Loobani AcademyAbstract
Acute renal failure (ARF) is also called acute kidney injury(AKI),which is a clinical syndrome of sudden decrease of glomerular filtration function(GFR). Dogs with acute onset and obvious clinical symptoms, often characterized by acute urine volume, electrolyte disorders, acid-base balance disorders and inability to excrete metabolites, rapid increases in blood urea nitrogen and creatinine, and acute uremia. If the kidney tissue is not completely damaged, potential compensatory function can occur. In many cases, with careful treatment and care, the affected dog can regain adequate kidney function to maintain a normal life.In this case,i will introduce the diagnosis and treatment methods to AKI in canine.
Key words: Canine,diagnosis,treatment,AKI
Basic information
Name: DU DOU
Breed: Poodle
Sex: Female (castrated)
Age: 3 years old
Body weight: 10.5kg
History: Complete vaccination and deworming,canine distemper virus infection when she was young.
Owner took her to park recently, playing water in the outdoors during that time and eat a lot of mankind food(including purples). Yesterday ,the dog was found start to appear vomiting and weak.Owner found it lose appetite and in lower spirits than usual. So decide to took her to the hospital. Vaccinate history is completed and deworming in this year.
Physical examination:
Body weight 10.5kg,temperature 39.7℃,respiratory rate was 36/min,heart rate: 124 beats/min. No obvious murmurs in breathing. Mouth mucosa was red,capillary refill time(CRT)<2s,body condition score(BCS)was 6/9 which can no touch the ribs in palpation. The patient was presented with highly depression situation. Dry coat and nose. Abdominal palpation was found painful and swelling in the latter abdomen which was a position of the kidneys. There were mild dental calculus and gingivitis in oral examination. The surface hair of skin were bad. Mild dehydration was not found. Palpation the rate of the femoral artery was equal with the heart rate.
Laboratory examination
Complete Blood Count (CBC) examination for Day 1
Project | Result | Reference Range |
WBC | 19.8×103/uL | 6.0~17.0 |
RBC | 8.57×106/uL | 5.5~10 |
HGB | 14.6g/dL | 12.0~18.0 |
HCT | 53.1% | 37~55 |
MCV | 66fL | 60~77 |
MCH | 21.7pg | 19~24.5 |
MCHC | 32.9g/dL | 30~37 |
PLT | 247×103/uL | 200~500 |
LYM% | 23.5% | 12~30 |
OTHR% | 90.8% | 60~86 |
EO% | 5.7% | 2~10 |
LYM# | 0.3×103/uL |
|
OTHR# | 6.5×103/uL |
|
EO# | 0.4×103/uL |
Interpretation: There was a mild increased in the leukocyte line. Red blood cell count and HCT indicate a possibility of dehydration that may have a low liquid volume,combined with the performance of the patient.
Idexx Catalyst biochemistry CHEM15
Project | Result | Reference Range |
ALB | 1.9g/dL | 2.3-4.0 |
ALT | 128U/L | 10-100 |
ALKP | 786U/L | 23-212 |
AMYL | 1450U/L | 500-1500 |
AST | 112 U/L | 0-50 |
BUN | 46.1mg/dL | 7-27 |
CREA | 590mg/dL | 0.5-1.8 |
CK | 138U/L | 10-200 |
GGT | 8U/L | 0-7 |
LIPA | 1560U/L | 200-1800 |
PHOS | 4.96mg/dL | 2.5-6.8 |
TP | 4.8g/dL | 5.2-8.2 |
TBIL | >1000mg/dL | 0-0.9 |
GLOB | 2.9g/dL | 2.5-4.5 |
GLU | 39mg/dL | 74-143 |
CHOL | 355mg/dL | 110-320 |
CA | 8.7mg/dL | 7.9-12.0 |
Interpretation: There was a obvious increase in ALT,ALKP,AST,BUN,CREA,TBIL,GGT,LIPA,CHOL which is a cue for the cell injury and dehydration. No obvious abnormalities in other biochemical indicators. If kidney function is close to normal, small changes in creatinine are accompanied by large changes in GFR. When renal function is significantly impaired, there are larger changes in creatinine and smaller changes in GFR. Therefore,serum creatinine is an insensitive indicator of mild renal insufficiency. Creatinine increases beyond the reference range until 75% of renal function loss occurs
The result of the CRP testing
Project | Result | Reference Range |
CRP | 24.0mg/L | <10mg/L |
Interpretation:The increased of CRP was higher than normal indicating the existence of mild acute inflammation or tissue cell damage in the body.
The PCR result of infectious examination
Project | Result |
Leptospira | (+) |
Diagnosis
Acute kidney injury
The diagnosis methods in Canine Acute kidney injury usually used in veterinary clinical are consist of the physical examination findings or history,laboratory examination such as complete blood count,Biochemistry profile,symmetric dimethylarginine(SDMA) analysis,cytology,biopsy,histopathology, radiography,ultrasonography and even using advanced imaging. And in some situation,doctor will also take polymerase chain reaction(PCR)assay to look for the cue with acute kidney injury.
IT was difficult to diagnose acute kidney injury because multiple cause can lead to the disease. And,the categories of kidney injury are consist of different period like prerenal disease,intrinsic disease and postrenal disease which we will talk in the conclusion part. There are two main staging systems which are used to evaluate the acute kidney injury in dog,So based on serum creatinine results from biochemistry profile, there are two main canine AKI staging systems. But be attention that neither staging systems have been evaluated in cats. One such system is the modification of the International Society for Renal Interests (IRIS) program, which consists of phase I-V. Each stage can also be divided according to urine volume (i.e. oliguria, non-oliguria). Another system is the Veterinary Acute Kidney Injury (VAKI) Programme, which consists of four phases
According to the obvious result of the biochemistry profile and the history that eating purples,we had a highly suspect that the dog was suffer from acute kidney injury. Since lack of more examination in this case,the other cause may not be excluded.
Treatment
1. Amoxicillin clavulanic acid:15mg/kg s.c q24h
2.Gastroprotectants of omeprazole:1mg/kg s.c q24hrs
3.Furosemide: 2mg/kg q6h i.v
4.LRS + 0.9% NaCl solution(1:1) 55mL/kg ivgtt
5.Metoclopramide 0.01mg/kg/hr i.v CRI
6.Sucralfate 250mg p.o q12hrs
The target of treatment is to maintain and restore the renal hemodynamics. Promoting cell self-recovery.Increasing solute excretion.Reducing the toxicity of nephrotoxic materia.Maintaining urine output.Correcting the abnormalities of the fluid of acid-base and electrolyte. Treatment is more successful in the initiation stage and extension of AKI. Patients with poorly responding to acute renal injury are usually need to be hospitalized for at least a few days to treated with the body maintenance or recovery. The underlying cause of AKI must be identified and managed appropriately. For example, the grape/raisin poisoning in this case.NSAIDS drug are used with caution in AKI.
Extensive monitoring is required in AKI. Monitoring volume overload in patients treated with IV fluids is critical. Hydration status, respiration and heart rate, thoracoscopic auscultation, and weight measurements were performed at least every 4-6 hours during infusion therapy. Measurement of central venous pressure (CVP) can detect volume overload early in some report. A CVP of 5-7 cm H2O above baseline or an absolute CVP of > 10cm H2O indicates capacity overload,but it is hard to use this method in clinical. Blood pressure monitoring is also critical, as both hypotension and hypertension can lead to increased kidney damage. Hypertension is common in patients with AKI but is not an indicator of the severity of kidney damage. The development of hypertension during IV therapy is indicative of volume overload. Monitoring filled cell volume and total solids can provide an estimate of fluid balance.
After 7days of therapy,the patient has been recovery,and further examination about the function of kidney such as biochemistry and SDMA assay should be evaluated one month later.
The examination during the 3 days of therapy
Complete Blood Count (CBC) examination after therapy
Project | Result | Reference Range |
WBC | 16.8×103/uL | 6.0~17.0 |
RBC | 6.36×106/uL | 5.5~10 |
HGB | 16.4g/dL | 12.0~18.0 |
HCT | 46.1% | 37~55 |
MCV | 65fL | 60~77 |
MCH | 22.6pg | 19~24.5 |
MCHC | 33.1g/dL | 30~37 |
PLT | 201×103/uL | 200~500 |
LYM% | 20.5% | 12~30 |
OTHR% | 86.4% | 60~86 |
EO% | 2.1% | 2~10 |
LYM# | 0.1×103/uL | |
OTHR# | 4.5×103/uL | |
EO# | 0.1×103/uL |
Conclusion
Definition and pathophysiology
Acute kidney injury (AKI), formerly known as acute renal failure (ARF), is a sudden and severe decline in kidney function that resulting in uremic waste retention,Abnormal circulating fluid and electrolyte and the acid base imbalance.
Because the kidneys receive about 20-25% of circulating cardiac output, they are susceptible to ischemic injury. Ischemia can lead to renal hypoperfusion, reduced renal toxin distribution volume, reduced renal tubular flow, and increased vasoconstriction. In order to maintain perfusion of the heart and brain in the presence of hemodynamic abnormalities, renal vasoconstriction leads to a decrease in glomerular filtration rate (GFR). Secondary hypotension (mean arterial pressure < 80mmhg) results in loss of the automatic regulation that normally helps maintain the renal perfusion.
Toxins can also cause the damage of kidney, especially blood-borne toxins. The surface of glomerular capillaries provides a large space for toxin-endothelial cell interactions. Tubular mechanisms increase the concentration of toxins in the distal kidney, high oxygen consumption and metabolic activity, and transcellular transport devices also contribute to the sensitivity of the kidney to toxins. Cortical structures (such as proximal tubules and Henle loops) have a high metabolic rate and receive 90% of the blood circulation in the kidney, and are prone to ischemic and toxic damage.
Type III hypersensitivity is associated with AKI in dogs injected with 25% human serum albumin. Sepsis can reduce glomerular capillary pressure which is another potential cause of AKI. Activate the inflammatory cascade.And lead to obstruction of the renal tubules. These changes lead to endothelial dysfunction, altered hemostasis, accelerated apoptosis, and induction of immunosuppression.
Phase of AKI
Initiation Phase:AKI totally has four stages. In the initial stage, motivational insults occur in the kidneys. GFR of kidney Direct tubular damage occurs, resulting in hypoxia and ATP depletion. ATP depletion leads to free radical formation, which also leads to further cell damage and changes in Na/K ATPase pumps. Abnormal Na/K ATPase pump function will lead to abnormal solute and electrolyte movement. The cells’ basement membrane connections are damaged, causing the cells to enter the tubular lumen to form a tubular cast. Tubular casting increases glomerular back pressure and further reducing of GFR. Renal ischemia can be aggravated by inflammation and constriction of afferent arterioles. The initial phase can last from several hours to several days, and clinical symptoms may not be present. Therapeutic interventions can prevent progression to subsequent stages.
Extension Phase:This phase will last for 1-2 days. Ischemia, hypoxia, inflammation, and cell damage persist. Additional endothelial damage, apoptosis, leukocyte activation and adhesion, and vascular congestion will Therapeutic interventions may or may not be successful at this stage.
Maintenance Phase:During the maintenance phase, GFR reached its lowest point. Urine volume may increase or decrease. Tubular cells begin to proliferate and migrate to rebuild tubular integrity. Blood flow ofthe kidney can return to normal. Apoptosis may be occurring. Irreversible kidney damage may occur. The maintenance period is 1-2 weeks.
Recovery Phase:Renal tubules are repaired during the recovery phase. GFR is elevated, but may not return to normal. Polyuria can occur with the restoration of tubular function and the accumulation of solute by osmotic diuresis. It can take weeks to months for kidney tissue to repair and regenerate.
Categories and Etiologies
Pre-renal disease: Prerenal of AKIis secondary to insufficiency of renal blood flow, abnormal perfusion pressure, or imbalance of renal vascular resistance is usually a complication of other diseases that cause systemic hemodynamic abnormalities. It does not initially cause renal morphological abnormalities and can be reversed by correction of hemodynamic changes. It is possible that the causes include hypovolemia, bleeding, hypotension, sepsis, anesthesia, renal vascular thrombosis, congestive heart failure, arrhythmia, trauma, burns, moderate fever, transfusion reaction, hypoproteinemia, non-steroidal anti-inflammatory drugs (NSAID), angiotensin-converting enzyme inhibitors, and liver failure.
Intrinsic disease:Endogenous AKI occurs in morphological changes of renal vessels, glomeruli, tubules or interstitium. Pre-renal AKI can eventually lead to this stage ofl AKI. Intrinsic AKI is one of the most challenging forms to treat. Possible causes include pyelonephritis, feline infectious peritonitis (cats), sepsis, leptospirosis (dogs), immune-mediated glomerulonephritis, Rocky Mountain macular fever (dogs), Lyme disease (dogs), hypercalcemia, amyloidosis, acute pancreatitis, neoplasia (the most common form of lymphoma), and certain toxins. In a study of 32 cats with congenital AKI, nephrotoxins account for 18 cases. It is known that the nephrotoxins include lilli (cat), non-steroidal anti-inflammatory drugs, ethylene glycol, bissex B, aminoglycoside, doxorubicin, cisplatin, hemoglobin, myoglobin, snake or bee venom, mushrooms, cyclosporine, azathioprine, pesticides, radiocontrast agents (such as iodohexanol), mannitol and other diuretics, vitamin D metabolites (such as pet food phase) Kidney poisoning, rodent drug nephropathy), heavy metals, grapes/raisins (dogs), and melamine (e.g. pet food related nephrotoxins).In this case,grapes are considered to be a toxin to our patient.
Post-renal diseases:Postrenal of AKI occurs when urine leaks into the abdomen, urethra obstruction, bilateral ureteral obstruction, or unilateral ureteral obstruction may happen with normal renal function. Urinary tract obstruction reduces renal clearance and increases renal back pressure. Possible causes include urethral or kidney stones, urethral or ureter stenosis, tumors, mucus obstruction, and trauma. Although postrenal AKI can be quickly corrected by treating the underlying cause, postrenal AKI can lead to intrinsicof
