Renal Amyloidosis in CatsRenal Amyloidosis in cats can be both familial and inherited.
Familiar is used when the disorder occurs more frequently in cats than you would think by chance by has not been proven by inheritance.Renal Amyloidosis usually effects young to middle aged cats.
One usually thinks of the Abyssinisian breed with familial renal Amyloidosis but other breeds are affected.
The symptoms for renal Amyloidosis are weight loss, poor hair coat, large water intake, frequent urination, anorexia and tiredness add bad breath to name a few. There are phosphorus binders such as Amphojel, Basaljel, or Alternagel that may help since research is pointing more to the damaging effects of phosphorus intake rather than high protein intake..
Renal Disease in Cats
"There is no specific treatment. Symptomatic treatment should correct disorders caused by renal failure according to the degree of insufficiency, avoid the effects of the nephrotic syndrome by the administration of diuretics (furosemide 2 to 4 mg/kg once to twice a day), correcting hypertension, avoid complications due to thromboembolism: (Aspirin 2 mg/kg every 3 days)."
Familial Amyloidosis in Abyssinian Cats
"DMSO is used because of its anti-inflammatory effects which may inhibit
the process of amyloid deposition and therefore should be used early in the
onset of the disease...Colchicine seems to slow the production of amyloid. Its role in cats
is not clear although in humans it does seem to slow the disease process.
Its primary role in humans is to prevent the onset of the disease in those
Feline Renal Failure also mentions treatments
Selected Diseases of the Feline Kidney
"Spontaneous systemic amyloidosis ... Affected Abyssinian cats usually are presented for poor haircoat, weight loss, polydipsia, polyuria, lethargy, and anorexia"
Links on dietary research for renal disease
Feline Renal Amyloidosis
Renomegaly in Dogs and Cats .
1. Differential Diagnoses
MLD Cuypers, AM Grooters, J Williams, BP Partington
Louisiana State Univ,Sch Vet Med,Dept Vet Clin Sci,Baton Rouge,LA 70803 USA
Compendium on Continuing Education for the Practicing Veterinarian, 1997, 19,9, 1019
Detection of renomegaly is important because, when combined with other clinical information (such as signalment and history), it provides a narrow list of differential diagnoses. Clinicians who are familiar with the potential causes of renomegaly can often quickly arrive at a definitive diagnosis with the aid of radiographic, ultrasonographic, cytologic, or histopathologic information. Renomegaly is caused by various pathophysiologic processes, such as infiltration of the renal parenchyma by inflammatory or neoplastic cells, alteration of renal structure by developmental disorders or renal insult, and distortion of the collecting system secondary to urinary tract obstruction. In this review, the causes are grouped into several categories for ease of discussion: renomegaly caused by diffuse renal parenchymal disorders, such as acute renal failure, amyloidosis, renal lymphoma, pyogranulomatous nephritis secondary to feline infectious peritonitis, and renal hypertrophy; renomegaly caused by focal or multifocal parenchymal disorders, such as polycystic kidney disease and primary or metastatic renal neoplasia; renomegaly caused by subcapsular and perirenal disorders, such as perinephric pseudocysts and subcapsular and perirenal hematomas and abscesses; and renomegaly caused by collecting system disorders, such as hydronephrosis and acute bacterial pyelonephritis. Part II of this review will focus on the diagnostic approach to patients with renomegaly.
Renomegaly in Dogs and Cats .2.
AM Grooters, MLD Cuypers, BP Partington, J Williams, RD Pechman
Louisiana State Univ,Sch Vet Med,Dept Vet Sci,Baton Rouge,LA 70803 USA
Compendium on Continuing Education for the Practicing Veterinarian, 1997,19, 11, 13
Renomegaly is an important clinical finding in small animal patients, not only because it provides a fairly narrow list of differential diagnoses but also because it is easily investigated using minimally invasive imaging techniques and fine-needle aspiration. Kidney enlargement may result from various pathophysiologic processes, such as infiltration of the renal parenchyma by inflammatory or neoplastic cells, alteration of renal structure by developmental disorders or renal insult, and distortion of the collection system secondary to urinary tract obstruction. For ease of discussion, causes of renomegaly can be grouped into several categories - diffuse parenchymal disorders, such as acute renal failure, amyloidosis, renal lymphoma, pyogranulomatous nephritis secondary to FIP, and renal hypertrophy; focal or multifocal parenchymal disorders, such as polycystic kidney disease and primary or metastatic renal neoplasia; subcapsular and perirenal disorders, such as perinephritic pseudocysts and subcapsular hematomas; and collecting system disorders, such as hydronephrosis and bacterial pyelonephritis. The diagnostic approach to renomegaly is straightforward. When enlargement of one or both kidneys is identified during physical or radiographic examination, a list of differential diagnosis is formulated based on signalment, clinical signs, laboratory abnormalities, and survey radiographic findings. This is followed by specific evaluation of the kidneys using contrast radiography or ultrasonography, which provides a more complete assessment of the renal parenchyma and collecting system. In some patients, ultrasonography or contrast radiography may provide a definitive diagnosis. In others, fine-needle aspiration or needle core biopsy of the kidney is required to obtain a definitive diagnosis.
EUKANUBA VETERINARY DIETS (R) RENAL MANAGEMENT SYSTEM (R), Nitrogen Trap (R) Fibre System using fermentable fibres-fructooligosaccharides,beet pulp,and gum arabic to utilize the colon to aid the kidneys.Results in a 34% increase in fecal nitrogen excretion,decreases urinary nitrogen excretion,decreases reliance on kidneys for nitrogen excretion,decreases the need for drastic protein restriction. Nutritional Kidney Formula(R)Early Stage,Nutritional Kidney Formula(R)Advanced Stage . Moderate high quality protein levels,added potassium citrate,low phoshorus levels,adjusted omega-6:omega-3 fatty acid ratio
IAMS International,POBox 57012,5605 AA Eindhoven,NL Fax:(31)-(0)40-2519802
IAMS UK ,Unit 2,Meadow Brook Industrial Estate,Maxwell Way,Crawley,West Sussex RH10 2SA Tel.01293-572100
IAMS U.S.A. Tel.1-800-535-8387
Dietary management of feline chronic renal failure: where are we now? In what direction are we headed?
D J Polzin, C A Osborne, S Ross, F Jacob
Journal of Feline Medicine & Surgery , Volume 2, Number 2 , June 2000,p 75-82
Dietary modification is of primary importance in managing cats with chronic renal failure. Diets designed for cats with chronic renal failure are typically formulated to be pH neutral and contain reduced quantities of protein, phosphorus and sodium and an increased quantity of potassium. These changes in diet formulation are designed to ameliorate clinical signs of renal failure by adapting dietary intakes to meet the limited ability of failing kidneys to adapt to the normal range of dietary intakes. Important recent clinical trials support the therapeutic value of dietary therapy in cats with chronic renal failure.
Method of treating renal disease by administering IGF-I and IGFBP-3
Higley; Howard R., Mountain View, CA Maack; Christopher A., El Cerrito, CA
ASSIGNEES: Celtrix Pharmaceuticals, Inc., Santa Clara, CA
Treatment with IGF/IGFBP-3 complex increases renal tubular mass and potentiates and/or stimulates kidney function in subjects suffering from acute and chronic renal failure or insufficiency resulting from such disorders as glomerulonephritis, glomerulosclerosis, interstitial nephritis, acute tubular necrosis due to ischemia and drug-induced toxicity, diabetic and autoimmune nephropathies and renal dysfunction due to acute and chronic rejection episodes in post-transplantation patients.
1. A method of treating a renal disorder in a subject, said renal disorder selected from the group consisting of diabetic nephropathy and autoimmune nephropathy, said method comprising administering to said subject an effective amount of insulin-like growth factor (IGF) and insulin like growth factor binding protein 3 (IGFBP-3).
Early Markers of Nephrotoxicity
R. G. Price
Division of Life Sciences, King's College London, UK
Comparative Clinical Pathology Volume 11 Issue 1 (2002) pp 2-7
The kidney is susceptible to a wide range of nephrotoxins which vary in their effect from mild renal dysfunction to severe damage and end-stage renal failure. The identification of the presence of early renal damage, and also of individuals at risk of developing renal dysfunction, is important in order that corrective therapies can be applied at an early stage. However, glomerular filtration rate (GFR) is unlikely to fall until 50% of nephrons have ceased to function. A major challenge is to provide measurements, both qualitative and quantitative, that give an early indication of the initial site of renal damage before gross deterioration in kidney function has occurred. Nephrotoxic exposure results in a cascade of events of gradually increasing severity. Initially, functional changes occur which, if exposure continues, then progress past a point of no return leading ultimately to renal failure. Most biomarkers measure the effect of a toxin on the kidney, but some are insensitive, making it difficult to measure accurately the extent to which the kidney has been exposed. Used selectively, biomarkers are able to give information on the stage and severity of the damage/disease process. To be useful, a biomarker should be easily measured by robust inexpensive procedures, which can be carried out on random or timed urine samples. The effect of nephrotoxic agents is best assessed with a small battery of tests that can be followed by more specialized tests to confirm the severity and type of renal damage that has occurred.
Effects of the angiotensin converting enzyme inhibitor benazepril in cats with induced renal insufficiency.
Brown SA, Brown CA, Jacobs G, Stiles J, Hendi RS, Wilson S.
Dept of Physiol and Pharmacol, College of Veterinary Medicine, University of Georgia, Athens 30602, USA.
Am J Vet Res 2001 Mar;62(3):375-83
OBJECTIVE: To determine effects of the angiotensin converting enzyme inhibitor benazepril in cats with induced renal insufficiency. ANIMALS: 32 cats. PROCEDURE: Renal mass was surgically reduced, and cats were assigned to 1 of 4 eight-cat groups. Group 1 received placebo, whereas groups 2, 3, and 4 received benazepril hydrochloride orally once daily for approximately 6.5 months at the following doses: group 2, 0.25 to 0.50 mg/kg of body weight; group 3, 0.50 to 1.00 mg/kg; and group 4, 1.00 to 2.00 mg/kg. Arterial blood pressures, glomerular filtration rate (GFR), and renal plasma flow were determined before treatment and during the treatment period. Other determinants of renal hemodynamics were measured by use of micropuncture techniques. Renal biopsy specimens were examined microscopically. RESULTS: Compared with cats that received placebo, mean systolic arterial blood pressure was significantly less and GFR significantly greater in cats that received benazepril. Glomerular capillary pressure and the ratio of efferent to afferent arteriolar vascular resistance were also significantly less in treated cats. However, histologic differences in renal specimens were not detected. CONCLUSIONS AND CLINICAL RELEVANCE: Treatment with benazepril sustained single nephron GFR in remnant nephrons of cats with induced renal insufficiency. Administration of benazepril was also associated with a small but significant reduction in degree of systemic hypertension and an increase in whole kidney GFR. Benazepril may be an effective treatment to slow the rate of progression of renal failure in cats with renal disease.
Effects of dietary polyunsaturated fatty acid supplementation in early renal insufficiency in dogs
SA Brown, CA Brown, WA Crowell, JA Barsanti, CW Kang, T Allen, C Cowell, DR Finco
Univ Georgia,Dept Physiol & Pharmacol,Diagnost Lab,Athens,GA 30602 USA
Journal of Laboratory and Clinical Medicine, 2000, Vol 135, Iss 3, pp 275-286
Dietary supplementation with polyunsaturated fatty acids (PUFAs) alters the course of experimental kidney disease in dogs. In particular, supplementation with omega-6 PUFAs hastens the decline of kidney function, and omega-3 PUFAs are renoprotective. We investigated the early stages of renal insufficiency to determine whether PUFA supplementation altered the magnitude of hypercholesterolemia or glomerular hemodynamics. Two months after 11/12 nephrectomy, dogs were randomly divided into three groups of 6 animals each. Each group of dogs was then fed a low-fat basal diet supplemented with one of three sources of lipid to achieve a final concentration of 15% added fat. Fat sources were rich in omega-3 PUFAs (menhaden fish oil, group FO), omega-6 PUFAs (safflower oil, group SO), or saturated fatty acids (beef tallow, group C). Early in renal insufficiency, before significant kidney damage, group FO had a lower (P < .05) serum cholesterol concentration and tended to have a lower urinary prostaglandin E2 (PGE2) and thromboxane A2 (TxA2) excretion than group C. In contrast, group SO had a higher mean glomerular capillary pressure (P < .05) and more glomerular enlargement (P < .05) and tended to have higher eicosanoid excretion rates than group C, These differences in lipid metabolism, glomerular hypertension and hypertrophy, and urinary eicosanoid metabolism could explain, in part, the beneficial effects of omega-3 PUFAs and the detrimental effects of omega-6 PUFAs when administered on a long-term basis in this model of renal insufficiency.
Vet Clin North Am Small Anim Pract. 2001 Mar;31(2):393-9, viii. :
Congenital and inherited renal disease of small animals.
Department of Clinical Sciences, College of Veterinary Medicine and Biological Sciences, Colorado State University, Fort Collins, Colorado, USA.
Congenital renal diseases are present at birth and may be determined genetically; familial renal disorders occur in related animals with a higher frequency than would be expected by chance, and frequently are inherited. The most common familial disorders in cats and dogs include renal amyloidosis, renal dysplasia, polycystic kidneys, basement membrane disorders, and tubular dysfunction (Fanconi's syndrome). This article alerts the veterinarian to commonly observed congenital and hereditary conditions of the kidneys in small animals.
J Small Anim Pract. 1998 Sep;39(9):442-7.:
Generalised amyloidosis in two Siamese cats: spontaneous liver haemorrhage and chronic renal failure.
Godfrey DR, Day MJ
Nine Lives Veterinary Practice for Cats, West Midlands.
Two cases are reported, illustrating the antemortem diagnosis of systemic amyloidosis in Siamese cats. A cat presenting with inappetence and depression was diagnosed as having systemic amyloidosis with spontaneous haemorrhage from the liver. In another cat from the same breeding cattery, chronic renal failure due to systemic amyloidosis was an incidental finding. Little treatment was possible in either case and both were later euthanased. The two cats had similar renal and hepatic pathology but different signs of disease
J Comp Pathol. 1986 Jul;96(4):387-98. :
Tissue distribution of amyloid deposits in Abyssinian cats with familial amyloidosis.
DiBartola SP, Tarr MJ, Benson MD.
The tissue distribution of amyloid deposits was studied in 15 related Abyssinian cats with familial amyloidosis. There was interstitial medullary amyloidosis in the kidneys of all 15 cats but only 11 had detectable glomerular involvement. The thyroid glands, stomach and colon were affected in all cats examined. Most of the cats also had amyloid deposits in the small intestine, spleen, heart, adrenals, pancreas, liver, lymph nodes and bladder. In 50 per cent or fewer of the cats examined, there was involvement of the parathyroids, lung and gonads. The central nervous system was not involved in any of the 3 cats evaluated. In 8 of the cats, no concurrent inflammatory disease could be detected. The tissue distribution of amyloid deposits resembled that found in other breeds of domestic cats with systemic amyloidosis. Despite the wide tissue distribution of amyloid deposits, clinical signs were related to renal amyloidosis. Familial amyloidosis in the Abyssinian cat may represent a valuable spontaneous animal model for the study of Familial Mediterranean Fever in man and the pathogenesis of reactive amyloidosis in general.
Lab Invest. 1985 May;52(5):485-9. :
Isolation and characterization of amyloid protein AA in the Abyssinian cat.
DiBartola SP, Benson MD, Dwulet FE, Cornacoff JB.
Amyloid fibrils were isolated by extraction in deionized water from the kidneys of an Abyssinian cat with familial renal amyloidosis. The fibrils were suspended in a buffer containing 6 M guanidine hydrochloride and reduced and alkylated using dithiothreitol and iodoacetid acid. The resulting amyloid fibril subunit protein was isolated by chromatography on a column of Sepharose CL6B. It was fragmented using cyanogen bromide, and the resultant peptides were separated by reverse phase high performance liquid chromatography. The protein was characterized by determination of the amino acid sequence of the cyanogen bromide fragments using a Beckman 890C sequencer. The primary structure of this amyloid fibril subunit protein showed strong homology with amyloid protein AA found in man and animals with spontaneous and experimentally induced reactive systemic amyloidosis. This study confirms the reactive nature of familial renal amyloidosis in the Abyssinian cat and suggests that this disease may be a valuable spontaneous animal model for the study of familial Mediterranean fever in man.
Vet Pathol. 1984 Jan;21(1):33-8. :
Familial renal amyloidosis in Abyssinian cats.
Boyce JT, DiBartola SP, Chew DJ, Gasper PW.
Medullary and glomerular amyloidosis, papillary necrosis, and secondary interstitial disease were diagnosed in eight related adult Abyssinian cats from two catteries. The lesions were similar to those in two unrelated mongrel cats with renal amyloidosis. Ultrastructurally, the patterns of amyloid deposition were as described in other species, although medullary deposition predominated. Potassium permanganate oxidation blocked Congo red staining of the deposits suggesting that they contained amyloid A protein (secondary amyloid). The disease may be a model of familial secondary amyloidosis and offers an opportunity to study the pathogenesis of both amyloid deposition and papillary necrosis. The histochemical characteristics of feline renal amyloid require careful attention to technique. Section thickness affects Congo red affinity and both dichroism as well as birefringence should be considered when interpreting staining reactions. Thioflavine-T may be the preferred stain for identification of small deposits of amyloid. Variation in section thickness markedly affected the degree of potassium permanganate oxidation
J Am Vet Med Assoc. 1982 Jul 15;181(2):139-42. :
Renal amyloidosis in related Abyssinian cats.
Chew DJ, DiBartola SP, Boyce JT, Gasper PW.
Renal amyloidosis was diagnosed in 8 related Abyssinian cats. The kidneys were characterized pathologically by medullary interstitial and glomerular amyloid deposition, interstitial fibrosis, and papillary necrosis. Amyloid deposits were birefringent under polarized light after Congo red staining, were thioflavine-T positive, and lost Congo red staining after permanganate oxidation. Four of the cats were evaluated clinically. Two of these cats were terminally uremic, with nonregenerative anemia, azotemia, hyperphosphatemia, metabolic acidosis, mild hyperglycemia, isosthenuria, proteinuria, cylindruria, and mild hematuria. The remaining 2 cats were only moderately azotemic. Three of the cats had severe gingivitis and all 4 cats had hyperproteinemia due to hyperglobulinemia.
Arch Pathol Lab Med. 1979 Aug;103(9):475-8. :
Concurrent feline immune-complex nephritis. Tubular antigen-positive and renal amyloidosis.
Saegusa S, Shimizu F, Nagase M, Kasegawa A.
We describe tubular antigen-positive immune-complex nephritis in a case of feline renal amyloidosis. Amyloid deposition was observed in mesangial area, and thickening of capillary walls was shown in the majority of the glomeruli. This case was also characterized with typical fluorescent granular depositions of cat IgG and C3 along the glomerular capillary walls as seen in human membranous glomerulonephritis. The fluorescent pattern of tubular antigen was identical with that of IgG and C3. Electron micrograph showed the thickening and irregularity of glomerular basement membranes, fusion of foot processes, and deposits of electron-dense or sometimes translucent materials, mostly in the intramembranous location. The causal sequence of the coincidental deposition of amyloid and immune complexes is discussed.