Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

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496 Chapter | 16 Kidney Function and Damage et al. , 1982 ; Newell et al. , 1997 ), but a decrease was reported after acepromazine alone ( Lourens et al. , 1982 ) and others found that GFR was slightly higher in anesthetized than in nonanesthetized dogs ( Balint and Forgacs, 1967 ), maybe as a consequence of the intravenous fluids. Anesthesia could lead to reduction of GFR in dogs with reduced renal mass ( Stone et al. , 1981 ). Thiopental anesthesia had no effect on GFR in sheep ( Cirio et al. , 1990 ). ● Hydration status: GFR was higher in dogs that were hyperhydrated, so hydration status should be standardized ( Kerr, 1958 ; Kunze et al. , 2006 ; Tabaru et al. , 1993 ). In cats, infusion of Ringer lactate at 1 to 2 ml/min produced on average a 40% increase of GFR ( Rasmussen et al. , 1985 ). In sheep, GFR was lower in summer than in winter because of hemoconcentration ( Nawaz and Shah, 1984 ). ● Diet: GFR was higher in dogs fed animal proteins rather than other proteins ( Bartges et al. , 1995a, 1995b, 1995d ; Kerr, 1958 ). It was higher with high levels of proteins in the diet in normal dogs and cats and after renal mass reduction ( Adams et al. , 1994 ; Bartges et al. , 1995c ; Bovee, 1992 ; Bovee and Kronfeld, 1981 ; Robertson et al. , 1986 ). In partially nephrectomized dogs, low- or high-sodium diets had little influence on GFR ( Greco et al. , 1994 ). In cats, GFR was moderately reduced by low-sodium diets (Buranakarl et al. , 2004 ), unchanged in cats receiving potassium-depleted food, but lowered when the same food was acidified with ammonium chloride ( Dow et al. , 1990 ). In cows, GFR was unchanged by mineral supply ( Hartmann et al. , 2001 ). GFR was higher in sheep fed a normal or high rather than a low protein diet ( Cirio and Boivin, 1990a, 1990b ; Cirio et al. , 1990 ; Eriksson and Valtonen, 1982 ; Rabinowitz et al. , 1973 ; Valtonen et al. , 1982 ). ● Meals: GFR increases ranging from 10% to 45% were observed after a meal of proteins in normal dogs and in dogs with renal mass reduction ( Bourgoignie et al. , 1987 ; Brown, 1992 ; Ewald, 1967 ; Jolliffe and Smith, 1932 ; Moustgaard, 1947 ; O’Connor and Summerill, 1976 ; Reinhardt et al. , 1975 ). This postprandial increase of GFR was not observed in dogs with experimental Fanconi’s syndrome ( Woods and Young, 1991 ). It was not reduced by fasting for more than 1 day ( Moustgaard, 1947 ). No difference in GFR was observed when ponies were fed twice a day or received the same amount of food every 2 h ( Clarke et al. , 1990 ). ● Exercise: GFR was unchanged by training in horses and dogs ( McKeever et al. , 1985, 2002 ) or by submaximal exercise for 20 or 60 min despite hemoconcentration ( Hinchcliff et al. , 1990 ; McKeever et al. , 1991 ). During effort under anaerobic conditions in horses, GFR decreased sharply then returned to prerun values within 15 min ( Schott et al. , 1991 ). ● Drugs: In dogs and sheep, GFR was increased by glucocorticoids, probably by an increase of plasma flow rate as in rats ( Baylis and Brenner, 1978 ; Gans, 1975 ). GFR was decreased by furosemide in dogs and cats ( Bostrom et al. , 2003 ; Hanna et al. , 1988 ). Controversial effects of NSAIDs were reported in dogs: either no change of GFR with meloxicam, carprofen, and ketoprofen ( Crandell et al. , 2004 ; Ko et al. , 2000 ; Narita et al. , 2005 ) or a moderate decrease with carprofen or ketoprofen ( Forsyth et al., 2000 ). GFR was moderately decreased after repeated excretory urograms in dogs ( Feeney et al. , 1980a ). In cats with experimental CRF, the ACE inhibitor benazepril increased GFR up to 30% ( Brown et al. , 2001 ), whereas ACE inhibitors could decrease GFR in sodium-restricted dogs ( Hall et al. , 1979 ). ● Biopsy: GFR was not affected after repeated renal biopsies in dogs ( Drost et al. , 2000 ; Groman et al. , 2004 ). b . Techniques of GFR Measurement The procedures used to calculate plasma clearances may also influence the results as they depend on the mathematical model chosen ( Heiene and Moe, 1999 ; Powers et al. , 1977 ; Watson et al. , 2002a ) and on the proposed limited sampling strategies ( Barthez et al. , 2001 ; Blavier et al. , 2001 ; Finco, 2005 ; Watson et al. , 2002a ). Others have suggested measuring the concentration of an exogenous marker at a given time after injection (e.g., P-Creatinine after I.V. load in dogs) ( Labato and Ross, 1991 ; Watson et al. , 2002a ). The measurement of creatinine concentrations by Jaffé technique (discussed earlier) led to erroneously high values for creatinine clearance in early studies. Because of the larger proportion of interfering substances in plasma than in urine with the Jaffé technique, P-Creatinine was overestimated in comparison to U-Creatinine (e.g., in dog urine) ( Shannon et al. , 1932 ). This discrepancy between creatinine and inulin clearances does not exist when the measurements are based on the more accurate enzymatic techniques ( Finco et al. , 1993 ). The results of GFR determination may vary according to the technique so their transferability is limited ( Driehuys et al. , 1998 ; Finco, 2005 ; Gagnon et al. , 1971 ; Izzat and Rosborough, 1989 ; Oester et al. , 1968 ; Rogers et al. , 1991 ), and caution is required when using decision limits from other laboratories or from the literature. Correcting factors have been proposed in some cases, for instance, for iohexol plasma clearance and exogenous creatinine urinary clearance in dogs ( Finco et al. , 2001 ; Gleadhill and Michell, 1996 ). However, such results remain controversial. The estimation of GFR based on iohexol clearance, for example, was considered reliable in dogs and cats ( Brown et al. , 1996 ), whereas others showed differences of up to 0.95 ml/min/kg with creatinine clearance ( Miyamoto, 2001b ). The urine clearance of endogenous creatinine and the urine and plasma clearance of exogenous creatinine gave similar results ( Finco et al. , 1981, 1991 ; Lee et al. , 1983 ; Watson et al. , 2002a ), but plasma DTPA clearance was 1.15 time higher than plasma iohexol clearance in dogs ( Moe and Heiene, 1995 ).
6 5 4 3 2 1 0 Dog Cat Equine Cattle Sheep Goat
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Preface It has been more than a dec
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viii Contributors Björn P. Meij (5
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2 Chapter | 1 Concepts of Normality
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10 Chapter | 1 Concepts of Normalit
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Chapter 2 Comparative Medical Genet
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I. Introduction 29 Green Red Green
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I. Introduction 31 A1 genetic map d
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I. Introduction 33 of genomes of va
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36 Chapter | 2 Comparative Medical
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46 Chapter | 3 Carbohydrate Metabol
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IX. Disorders of Carbohydrate Metab
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X. Disorders of Ruminants Associate
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X. Disorders of Ruminants Associate
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References 79 Kaneko , J. J. , Luic
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Chapter 4 Lipids and Ketones Michae
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II. Long Chain Fatty Acids 83 FIGUR
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II. Long Chain Fatty Acids 85 Plasm
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IV. Phospholipids 87 The regulation
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V. Cholesterol 89 V. CHOLESTEROL A.
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VI. Lipoproteins 91 TABLE 4-1 Compo
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VI. Lipoproteins 93 TABLE 4-2 Apoli
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96 Chapter | 4 Lipids and Ketones B
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98 Chapter | 4 Lipids and Ketones
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Chapter 5 Proteins, Proteomics, and
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III. Metabolism of Proteins 119 C .
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IV. Plasma Proteins 121 NH 4 HCO
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V. Methodology 123 molecule. The gl
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V. Methodology 125 has occurred wil
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V. Methodology 127 Although attempt
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V. Methodology 129 kD 94 67 43 2 2
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V. Methodology 131 D . Specific Pro
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VI. Normal Plasma and Serum Protein
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VII. Interpretation of Serum Protei
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References 149 Andersson , M. , Ste
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References 151 response of haptoglo
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References 153 dogs with metastasiz
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References 155 Watson , T. D. G. (
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158 Chapter | 6 Clinical Veterinary
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V. Methods for Evaluation of the Im
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VI. Laboratory Diagnosis of Disease
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Chapter 7 The Erythrocyte: Physiolo
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II. Hematopoiesis 175 progenitor ce
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III. Developing Erythroid Cells 177
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IV. Mature RBC 185 immune-mediated
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IV. Mature RBC 187 TABLE 7-3 Erythr
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IV. Mature RBC 189 TABLE 7.5 Erythr
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IV. Mature RBC 191 Echinocyte forma
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IV. Mature RBC 193 Pig RBC isoantig
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IV. Mature RBC 195 occurs in chicke
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IV. Mature RBC 197 inorganic phosph
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IV. Mature RBC 199 (a) FIGURE 7-6 T
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IV. Mature RBC 201 RBC 2,3DPG incre
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IV. Mature RBC 203 mechanisms would
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IV. Mature RBC 205 released during
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IV. Mature RBC 207 reduced by ascor
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V. Determinants of RBC Survival 209
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V. Determinants of RBC Survival 211
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VI. Inherited Disorders of RBCs 213
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described in people. They include a
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References 221 Boas , F. E. , Forma
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References 223 Della Rovere , F. ,
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References 225 Gedde , M. M. , Davi
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References 227 phosphofructokinase-
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References 229 Knight , A. P. , Las
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References 231 Martinovich , D. , a
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References 233 Pearson , W. , Boerm
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References 235 Shadduck , R. K. ( 1
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References 237 Tennant , B. , Dill
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References 239 Williams , D. M. , L
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Chapter 8 Porphyrins and the Porphy
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II. Porphyrins 243 two vinyl groups
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II. Porphyrins 245 TABLE 8-2 Nomenc
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IV. Porphyrias 247 6. Uroporphyrins
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IV. Porphyrias 249 i . Urine It is
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IV. Porphyrias 251 to localize the
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IV. Porphyrias 253 FIGURE 8-6 Metab
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IV. Porphyrias 255 estrogens. The d
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References 257 and hexachlorobenzen
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Chapter 9 Iron Metabolism and Its D
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II. Iron Distribution 261 plasma of
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IV. Plasma Iron Transport 263 pathw
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VI. Iron Metabolism in Cells 265 of
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VI. Iron Metabolism in Cells 267 in
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VII. Tests for Evaluating Iron Meta
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VII. Tests for Evaluating Iron Meta
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VIII. Disorders of Iron Metabolism
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References 279 ( Norrdin et al ., 2
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References 281 Fresco , R. ( 1981 )
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References 283 Moore , C. V. , Duba
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References 285 Weiden , P. L. , Hac
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288 Chapter | 10 Hemostasis TABLE 1
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292 Chapter | 10 Hemostasis The pro
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294 Chapter | 10 Hemostasis exhibit
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298 Chapter | 10 Hemostasis that is
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302 Chapter | 10 Hemostasis However
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304 Chapter | 10 Hemostasis 2. Comp
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306 Chapter | 10 Hemostasis is a re
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308 Chapter | 10 Hemostasis 2. Asse
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310 Chapter | 10 Hemostasis necessi
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312 Chapter | 10 Hemostasis disease
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314 Chapter | 10 Hemostasis concent
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316 Chapter | 10 Hemostasis the rol
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318 Chapter | 10 Hemostasis proport
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320 Chapter | 10 Hemostasis a consi
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322 Chapter | 10 Hemostasis Bakhtia
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324 Chapter | 10 Hemostasis Dowd ,
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326 Chapter | 10 Hemostasis Kier ,
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328 Chapter | 10 Hemostasis Nielsen
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330 Chapter | 10 Hemostasis Tablin
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332 Chapter | 11 Neutrophil Functio
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352 Chapter | 12 Diagnostic Enzymol
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380 Chapter | 13 Hepatic Function L
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382 Chapter | 13 Hepatic Function e
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384 Chapter | 13 Hepatic Function p
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386 Chapter | 13 Hepatic Function m
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388 Chapter | 13 Hepatic Function s
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390 Chapter | 13 Hepatic Function f
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392 Chapter | 13 Hepatic Function T
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394 Chapter | 13 Hepatic Function 2
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396 Chapter | 13 Hepatic Function u
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398 Chapter | 13 Hepatic Function 2
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400 Chapter | 13 Hepatic Function c
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402 Chapter | 13 Hepatic Function F
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404 Chapter | 13 Hepatic Function A
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406 Chapter | 13 Hepatic Function E
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408 Chapter | 13 Hepatic Function K
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410 Chapter | 13 Hepatic Function R
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412 Chapter | 13 Hepatic Function W
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414 Chapter | 14 Gastrointestinal F
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Page 479 and 480: References 481 Engel , A. G. ( 2004
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Page 483 and 484: Chapter 16 Kidney Function and Dama
Page 485 and 486: II. Kidney Morphology and Function
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Page 527 and 528: Chapter 17 Fluid, Electrolyte, and
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546 Chapter | 17 Fluid, Electrolyte
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VIII. Clinicopathological Indicator
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References 555 plasma water, electr
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References 557 Krzywanek , H. ( 197
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562 Chapter | 18 Pituitary Function
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606 Chapter | 19 Adrenocortical Fun
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624 Chapter | 20 Thyroid Function a
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630 Chapter | 20 Thyroid Function S
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632 Chapter | 20 Thyroid Function a
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634 Chapter | 20 Thyroid Function O
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636 Chapter | 21 Clinical Reproduct
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664 Chapter | 22 Trace Minerals the
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666 Chapter | 22 Trace Minerals the
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668 Chapter | 22 Trace Minerals P i
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670 Chapter | 22 Trace Minerals be
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Copper Cuproreductase Cytochromes C
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674 Chapter | 22 Trace Minerals 2 .
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676 Chapter | 22 Trace Minerals Cor
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678 Chapter | 22 Trace Minerals inf
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682 Chapter | 22 Trace Minerals VI
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684 Chapter | 22 Trace Minerals red
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686 Chapter | 22 Trace Minerals of
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688 Chapter | 22 Trace Minerals Per
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692 Chapter | 22 Trace Minerals Liu
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Chapter 23 Vitamins Robert B. Rucke
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III. Fat-Soluble Vitamins 697 TABLE
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III. Fat-Soluble Vitamins 699 Carot
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III. Fat-Soluble Vitamins 701 Major
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III. Fat-Soluble Vitamins 703 doses
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III. Fat-Soluble Vitamins 705 Diet
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III. Fat-Soluble Vitamins 707 conta
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III. Fat-Soluble Vitamins 709 immun
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IV. Water-Soluble Vitamins 711 are
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IV. Water-Soluble Vitamins 713 abil
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IV. Water-Soluble Vitamins 715 5’
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IV. Water-Soluble Vitamins 717 H 2
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IV. Water-Soluble Vitamins 719 Enzy
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722 Chapter | 23 Vitamins When biot
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724 Chapter | 23 Vitamins Cyanocoba
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726 Chapter | 23 Vitamins V . VITAM
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728 Chapter | 23 Vitamins nature, r
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730 Chapter | 23 Vitamins Stites ,
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732 Chapter | 24 Lysosomal Storage
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Chapter 25 Tumor Markers Michael D.
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II. Serum Tumor Markers 753 also be
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III. Flow Cytometry 755 cancer of t
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V. Immunohistochemistry/Immunocytoc
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V. Immunohistochemistry/Immunocytoc
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References 761 analysis will facili
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References 763 Fernandez , N. J. ,
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References 765 Meinecke , B. , and
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References 767 Walter , J. ( 2000 )
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770 Chapter | 26 Cerebrospinal Flui
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TABLE 26-7 Continued Constituent Ro
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Chapter 27 Clinical Biochemistry in
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II. Hepatotoxicity 823 Therefore, A
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III. Nephrotoxicity 825 suggested a
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IV. Toxins Affecting Skeletal and C
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VII. Toxins Affecting Erythrocytes
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VIII. Toxins Affecting Hemoglobin a
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IX. Toxins Affecting the Nervous Sy
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References 835 Plants classified as
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References 837 Solaiman , S. G. , M
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840 Chapter | 28 Avian Clinical Bio
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Budgerigar ALAT (IU/g tissue) Budge
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874 Appendix | I SI Units TABLE E S
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Appendix II Conversion Factors of S
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Appendix IV Stability of Serum Enzy
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Appendix VI Nomogram for Computing
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t0100 Appendix VIII Blood Analyte R
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884 Appendix | VIII Blood Analyte R
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890 Appendix | IX Blood Analyte Ref
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Appendix X Blood Analyte Reference
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Appendix XI Blood Analyte Reference
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Appendix XII Urine Analyte Referenc
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902 Appendix | XIII Cerebrospinal F
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904 Appendix | XIV Cerebrospinal Fl
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