Proteinuria is a marker and mediator of chronic kidney disease (CKD). In clinical practice, the urinary protein‐to‐creatinine ratio (UP/C) is of limited usefulness, because it indicates only the magnitude of proteinuria and not the origin of the loss (glomerular or tubular). The complete assessment of proteinuria includes quantitative and qualitative evaluations, both of which are required in order to optimize the therapy. In addition to measuring the UP/C, we performed SDS‐PAGE and western blotting to determine the expression of albumin, vitamin D‐binding protein (VDBP), retinol‐binding protein (RBP), and Tamm‐Horsfall protein (THP) in urine samples of 49 dogs: healthy (control) dogs (n = 9); and dogs with CKD (n = 40), stratified by stage. In the dogs with stage 3 or 4 CKD, there was a predominance of tubular proteins. Neither VDBP nor RBP was observed in the urine of the control dogs. Among the dogs with stage 1 or 2 CKD, VDBP and RBP were detected in those without proteinuria or with borderline proteinuria. The expression of urinary albumin was significantly higher in the stage 4 group than in any other group (P ≤ 0.01). In the stage 4 group, urinary THP was either undetectable or lower than in the control group (P ≤ 0.01). In conclusion, urinary VDBP and RBP might act as early markers of kidney injury, and a decrease in urinary THP could be an indicator of CKD progression.

RESUMO Foi proposta uma revisão das terminologias empregadas para a descrição das alterações renais e também sugerida uma classificação em estágios para a doença renal crônica à semelhança da medicina humana pela IRIS (International Renal Interest Society) INTRODUÇÃOSempre foi de grande interesse a padronização dos termos e conceitos relativos às doenças renais crônicas em cães e gatos, com o intuito de auxiliar no diagnóstico, no prognóstico e no tratamento (BROWN, 1999). Tradicionalmente, os termos doença renal, insuficiência renal, falência renal, azotemia e uremia têm sido empregados como sinônimos para descrever processos patológicos renais, o que implica diagnóstico equivocado e muitas vezes ocasiona a indicação de terapia inadequada (POLZIN et al., 2005). As doenças renais podem acometer os glomérulos, os túbulos, o tecido intersticial e/ou os vasos sanguíneos, e as afecções podem ter origem hereditária/congênita, infecciosa e tóxica (toxinas endógena ou exógena), ser imunomediada, por desequilíbrios eletrolíticos (hipercalcemia e hipocalemia no felino), e traumática (POLZIN, 2008). O rim é um órgão de múltiplas funções orgânicas (excretória, regulatória e biossintética) (POLZIN et al., 2005) e, para preservar a homeostase, não é necessária a presença do número original de néfrons, mas sim o suficiente para manter as funções. A falência renal retrata a disfunção máxima do órgão, e a insuficiência renal designa os quadros em que há perda de função renal, mas há ainda a tentativa de compensação por meio da -REVISÃO BIBLIOGRÁFICA -

There was no strong evidence that oxidative stress was associated with higher degrees of anemia in dogs with CKD.

Abstract:The increase of urinary fractional excretion of phosphorus (uFEP) may indicate phosphorus retention before the onset of hyperphosphatemia in the early stages of chronic kidney disease (CKD). The hypothesis of this study is whether uFEP may increase during the early stage of CKD as a compensatory mechanism to prevent hyperphosphatemia as well as whether hyperphosphatemia in the late stages is associated with increase or decrease in uFEP in dogs with naturally occurring CKD; therefore, the aim of this study was to determine the uFEP in CKD dogs with different stages. Forty-nine CKD dogs were included, and they were divided into stage 1 (serum creatinine < 1.4 mg/dL), stage 2 (serum creatinine 1.5 to 2.0 mg/dL), stage 3 (serum creatinine 2.1 to 5.0 mg/dL) and stage 4 (serum creatinine > 5.0 mg/dL), according to the IRIS staging criteria. The stage 3 was subdivided into stage 3-A (serum creatinine 2.1 to 3.5 mg/dL) and stage 3-B (serum creatinine 3.6 to 5.0 mg/dL). The control group comprised 10 dogs, and uFEP ≤ 40% was considered as normal. A progressive increase in uFEP along the progression of CKD was found. However, similar results of uFEP levels were observed in late CKD, since there were no differences between stages 3 (A, B) and 4. Interestingly, some CKD dogs with stage 4 showed normal or reduced uFEP, besides hyperphosphatemia; conversely, some dogs in early CKD had increased uFEP values and normophosphatemia. Our findings suggest that uFEP may act as a compensatory mechanism to avoid the onset of hyperphosphatemia in early CKD, but not in later stages. uFEP assessment may be considered as an additional tool for the diagnostic and monitoring of phosphate disorders in dogs with CKD, since it may help to identify disturbances of phosphorus balance. More studies are needed to elucidate the role of uFEP in phosphorus homeostasis in dogs with CKD.