-18 month old female spayed Persian presented in acute renal failure. Progressed to anuric renal failure with no response to lasix.
-Indoor only, fully vaccinated, no plants in house, no access to garage, no known exposure to toxins. Did get single metacam injection in February associated with OHE.
-U/S showed large amount free abdominal and pleural fluid
-Hypoechoic pancreas and liver
-Hyperechoic, clumpy-appearing mesentery
-Normal lymph nodes
-Mild corrugation of bowel (I assume secondary to peritonitis)
-18 month old female spayed Persian presented in acute renal failure. Progressed to anuric renal failure with no response to lasix.
-Indoor only, fully vaccinated, no plants in house, no access to garage, no known exposure to toxins. Did get single metacam injection in February associated with OHE.
-U/S showed large amount free abdominal and pleural fluid
-Hypoechoic pancreas and liver
-Hyperechoic, clumpy-appearing mesentery
-Normal lymph nodes
-Mild corrugation of bowel (I assume secondary to peritonitis)
-No fluid tap done.
-Kidneys length is ~4.1 – 4.3 cm.
Due to poor clinical response and severe findings on U/S, owners elected euthanasia with no post. However, I’m curious what the most likely etiologies are.
Thanks,
Suzanne
Comments
Could FIP or Renal Lymphoma
Could FIP or Renal Lymphoma be rule outs?
Could FIP or Renal Lymphoma
Could FIP or Renal Lymphoma be rule outs?
Sounds toxic or FIP/other
Sounds toxic or FIP/other infectious… kidneys are non descript minor hyperechoic cortices. How about doing a post mortem US guided renal bx?
I was doing the U/S for a
I was doing the U/S for a colleague. I told her it was likely a toxin or FIP but just wanted to make sure I didn’t miss a more likely diagnosis.
Thanks!
Suzanne
Sounds toxic or FIP/other
Sounds toxic or FIP/other infectious… kidneys are non descript minor hyperechoic cortices. How about doing a post mortem US guided renal bx?
I was doing the U/S for a
I was doing the U/S for a colleague. I told her it was likely a toxin or FIP but just wanted to make sure I didn’t miss a more likely diagnosis.
Thanks!
Suzanne
Most likley would be toxic –
Most likley would be toxic – any possiblity of exposure to Tiger lily flowers?, however, with the ascites bladder rupture also possible.
Lasix has been shown to have no effect in managing acute kidney injury cases.
I believe they used it in
I believe they used it in order to induce diuresis (which did not work). Do you use mannitol in anuric renal failure?
No possible exposure to lilies per owner.
Thanks.
Most likley would be toxic –
Most likley would be toxic – any possiblity of exposure to Tiger lily flowers?, however, with the ascites bladder rupture also possible.
Lasix has been shown to have no effect in managing acute kidney injury cases.
I believe they used it in
I believe they used it in order to induce diuresis (which did not work). Do you use mannitol in anuric renal failure?
No possible exposure to lilies per owner.
Thanks.
Treatment is aimed at
Treatment is aimed at correcting dehydration and maintaining renal p[erfusion and blood pressure (MAP > 60 mmHg). Poor response with Lasix and mannitol Abstract from a recent paper on sepsis induced AKI:
Objective – To review the unique pathophysiology of sepsis-induced acute kidney injury (AKI) and highlight the relevant aspects of the Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guidelin for Acute Kidney Injury that may apply to veterinary patients.
Data Sources – Electronic search of MEDLINE database.
Human Data Synthesis – Sepsis-induced AKI is diagnosed in up to 47% of human ICU patients and is seen as a major public health concern associated with increased mortality and increased progression to chronic kidney disease (CKD). Consensus criteria for the definition and classification of AKI has allowed for accurate description of the epidemiology of patients with AKI. AKI develops from a complex relationship between the initial insult and activation of inflammation and coagulation. In contrast to the traditional view, clinical and experimental data dispute the role of renal ischemia-reperfusion in the development of sepsis-induced AKI.
Renal tubular dysfunction with activation of the tubuloglomerular feedback mechanism appears to be a crucial contributor to sepsis-induced AKI. Furosemide and n-acetylcysteine (NAC) do not appear to be helpful in the treatment of AKI. Hydroxyethyl starches (HES), dopamine, and supraphysiological concentrations of chloride are harmful in patients with AKI.
Veterinary Data Synthesis – Community and hospital-acquired AKI is a significant factor affecting survival in critical ill patients. Sepsis-induced AKI occurs in 12% of dogs with abdominal sepsis and is an important contributor to mortality. Early detection of AKI in hospitalized patients currently offers the best opportunity to improve patient outcome. The use of urinary biomarkers to diagnose early AKI should be evaluated in critical care patients.
Conclusion – Veterinary clinical trials comparing treatment choices with the development of AKI are needed to make evidence-based recommendations for the prevention and treatment of AKI.
J Vet Emerg Crit Care 2015; 25(2): 200–209
Treatment is aimed at
Treatment is aimed at correcting dehydration and maintaining renal p[erfusion and blood pressure (MAP > 60 mmHg). Poor response with Lasix and mannitol Abstract from a recent paper on sepsis induced AKI:
Objective – To review the unique pathophysiology of sepsis-induced acute kidney injury (AKI) and highlight the relevant aspects of the Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guidelin for Acute Kidney Injury that may apply to veterinary patients.
Data Sources – Electronic search of MEDLINE database.
Human Data Synthesis – Sepsis-induced AKI is diagnosed in up to 47% of human ICU patients and is seen as a major public health concern associated with increased mortality and increased progression to chronic kidney disease (CKD). Consensus criteria for the definition and classification of AKI has allowed for accurate description of the epidemiology of patients with AKI. AKI develops from a complex relationship between the initial insult and activation of inflammation and coagulation. In contrast to the traditional view, clinical and experimental data dispute the role of renal ischemia-reperfusion in the development of sepsis-induced AKI.
Renal tubular dysfunction with activation of the tubuloglomerular feedback mechanism appears to be a crucial contributor to sepsis-induced AKI. Furosemide and n-acetylcysteine (NAC) do not appear to be helpful in the treatment of AKI. Hydroxyethyl starches (HES), dopamine, and supraphysiological concentrations of chloride are harmful in patients with AKI.
Veterinary Data Synthesis – Community and hospital-acquired AKI is a significant factor affecting survival in critical ill patients. Sepsis-induced AKI occurs in 12% of dogs with abdominal sepsis and is an important contributor to mortality. Early detection of AKI in hospitalized patients currently offers the best opportunity to improve patient outcome. The use of urinary biomarkers to diagnose early AKI should be evaluated in critical care patients.
Conclusion – Veterinary clinical trials comparing treatment choices with the development of AKI are needed to make evidence-based recommendations for the prevention and treatment of AKI.
J Vet Emerg Crit Care 2015; 25(2): 200–209