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| The Mastiff Sweet Spot > Message Board > CYSTINURIA POSITIVE DOGS |
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| acslinda Registered: 05/06/06 Posts: 5,602 | 07/29/08 at 10:06 AM Ok peeps, it is time to get this information out in the open so | ||||||||||||||||||||||||||||||||
| Sandragon Registered: 06/18/06 Posts: 4,192 | 07/29/08 at 10:29 AM This is Danny Boy. The dog that the Danny Fund was set up to honor!
CERTIFIED PEDIGREERegistered Name: Renrock Danny Boy O'NanjayReg. #: WP789833/06 Sex: Male Date Whelped: 7/1/1997 Color: ______________________________ Notes: MCOAsp98 -Ch. Deer Run Wycliff -Ch. Deer Run Ivan | -Tasha Farley's First Lady -Ch. Deer Run Ezekiel | OFA MF426 | -Ch. Grand Duke O'Fern | -Le Mar's Sally | -Le Mar's Little Gem -Ch. Old School Primo Remo Major| Thyroid Normal | -Ch. Deer Run Noah Massalane | | -Deer Run Florister Rufus | | | -Ch. Nanjemoy's Etasha| -Ch. Old School Ursa Major | | -Ch. Hannibal of Makar | -Old School Trouble | -Mistress Julia of Massalane-Nanjay's Black Star In MyCrown| | -Ch. Gulph Mills Mugger| | -Ch. Gulph Mills Mulcher| | | -Ch. Greenbranch Macushla| | -Ch. Gulph Mills Ajax III | | | | -Tamarack Donner| | | -Ch. Lady Natassia Of Apple Creek| | | -Ch. Lady Pebbles Of Apple Creek| -Nanjay's Black Jewel Of Lyndon| | -Ch. Bournewood Edwin| | -Ch. Harper of Lyndon| | | OFA MF-282 -Ch. Oak Ridge's Aquila | -Lyndon Window Chimes Lyra| OFA good MF577G30F| -Peach Farm Jacob| -Jacob's High Buttons| OFA MF-299-T -Jalaine Daisy- | -Ch. Deer Run Ezekiel| -Ch. Burns Hall Zackery| | OFA good MF1175G42M CERF-Ch. Thorchelseaias Noel| -Am.Can.Ch. Matts Joshua Of Dogwood Knoll| | | -Rapscallion's Sir Winston| | -Ch. Burns Hall Nicole | | OFA fair MF1223F53F-Ch. Night Stalker Sarah Anne| -Ch. Lionsire Run'n Bear Samson| | OFA excellent MF2003E28M| -Ch. Deer Run Ivan | | | -Ch. Deer Run Ezekiel| | | | OFA MF426 -Le Mar's Sally| | -Lionsire Girl With The Curl| | | -Sheila's Christian Samson| | -Christian Bristol Cream| | -Ch. Zachary's Lady Titan-Running Bear's Rogue Of Nanjay | -Ch. Altom's Paulas Pride| -Emphil's Montana Of Wildacres | | -Emeline Mayflower of Columbo | -General Lee Bigfoot | | | -Sir Cassius Of Rockcliff | | -Sara Lee Wycliff | | -Babe Ruth -Gabriela's Abbilene | -Ch. Willowledge Caius| -Vegte's Milo Of Belly Acres | | -Ch. Camelot's Rock Of Gibraltor -Elaine's Daisey Magnolia | -Samuel Jaws Easter -Vegte's Tooty Of Belly Acres -Princess Of ColdwaterI hereby certify that this pedigree is true and correct to the best of my knowledge and beliefSigned By: __________________________________________________ Signature: __________________________________________________ Date: ______________________________ Address: __________________________________________________ _________________________ | ||||||||||||||||||||||||||||||||
| Fanchone1 Registered: 06/05/08 Posts: 10 | 07/29/08 at 10:31 AM My boy is positive: | ||||||||||||||||||||||||||||||||
| Sandragon Registered: 06/18/06 Posts: 4,192 | 07/29/08 at 11:55 AM | ||||||||||||||||||||||||||||||||
| RollingRock Registered: 05/22/08 Posts: 28 | 07/29/08 at 03:03 PM My dog is also Cystinuria Positive. He is the littermate to above Windfall's Full of Gusto. | ||||||||||||||||||||||||||||||||
| medievalmastiff Registered: 05/07/06 Posts: 469 | 07/29/08 at 07:56 PM This the first C+ boy. The second is out of his littermate sister. | ||||||||||||||||||||||||||||||||
| Teresa Registered: 10/28/07 Posts: 1,370 | 07/29/08 at 11:17 PM Pedigree for Newt
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| acslinda Registered: 05/06/06 Posts: 5,602 | 07/30/08 at 12:34 AM This may seem redundant, but I think this post, written by Cystinuria genetics – Tracy Eberheart With the mode of transmission still incomplete, and the models that follow may have another factor UPenns recommendations are pretty clear. The still believe it to be x linked recessive with incomplete penetrance ( this would be the reason that you would not see as many positives out of the littler as you would expect.) there is another factor in play, and It is my understanding that there may be studies coming in soon that would link the xfactor recessive with the coupling with the other factor ( I will not say until the studies prove it so but it may be related to a factor many have not considered yet) so UPENN recommendations of .......... simple X-linked inheritance of the disease.
the sons who receive their mother’s mutant version of the gene, also referred to as the mutant allele, will have the disease, since their only copy of the gene is a mutant version . The sons who get her normal allele will be normal. Therefore, on average, 1/2 of the sons will be normal, and 1/2 will be affected. The daughters of the carrier female by normal male breeding will all get a normal allele from their normal father. They will get either a normal allele or a mutant allele from their mother. Therefore, while all of the daughters will be clinically normal, approximately 1/2 of them will be carrier females. There are two important issues to consider here.
o The proportion 1/2 stated above is an average. Each offspring has a 50:50 chance of getting the mutant allele from the mother. Consequently, it is possible, by chance, that a carrier mother will not give her mutant allele to ANY of her offspring, particularly, if she does not produce many pups. (Think of tossing a coin for example three times and getting three heads in a row. You wouldn’t be too surprised.) Consider a litter of six, containing three females. If, by chance, none of the three male puppies received a mutant allele from their carrier dam, this carrier female would not be recognized as a carrier because she did not produce any affected offspring, and her daughters would not be recognized as being at risk of being carriers themselves.
information, there is no way to know if the normal-appearing female is normal or a carrier. In the case of cystinuria, the only way to identify a carrier female is from knowledge of her parents or offspring. If a female had an affected parent, she is an obligate carrier, having only the possibility of getting a mutant allele from that parent. Or, if the female produced an affected offspring, that offspring had to get a mutant allele from the mother, making her a carrier. This emphasizes why family information is so important.
Normal female to affected male – The normal female can only contribute normal alleles to her offspring, while the affected male contributes his only X chromosome, which carries the mutant allele, to all of his daughters, and contributes his Y chromosome to his sons. Therefore, all males produced from this type of mating will be normal and ALL females produced will be CARRIERS. Important issues here are: o Carrier and normal females are indistinguishable, so without additional information, it would not be possible to know if the normal-appearing female used for mating was normal or a carrier.
father’s only X chromosome, which has a mutant allele in an affected male. This is a case where additional information allows us to differentiate between normal and carrier females. • Affected female to normal male – The affected female has only mutant alleles to contribute to her offspring, and the normal male has only normal alleles. Consequently, ALL male puppies are AFFECTED (they get their X chromosome from their mother), and ALL female offspring are CARRIERS. Remember that: o Due to anatomical differences, unlike affected males, affected females are much less likely to form stones that will cause clinical problems, and in the absence of urine testing, are very likely to be undetected. Carrier female to affected male – Here, the mother contributes either a mutant allele, or a normal allele, while the father has only a mutant allele to contribute. On average, 1/2 of the daughters will be affected and 1/2 will be carriers. Of the sons, on average, 1/2 will be affected and 1/2 will be normal. Therefore, on average, 1/2 of any litter will be affected. The important issues are: o As explained above, the 1/2 ratios are the average that would be seen from this type of mating. Within a single litter, the actual ratios will vary. Litters from this type of mating could range from containing no affected dogs to containing all affected dogs.
• Affected female to affected male – All offspring will be affected. In the case of cystinuria, they may not all form stones or develop clinical signs of the disease. o This is a good place to reiterate the additional complications present for cystinuria in particular. In the case of cystinuria, we know that there can be cystinuric dogs without uroliths, and that uroliths often form for the first time after a dog has been bred. For both of these cases, mutant alleles that are not detected in the parents are passed from parent to offspring. The bottom line is that the breeding of affected dogs of either gender or of carrier females will transmit mutant alleles to offspring and may produce cystinuric animals. Complicating factors in making breeding decisions are the facts that we do not yet have any estimate of the rate at which dogs with excess cystine in the urine develop clinical manifestations of the disease. We do know that dogs that have had only negative NP test results have formed cystine stones. What this tells us is that, presumbably due to the variability of cystine levels in the urine , a single or even a few NP test results do not necessarily give a complete understanding of renal cystine transport in a dog.
If a dog is found to be positive it should not be bred period, I dont really care that you have built a line on it. With the mode of inheritence more than likely x linked recessive with a cofactor influencing it, the siblings should also be spayed/neutered, they are more than likely carrying the mutant gene, and the expression of that gene is dependant on the cofactor being expressed also. It is hard enough every day to take care of these big guys, foods, regular vet expenses ect, why throw in a known problem in the mix??
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| Sandragon Registered: 06/18/06 Posts: 4,192 | 07/30/08 at 07:55 PM Registered Name: Windfalls Trophy Buck | ||||||||||||||||||||||||||||||||
| Sandragon Registered: 06/18/06 Posts: 4,192 | 07/30/08 at 10:50 PM Registered Name: De Vine Farm's Hooch | ||||||||||||||||||||||||||||||||
| Sandragon Registered: 06/18/06 Posts: 4,192 | 07/30/08 at 10:54 PM To whom it may concern: | ||||||||||||||||||||||||||||||||
| Sandragon Registered: 06/18/06 Posts: 4,192 | 07/30/08 at 10:56 PM
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| smokerise Registered: 09/30/06 Posts: 57 | 07/31/08 at 04:03 PM My past boy Hillsides Sir Gulliver (Fawn) ws05924803 | ||||||||||||||||||||||||||||||||
| Sandragon Registered: 06/18/06 Posts: 4,192 | 07/31/08 at 06:46 PM My past boy Hillsides Sir Gulliver (Fawn) ws05924803 | ||||||||||||||||||||||||||||||||
| smokerise Registered: 09/30/06 Posts: 57 | 08/01/08 at 03:37 PM Thank you Lorie | ||||||||||||||||||||||||||||||||
| Sandragon Registered: 06/18/06 Posts: 4,192 | 08/02/08 at 10:56 AM Tigris Stella Bella, daughter of a positive male, and daughter also of a carrier (her litter brother Lumpy was positive, but never bred, his being positive proved that their mother was a carrier). Stella produced two positive sons, one in each of her two litters, Tigris Tyger Tyger (OFA Excellent but neutered young), and Tigris Black Forest Cake (who tested negative before being sold). Stella's other sons were tested several times and never tested positive. Stella, being the daughter of a carrier and a positive, had a 50/50 chance of being one of the extremely rare positive females, but tested negative multiple times and was clear by necropsy after her death. In other words, she did not HAVE Cystinuria, she was "only" a carrier. -------------------------------------------------------------- laurie (Mother Mastiff) Registered Name: Tigris Stella Bella Reg. #: WP895807/02 Sex: Female Date Whelped: 2/15/1997 Color: fawn brindle Notes: OFAg MF3771G31F-T,OFEL,OFPg,OFEP,MFCA,CERF1&12,STUD11/99 -Belbeck Plantation Boss -Eng.Ch. Trevabyn Black Ice | -Coopell Malanese -Farnaby Touch Of Class At Trev | | -Eng.Ch. Parcwood W. Bear Esq of Lesdon | -Farnaby Special Features | OFA excellent -Dark Devina Of Farnaby -Farnaby Fearful Symmetry ,CGC | OFA good MF1362F27G OFEL MFPA14 CERF| -Eng.Ch. Glynpedr Dom Perignon | vWD Clear Thyroid Normal | -Eng.Ch. Damaria Count Magnum | | | -Nandina Shady Lady Of Damaria | -Eng.Ch. Farnaby Fraze And Fable | | -Eng.Ch. Parcwood W. Bear Esq of Lesdon | -Farnaby Special Features | OFA excellent -Dark Devina Of Farnaby -Am.UKC.Ch. Gold Coasts Woodrow F Call ,CGC,TDI | |OFA good MF2211G24M OFEL CERF -Willowledge J Johnson | |Thyroid Normal -Ch. Royalcourt Jonah | | | -Ch. Sanobar Saxon Queen | | -Ch. Willowledge Recon Sniper ,CD | | | | -Ch. Bournewood Edwin | | | -Royalcourt Jesabelle | | | -Sanobar Lady Ashton | -Gold Coasts Emelia | OFA good MF871G26F OFEL MF42-T CERF| -Ch. Ram's Gate Job | vWD Clear Thyroid Normal | -Ch. Gulph Mills Resounder | | | -Ch. Dame Sybil Of Greenbranch | -Walnut Hill Resolve ,TT | OFA fair MF438F CERF| -Hippocrates Mister Barry HM | vWD Clear Thyroid Normal -Winterwood Raconteur | -Ch. Greenbranch Lady Chelsea - | -Craig Goch Cadlyn | -Belbeck Plantation Boss | | -Monterosa Lovely Lady | -Eng.Ch. Trevabyn Black Ice | | | -Merripit's Kermit | | -Coopell Malanese | | -Coopell Merry Shadow | -Farnaby Touch Of Class At Trev | | | -Eng.Ch. Overnoons Mr. Micawber of Buck | | | -Eng.Ch. Parcwood W. Bear Esq of Lesdon | | | | -Eng.Ch. Farnaby Rainy Patch | | -Farnaby Special Features | | OFA excellent | -Farnaby Flattering Figure | | -Dark Devina Of Farnaby | | -Aunty Bobbetty Of Bulliff -Farnaby Well Turned Fraze |OFA good MF1853G34F OFEL CERF -Farnaby Lord Alexanderson |vWD Clear Thyroid Normal -Lesdon Lord FortescueOfFarnaby | | -Lesdon Lady Diana | -Farnaby Fair'n Square | | | -Nantymynydd Nefin | | -Wyaston Mary Rose | | -Nantymynydd Daphne -Farnaby Magic Moment | -Eng.Ch. Glynpedr Dom Perignon | -Eng.Ch. Damaria Count Magnum | | -Nandina Shady Lady Of Damaria -Farnaby Fortune Personified | -Eng.Ch. Parcwood W. Bear Esq of Lesdon -Farnaby Special Features OFA excellent -Dark Devina Of Farnaby I hereby certify that this pedigree is true and correct to the best of my knowledge and belief Signed By: __________________________________________________ Signature: __________________________________________________ Date: ______________________________ Address: __________________________________________________ _________________________ | ||||||||||||||||||||||||||||||||
| Tracy Registered: 05/30/06 Posts: 5,310 | 08/13/08 at 10:28 PM Ok, I was researching some autosomal recessive theories for a friend who has an amino acid issue. This information is collected about human cystinuria, and I think alot of points here are very very valid, esp the different types of cystinuria, and transmission, as well as treament. Forgive the cut and paste, I normally like to expalin things in my own words, but these double shifts are making me very tired!! How frequent is cystinuria? Cystinuria is the most common defect known in the transport of an amino acid. What is a transport defect? With such remarkable specificity, it is little wonder that sometimes there are defects in transport systems. Several dozen different diseases are now known to be due to transport defects. What causes cystinuria? Although cystine is not the only overly excreted amino acid in cystinuria, it is the least soluble of all naturally occurring amino acids. Cystine precipitates, or crystallizes out of urine and forms stones (calculi) in the kidney, ureter, bladder, or anywhere in the urinary tract. How is cystinuria treated? Cystine stones in many patients can be dissolved and new ones prevented by a high fluid intake. What high fluid intake means in this context is an absolute minimum of 4 liters (roughly 4 quarts) per day. An intake of 5 to 7 liters a day is ideal. The fluids must be spaced out, including through the night. It has been said that people with cystinuria must realize that "for them, water is a necessary drug." Alkalizing the urine: Another strategy that has been attempted to treat cystinuria is alkalization of the urine. The rationale is that in an alkaline (nonacidic) liquid, cystine tends to stay in solution and there it does no harm. To make the urine alkaline, sodium bicarbonate (and similar substances) have been used. This treatment is not without hazard because it can, while preventing cystine stones, lead to the formation of other types of kidney stones. Penicillamine: For people with cystinuria in whom a consistent, conscientious high fluid intake does not succeed in halting the formation of stones, another option available is regular treatment with a drug called penicillamine. Penicillamine (Cuprimine, Depen) acts to form a complex with cystine that is 50 times more soluble than cystine itselfWhat are the laboratory findings in cystinuria? This excess of amino acids in the urine constitutes aminoaciduria. Some persons (heterozygotes) carrying just one gene for cystinuria have aminoaciduria, although milder. There are actually 3 types of cystinuria. Carriers of 2 of these types of cystinuria (types II and III) show abnormal amounts of cystine in their urine. How is cystinuria inherited? There are, as mentioned, 3 types of cystinuria. They are termed cystinuria type I (abbreviated CSNU1), cystinuria type II (CSNU3), and cystinuria type III (CSNU3). Each type of cystinuria can be inherited as an autosomal recessive trait. For example, in a family each parent may have one CSNU1 gene (and a normal gene paired with it) while their boy or girl may have the misfortune of receiving the CSNU1 gene from both of them, thereby acquiring cystinuria. Cystinuria type I (CSNU1) is caused by a mutation (a change) in a gene (the SLC3A1 amino acid transporter gene) which is situated on chromosome 2p16. Cystinuria type 2 (CSNU2) is, quite remarkably, also caused by a gene in 2p16.3. Studies of families with both cystinuria I and cystinuria II have shown that the genes for CSNU1 and 2 are at exactly the same spot in chromosome 2p16.3 and in fact both involve the same gene (the SLC3A1 amino acid transporter gene). CSNU1 and 2 are therefore said to be allelic. The fact that CSNU1 and 2 are allelic means that genetic compounds can form, producing three clinical types -- persons with not just CSNU1/CSNU1 and CSNU2/CSNU2 but also the compound type CSNU1/CSNU2. Cystinuria III (CSNU3) is due to a mutation at a separate location, namely at chromosome 19q13.1. So, when I very quickly read through this, there is a possiblity that we are looking at, possibly based on the human model, different types of cystinuria, which have different loci on the genes for transmission. This would certianly explain why we dont see the direct autosomal transmission that we think it should follow. | ||||||||||||||||||||||||||||||||
| slobber2 Registered: 05/08/06 Posts: 2,682 | 08/14/08 at 08:47 PM Hi Tracy :>) | ||||||||||||||||||||||||||||||||
| Sandragon Registered: 06/18/06 Posts: 4,192 | 08/14/08 at 09:31 PM "Urolithiasis in Dogs Astrid Hoppe,DVM, PhD
CYSTINE UROLITHIASIS
Etiopathogenesis and biological behavior Cystinuria is an inborn metabolic disease characterized by excessive urinary excretion of cystine and the dibasic amino acids lysine, arginine, and ornithine. In normal dogs, circulating cystine is freely filtered at the glomerulus, and most of it is actively reabsorbed in the proximal tubules. Cystinuric dogs reabsorb a much smaller proportion of the amino acid from the glomerular filtrate, and some may even have net cystine excretion.20 The solubility of cystine in urine is pH dependent, and it is relatively insoluble in acid urine but becomes more soluble in alkaline urine. The exact mechanism of cystine urolith formation is unknown.Although increased urinary cystine excretion is found in both males and females, uroliths are most commonly found in males.
In a Swedish study, the urinary excretion of 20 amino acids was investigated in 24 stone-forming cystinuric dogs and 15 normal dogs. 21 Compared with the normal dogs, most cystinuric dogs showed significantly increased excretion of cystine, lysine, arginine, ornithine cystathionine, glutamic acid, threonine, and glutamine. A most significant finding was the great variation in urinary cystine excretion. Seven of 24 cystinuric dogs showed normal cystine excretion at the time. This suggests that factors other than excretion of cystine have to be considered as causes of the formation of cystine uroliths. In a recent study, the clinical features and metabolic renal abnormalitiesin 11 cystinuric Newfoundlands were described. 20 In this study, however, all affected dogs persistently excretedexcessive amounts of cystine compared with other related Newfoundlands without cystinuria. In the same study, the mode of inheritance of cystinuria was evaluated.Although clinical signs of urinary obstruction were observed only in males, cystinuric male and female offspring were produced from noncystinuric parents, consistent with an autosomal recessive mode of inheritance.
Obligate heterozygotes did not have clinical signs and had normal urinary cystine content and renal amino acid reabsorption. Surprisingly, cystine uroliths are often not recognized until maturity,with the average age of detection being approximately 3 to 5 years. Because cystinuria is an inherited defect, uroliths commonly recur within 6 to 12 months (in some dogs, within 4 to 8 weeks) unless prophylactic therapy is initiated. Apart from the uroliths, cystinuric dogs have no other defects and normal renal function, and the disease would have remained a physiological curiosity if cystine had not been the least soluble naturally occurring amino acid, and thus potentially leading to the formation of cystine uroliths. Characteristics, prevalence and diagnosis Cystine uroliths (Figure 4) account for 3.5% to 27% of the canine uroliths, probably depending on the breed of dogs encountered in specific surveys. Many breeds of dogs have been reported to develop cystine uroliths. In Sweden and Germany, cystine urolithiasis is particularly a problem in the dachshund, and it accounts for approximately 4% and 18.8% , respectively, of uroliths analyzed from the dog populations in those countries. 22
Although, cystinuria is found in both males and females, cystine uroliths have been reported most commonly in male dogs.22 The presence of flat hexagonal cystine crystals provides strong support for a diagnosis of cystinuria. However, not all dogs with cystine uroliths have concomitant cystine crystalluria. If a sufficient quantity of cystine is present in urine (>10 mmol/mol creatinine), the cyanide-nitroprusside test result for cystine will be positive.23 False-positive reactions due to medication with sulfur-containing drugs have been reported, but the author¢s experience is that this test is a reliable and simple diagnostic procedure. For quantitative measurement of urinary cystine excretion, 24 hour urine should be collected and quantified by, for instance, ion exchange chromatography.21
Treatment and prevention Current recommendations for dissolution and prevention of cystine uroliths encompass reducing the urine concentration of cystine and increasing the solubility of cystine in urine.Therapeutic approaches may be divided into four categories: reduction and change of dietary protein intake, aimed at reducing cystine production and excretion increase of diuresis increase of cystine solubility conversion of cystine to a more soluble compound.
Dietary modification Attempts have been made to design diets low in methionine to decrease the excretion of cystine in humans, mostly with disappointing results. At the Swedish University of Agricultural Sciences, we have used a protein-restricted diet designed for dissolution of canine struvite uroliths in two dogs with cystine uroliths; the uroliths did not dissolve. 23 Studies in humans conclude that, despite a defective proximal tubular reabsorption of cystine in cystinuria, the reabsorption can be increased by dietary sodium restriction.3 Our own preliminary studies indicatethat the effect of dietary sodium restriction in dogs might be the same as for humans. Increase of diuresis Increase of water intake provides a progressive reduction in urinary cystine concentration and reduces the likelihood of precipitation. Alteration of solubility Cystine solubility can be enhanced by inducing an alkaline pH, but the solubility does not increase significantly until the pH is above 7.5.Administration of bicarbonate and citrate, for example, has been advocated for improving solubility, but the author¢s clinical experience, as well as that of others, suggests that not much practical benefit is achieved. 23
Conversion to a more soluble compound Chemical modification of the cystine molecule into a more soluble form with D-penicillamine or 2-mercaptopropionylglycine (2-MPG) has been suggested. This would be expected to decrease cystine excretion into the urine and to diminish the likelihood of urolith formation (Figure 5). Although D-penicillamine is effective in preventing the formation, and sometimes the dissolution, of cystine uroliths, there are frequent complications that limit its use. In dogs, the most prominent side effect is vomiting. Another property of penicillamine is chelation of metals. In a study of 11 normal beagles given D-penicillamine orally and intravenously, significantly increased excretions of calcium, copper, zinc, chromium, cobalt, iron, and magnesium were found. 24
2-MPG is chemically related to D-penicillamine but has a higher oxidation-reduction potential and may therefore be more effective in a disulfide exchange reaction.A clinical study was performed on 25 cystinuric dogs receiving oral treatment with 2-MPG for periods of between 1 and 6 years. 23 The drug was effectivein urolith dissolution when given at a dose of approximately 40 mg/kg.Thus, in 15 dogs with uroliths found in the bladder on 17 occasions, complete urolith dissolution was achieved on 9 occasions (53%). For prophylactic therapy, a dose of 30 mg/kg isrecommended. Most dogs tolerate 2-MPG well, although transient side effects, such as thrombocytopenia, may occur. 23
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| Sandragon Registered: 06/18/06 Posts: 4,192 | 08/18/08 at 09:32 AM In some threads the topic has come up that you could make a dog cystinuric by the type of food fed. This is the responses to that. Both are posted with permission: diet and CystinuriaPosted by: "Windfall Mastiffs" windfallmastiffs@hughes.net mastiffs10Wed Aug 13, 2008 7:11 pm (PDT)Maybe this analysis will help: Most all make insulin in our body by the pancreas (I say most as there are Juvenile diabetics who don't make insulin) and that helps to control the blood sugar in our body and move it to the cells to store for energy. Well the more we eat, the most sugar we have, the more insulin we need to control the sugar. We can also help control the sugar levels with food or meds, which is what a diabetic must do or the levels get to high. Well we all make Cystine, it's just a matter of how the kidney's metabolize it, some have no problems (Normal), others have a problem (Cystinuric) and when they eat certain foods, the problem can be worse (form stones or just be diagnosed C+) and these are the ones who are detected easier, earlier etc... Okay, I'm tired and hope this makes sense! Jan __________________________________________________ _____________- | ||||||||||||||||||||||||||||||||
| slobber2 Registered: 05/08/06 Posts: 2,682 | 08/19/08 at 04:00 PM Good Post Lori :>0 | ||||||||||||||||||||||||||||||||
| smokerise Registered: 09/30/06 Posts: 57 | 09/26/08 at 06:35 PM My boy is positive Springhollows Mafia Don "Neiko" WS17501211 | ||||||||||||||||||||||||||||||||
| Sandragon Registered: 06/18/06 Posts: 4,192 | 09/26/08 at 09:34 PM
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| francesp1066 Registered: 10/31/06 Posts: 88 | 10/01/08 at 08:44 PM Last night I received the results and my Ziggy is Positive. Today tried to reach all my puppy owners. If you have any dogs from this line please test you mastiffs. This is very important. | ||||||||||||||||||||||||||||||||
| slobber2 Registered: 05/08/06 Posts: 2,682 | 10/01/08 at 09:13 PM Oh Damn Fran Im so sorry | ||||||||||||||||||||||||||||||||
| francesp1066 Registered: 10/31/06 Posts: 88 | 10/01/08 at 09:33 PM Yes, I was going to test him a few weeks before that but once I heard they were having a clinic I waited till then to do testing. | ||||||||||||||||||||||||||||||||
| Sandragon Registered: 06/18/06 Posts: 4,192 | 10/01/08 at 11:14 PM Thank you for posting. | ||||||||||||||||||||||||||||||||
| Moneletto Registered: 08/07/06 Posts: 216 | 10/14/08 at 06:44 PM Batista tested Positive | ||||||||||||||||||||||||||||||||
| francesp1066 Registered: 10/31/06 Posts: 88 | 10/14/08 at 09:31 PM Sire: Greiner Hall Nicholas | ||||||||||||||||||||||||||||||||
| francesp1066 Registered: 10/31/06 Posts: 88 | 10/14/08 at 10:33 PM Just thought I mention that I had Ziggy tested a second time and he came back positive again. | ||||||||||||||||||||||||||||||||
| Moneletto Registered: 08/07/06 Posts: 216 | 10/16/08 at 11:50 PM Has anyone taken there dog to UPenn personally for a blood draw and urine sample?? | ||||||||||||||||||||||||||||||||
| slobber2 Registered: 05/08/06 Posts: 2,682 | 10/17/08 at 01:51 AM HI :>) | ||||||||||||||||||||||||||||||||
| acslinda Registered: 05/06/06 Posts: 5,602 | 10/25/08 at 12:02 PM The Napotniks have been testing their dogs for Cystinuria (Yeah Stephen, cudos to you for testing - I wish more people would) and has asked me to postthe results. This is very good news for a lot of people.. "As for any speculation that Nic was the link, he is, unfortunately, gone from us. All we can say is that Neo is a Nic grandson, Brutus is a Nic great-grandson, and Grappa is a Nic grandson and great-great grandson, and all are negative. " Neo, Brutus and Grappa have all tested negative. | ||||||||||||||||||||||||||||||||
| slobber2 Registered: 05/08/06 Posts: 2,682 | 10/25/08 at 10:36 PM Thats wonderfull news :>) | ||||||||||||||||||||||||||||||||
| lamars Registered: 07/26/08 Posts: 29 | 07/26/09 at 07:11 PM I am the breeder of this dog he tested Positive they changed his diet and he never formed stones. He is now 8 years old. Pedigree for Lamars Woofus Maximus Mastiff Fawn Black Mask
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| lamars Registered: 07/26/08 Posts: 29 | 07/26/09 at 07:13 PM I am the co-owner and breeder of this dog Pedigree for Ch.Lamars Blues Clues Mastiff Fawn Black Mask
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| EileenDurante Registered: 06/05/06 Posts: 3,250 | 02/07/10 at 02:26 PM
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| EileenDurante Registered: 06/05/06 Posts: 3,250 | 02/20/10 at 04:50 PM Pedigree for Finney's Sir Noble Chuwee ( Cystinuria Positive )
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| MommaMorrison Registered: 03/09/10 Posts: 2 | 03/09/10 at 01:32 PM Hi Eileen! I'm new to this forum, and also new Mastiff owners as well! Our pup is almost 6 months old, and sweet as can be. | ||||||||||||||||||||||||||||||||
| slobber2 Registered: 05/08/06 Posts: 2,682 | 04/07/10 at 07:58 PM Hi Meg :>) | ||||||||||||||||||||||||||||||||
| kristiE Registered: 06/06/09 Posts: 136 | 04/08/10 at 01:57 AM Meg, | ||||||||||||||||||||||||||||||||
| Magnum Registered: 03/13/10 Posts: 513 | 06/17/10 at 05:17 AM A helpful link for "stones": http://homeocare.blogspot.com/2006/06/renal-stone.html |
Kim |
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