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Kidney: acute injury
Synonym(s): AKI
Introduction
- Definition: abrupt injury to the renal parenchyma, with or without a decrease in kidney function, as reflected by accumulation of uremic toxins or altered urine production.
- Cause: toxins/drugs, infection, renal ischemia, inflammation. Can be classified as community-acquired or hospital-acquired.
- Signs: uremia, oliguria (in most cases), anuria or polyuria (less commonly), dehydration, lethargy.
- Treatment: prompt treatment to limit renal damage.
- Prognosis: guarded, depending on underlying cause; mortality may be high and extensive renal damage may result in chronic renal failure.
Presenting signs
- Depending on severity of the injury.
- Acute uremia Uremia:
- Vomiting.
- Diarrhea.
- Anorexia.
- Nausea.
- Lethargy.
- Oral ulceration, appears in 3-5 days.
- Altered urinary production:
- Oliguria (relative if <2 ml/kg/h, or absolute if <1 ml/kg/h).
-
- Anuria (0-0.5 ml/kg/h).
- Polyuria (>2 ml/kg/h) in mild cases or in recovery phase.
- Abdominal pain in the sublumbar region (depending on etiology).
- Uremic encephalopathy (seizures, obtundation, coma) in very advanced cases.
- Uremic pneumonitis (respiratory distress).
- Hypervolemia and ventricular premature complex arrhythmias (if anuria/oliguria).
- Bradycardia, eg hyperkalaemia Hyperkalemia.
- Hypothermia or pyrexia, eg pyelonephritis Pyelonephritis, leptospirosis Leptospira spp.
Acute presentation
- Anuria.
- Uremic crisis.
Geographic incidence
- Leptospirosis is a cause of acute kidney injury which has a geographical influence, eg regions with higher annual rainfall and warm climates.
- Ethylene glycol toxicity Ethylene glycol poisoning is more common in colder climates.
Cost considerations
- If the owner can afford hemodialysis, it may improve survival and recovery rate. However, it is very expensive.
- Intensive fluid therapy and monitoring is moderate to expensive.
- Acute renal failure is rarely responsive to inexpensive therapy.
Special risks
Anesthesia
- Hyperkalemia Hyperkalemia and metabolic acidosis (pH <7.1) Acid base imbalance can cause severe cardiac problems and exacerbate neurological signs.
- Overdosage of drugs, since most drugs have some degree of renal clearance.
Intravenous contrast
- Pre-existing renal disease.
Pathogenesis
Etiology
Pre-renal AKI (hemodynamic)
- Hypovolemia: o Prolonged dehydration. o Fluid losses, eg gastrointestinal disease, hypoadrenocorticism Hypoadrenocorticism, diabetes insipidus Diabetes insipidus. o Diuretics Therapeutics: diuretics/vasodilators, ACE-Is ACE inhibitors: overview/ Angiotensin receptor blockers (ARBs). o Hypovolemic shock Shock: hypovolemic. o Hemorrhage/trauma. o Pancreatitis Pancreatitis or other causes of systemic inflammatory response syndrome Systemic inflammatory response syndrome (SIRS).
- Decreased cardiac output: o Cardiac disease; Heart: dilated cardiomyopathy (DCM), mitral valve disease (MVD). o Pericardial effusion Pericardial disease. o Sepsis Systemic inflammatory response syndrome (SIRS). o Anaphylaxis Anaphylaxis.
- Renal vasoconstriction: o Drugs (NSAIDs Analgesia: NSAID, ARBs, ACE-Is, norepinephrine) – can lead to intrinsic AKI. o Hepatorenal syndrome. o Hypercalcemia Hypercalcemia: overview Hypercalcemia.
- Systemic vasodilation: o Anesthesia/surgery. o Drugs, eg anti-hypertensives. o Sepsis.
Intrinsic AKI (tubular, glomerular, interstitial and vascular damage)
- Toxins:
- Ethylene glycol Ethylene glycol poisoning.
- Drugs:
- Antibiotics: aminoglycosides (neomycin Neomycin, gentamycin Gentamicin), polymixin B Polymyxin B, sulfonamides Trimethoprim, tetracycline Tetracycline.
- Amphotericin B Amphotericin B.
- NSAIDs (especially in dehydrated animal) Analgesia: NSAID.
- Doxorubicin Doxorubicin.
- Cisplatin Cisplatin.
- Methotrexate Methotrexate.
- Human albumin transfusion.
- Sucrose-containing human IV immunoglobulins.
- Cyclosporin Cyclosporin.
- Tacrolimus Tacrolimus (overdose).
- Vitamin D Vitamin D poisoning.
- Mercury.
- Hemoglobinuria Hemoglobinuria/myoglobinuria Myoglobinuria.
- Plants Poisonous Plants: lilies Lilies (Lilium and Hemerocallis species) (easter lily, day lily, tiger lily, Japanese show lily and rubrum lily); night blooming jessamine, Solanum malacoxylon.
- Grapes, raisins, currants Raisin poisoning.
- Contrast agents, eg isohexol.
- Fertilizers (containing melamine).
Sepsis and multiple organ dysfunction syndrome (MODS)
- Infection:
- Bacterial (pyelonephritis) Pyelonephritis.
- Leptospirosis Leptospira spp.
- Viral (FIP Feline immunodeficiency virus disease).
- Endotoxemia, eg E. coli infection Escherichia coli.
- Acute glomerulonephritis Glomerulonephritis.
- Renal lymphoma Kidney: neoplasia.
- Ischemia: renal artery thrombosis or occlusion Kidney: thromboembolism.
Post-renal AKI
- Ureteral/urethral obstruction:
- Urolithiasis Urolithiasis.
- Neoplasia Urethra: neoplasia.
- Feline lower urinary tract disease Feline lower urinary tract disease (FLUTD).
- Ureteric ligation Ureter: obstruction – surgical management.
- Urinary tract trauma, eg uroabdomen.
Predisposing factors
General
- Pre-existing renal damage with additional insult, eg reduced renal perfusion.
- Any cause of reduced renal blood flow.
Specific
- Anesthesia, especially without appropriate blood pressure monitoring and IV fluid support.
- Chemotherapy with cisplatin Cisplatin, methotrexate Methotrexate or doxorubicin Doxorubicin.
- Access to antifreeze (ethylene glycol) Ethylene glycol poisoning.
- Misuse of NSAIDs, aminoglycosides, diuretics or vasodilators.
- Intravenous contrast (especially in dehydrated/hypoperfused patients).
Pathophysiology
Four phases
- Induction phase: renal insult resulting in damage to renal parenchyma. However, clinical signs are often not apparent and make recognition challenging. Early intervention might make the injury potentially reversible; hours to 1-2 days.
- Extension phase: ongoing cellular injury progressing to cell death, with progressive decline in GFR, decreased urine output and loss of urine concentrating ability.
- Maintenance phase: elimination of inciting factors at this stage does not alter existing damage or rate of recovery; signs of uremia may be present; a prolonged maintenance phase is associated with slower recovery and increased likelihood of permanently reduced renal function.
- Recovery phase: progressive and variable restoration of renal function.
- Reduced renal blood flow → reduced oxygen and energy transport to cells → cell swelling and membrane damage → vasoconstriction and inflammatory mediator release → further vasoconstriction.
- Nephrons are damaged at different sites (glomerulus, tubular cell, intercellular junction, basement membrane) depending on etiology → acute decline in glomerular filtration rate → increased urea/creatinine, decrease in urine specific gravity → uremic signs, oliguria (sometimes anuria or polyuria), fluid and electrolyte imbalances, acidosis.
Timecourse
- Animals may die acutely, especially if the underlying cause is not detected and treated or if the oliguric/anuric phase persists.
- If treated appropriately, animals may recover, but the recovery phase can take >3 weeks of intensive care. Some patients may progress to develop chronic kidney disease (CKD) Chronic kidney disease.
Diagnosis
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Treatment
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Prevention
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Outcomes
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Further Reading
Publications
Refereed papers
- Recent references from PubMed and VetMedResource.
- Tolbert K & Stubbs E (2024) Rational use of gastroprotectants in cats: An evidence-based approach. J Feline Med & Surg 26 (8), 1098612X241274235 PubMed.
- Segev G, Cortellini S, Foster J D et al (2024) International Renal Interest Society best practice consensus guidelines for the diagnosis and management of acute kidney injury in cats and dogs. Vet J 305,106068 PubMed.
- Wun M K, Leister E, King T et al (2023) Acute kidney injury in 18 cats after subcutaneous meloxicam and an update on non-steroidal anti-inflammatory drug usage in feline patients in Australia. Aust Vet J 101 (3), 90-98 PubMed.
- Loane S C, Thomson J M, Williams T L & McCallum K E (2022) Evaluation of symmetric dimethylarginine in cats with acute kidney injury and chronic kidney disease. J Vet Intern Med 36 (5),1669-1676 PubMed.
- Siu K, Diaz A, Chadwick A, Keys D et al (2022) Urine bacterial culture growth and association with urine sedimentation and clinical findings in cats with acute kidney injury. J Feline Med Surg 24 (10), e295-e301 PubMed.
- Dijkman M A., van Roemburg R G, De Lange D W et al (2022) Incidence of Vitis fruit-induced clinical signs and acute kidney injury in dogs and cats. J Small Anim Pract 63 (6), 447–453 PubMed.
- Langston C &, Gordon D (2021) Effects of IV fluids in dogs and cats with kidney failure. Front Vet Sci 8, 659960 PubMed.
- Cook S, Whitby E, Elias N et al (2021) Retrospective evaluation of refeeding syndrome in cats: 11 cases (2013-2019). J Feline Med Surg 23 (10), 883-891 PubMed.
- Carvalho L, Kelley D, Labato M A & Webster C R (2021) Hyperammonemia in azotemic cats. J Feline Med Surg 23 (8), 700-707 PubMed.
- Mauro K D, Culler C A & Vigani A (2021) Emergency treatment with intermittent hemodialysis for amikacin overdose in a cat. J Vet Emerg Crit Care 31 (6), 813-817 PubMed.
- Chen H, Dunaevich A, Apfelbaum N et al (2020) Acute on chronic kidney disease in cats: Etiology, clinical and clinicopathologic findings, prognostic markers, and outcome. J Vet Intern Med 34 (4), 1496-1506 PubMed.
- Cooper R L & Labato M A (2011) Peritoneal dialysis in veterinary medicine. Vet Clin North Am Small Anim Pract 41 (1), 91-113 PubMed.
- Dorval P & Boysen S R (2009) Management of acute renal failure in cats using peritoneal dialysis: a retrospective study of six cases (2003-2007). J Feline Med Surg 11 (2), 107-115 PubMed.
- Worwag S & Langston C E (2008) Acute intrinsic renal failure in cats: 32 cases (1997-2004). JAVMA 232 (5), 728-732 PubMed.
- Sigrist N E (2007) Use of dopamine in acute renal failure. J Vet Emerg Crit Care 17 (2), 117-126 VetMedResource.
- Stokes J E & Forrester S D (2004) New and unusual causes of acute renal failure in dogs and cats. Vet Clin North Am Small Anim Pract 34 (4), 909-922 PubMed.
- Grauer G F (1998) Fluid therapy in acute and chronic renal failure. Vet Clin North Am Small Anim Pract 28 (3), 609-622 PubMed.
- Grauer G F (1996) Prevention of acute renal failure. Vet Clin North Am Small Anim Pract 26 (6), 1447-1459 PubMed.
- Ohashi F, Awaji T, Shimada T et al (1995) Plasma methylguanidine and creatinine concentrations in cats with experimentally induced acute renal failure. J Vet Med Sci 57 (5), 965-966 PubMed.
- Mealey K L & Boothe D M (1994) Nephrotoxicosis associated with topical administration of gentamicin in a cat. JAVMA 204 (12),1919-1921 PubMed.
Other sources of information
- Foster J D (2024) Acute Kidney Injury. In: Textbook of Veterinary Internal Medicine: Diseases of the Dog and the Cat. 9th edn. Eds: Ettinger S J, Feldman E C, Cote E. Elsevier Saunders, USA. pp 2073-2088.
- Blois S L (2024) Hyper- and Hypocoagulable States. In: Textbook of Veterinary Internal Medicine: Diseases of the Dog and the Cat. 9th edn. Eds: Ettinger S J, Feldman E C, Cote E. Elsevier Saunders, USA, pp 863-869.
- International Renal Interest Society (2023) IRIS Grading of AKI. Website: www.iris-kidney.com.
- Langston C (2010) Acute Uraemia. In: Textbook of Veterinary Internal Medicine. 7th edn. Eds: Ettinger S J & Feldman E C. W B Saunders, USA. pp 1969-1985.
- Chew D J & Gieg J A (2006) Fluid Therapy During Intrinsic Renal Failure. In: Fluid, Electrolyte and Acid-Base Disorders in Small Animals. Eds: Di Bartola S P. W B Saunders, USA. pp 518-540.
- Frenier S L & Dhein C R (1991) Diagnosis and Management of Acute Renal Failure. In: Consultations in Feline Internal Medicine 1. Ed: August J R. W B Saunders, USA. pp 281-288.