The Journal of small animal practice · 2025
Preliminary study investigating the role of estimated glomerular filtration rate, proteinuria and hypertension to inform on chronic kidney disease after acute kidney injury.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Cole L P, Pelligand L, Jepson R, Humm K
Аннотация
OBJECTIVES: To assess chronic kidney disease in dogs after azotaemic acute kidney injury utilising serum creatinine, symmetric dimethylarginine and estimated glomerular filtration rate.
MATERIALS AND METHODS: Client-owned dogs hospitalised for azotaemic acute kidney injury (T0) were evaluated at discharge (T1), 3 months (T2) and 12 (T3) months with serum creatinine and symmetric dimethylarginine measured. In non-azotaemic dogs (serum creatinine <145 μmol/L) at T1 and T2, glomerular filtration rate was estimated by iohexol clearance. Acute kidney injury grade and chronic kidney disease stage were determined according to International Renal Interest Society guidelines. Non-azotaemic dogs were considered to have kidney dysfunction if glomerular filtration rate was reduced ≥20% below the mean of the body weight category.
RESULTS: Fifteen dogs with azotaemic acute kidney injury were recruited. At T0 peak, acute kidney injury grade was III (n = 4), IV (n = 8) and V (n = 3). At T1, 10/15 dogs remained azotaemic. At T2, 3/15 dogs remained azotaemic; this persisted in 2/3 dogs at T3. One dog was euthanised prior to T3 due to progression of azotaemia (stage 4). Based on glomerular filtration rate assessment, 4/12 and 5/12 non-azotaemic dogs had evidence of kidney dysfunction at T2 and T3, respectively. Ten out of 15 dogs were classified as International Renal Interest Society chronic kidney disease stage 1 and 4/15 dogs were stage 2 and 1/15 dog that did not survive to T3 was stage 4.
CLINICAL SIGNIFICANCE: Persistent azotaemia occurs infrequently in dogs surviving beyond 3 months after acute kidney injury. Estimated glomerular filtration rate may identify continued kidney dysfunction in non-azotaemic dogs.
MATERIALS AND METHODS: Client-owned dogs hospitalised for azotaemic acute kidney injury (T0) were evaluated at discharge (T1), 3 months (T2) and 12 (T3) months with serum creatinine and symmetric dimethylarginine measured. In non-azotaemic dogs (serum creatinine <145 μmol/L) at T1 and T2, glomerular filtration rate was estimated by iohexol clearance. Acute kidney injury grade and chronic kidney disease stage were determined according to International Renal Interest Society guidelines. Non-azotaemic dogs were considered to have kidney dysfunction if glomerular filtration rate was reduced ≥20% below the mean of the body weight category.
RESULTS: Fifteen dogs with azotaemic acute kidney injury were recruited. At T0 peak, acute kidney injury grade was III (n = 4), IV (n = 8) and V (n = 3). At T1, 10/15 dogs remained azotaemic. At T2, 3/15 dogs remained azotaemic; this persisted in 2/3 dogs at T3. One dog was euthanised prior to T3 due to progression of azotaemia (stage 4). Based on glomerular filtration rate assessment, 4/12 and 5/12 non-azotaemic dogs had evidence of kidney dysfunction at T2 and T3, respectively. Ten out of 15 dogs were classified as International Renal Interest Society chronic kidney disease stage 1 and 4/15 dogs were stage 2 and 1/15 dog that did not survive to T3 was stage 4.
CLINICAL SIGNIFICANCE: Persistent azotaemia occurs infrequently in dogs surviving beyond 3 months after acute kidney injury. Estimated glomerular filtration rate may identify continued kidney dysfunction in non-azotaemic dogs.