloids by (1) increasing the solubility of crystalloids in urine, (2) increasing the volume of urine in which crystalloids are dissolved or suspended, and (3) reducing the quantity of calculogenic crystalloids in urine.