Exam 2 Flashcards
Function of Kidneys
Excretion
• Urea
• Creatinine
• Uric acid
• Bilirubin
• Drugs
Regulation
• Water, electrolytes
• Arterial pressure
• Acid-base balance
• Secretion, metabolism, excretion of hormones
• Gluconeogenesis
Regulation of Arterial Pressure by Kidneys
Short-term
• decreased perfusion -> secretes renin -> angiotensinogen -> angiotensin I -> angiotensin II by angiotensin converting
• angiotensin II is a strong vasodilator & only lasts for a few minutes
long-term
• excrete varying amounts of Na & H2O
Acid Base Regulation by Kidneys
o Bicarb resorption
o H+ secretion (hydrogen, sulfuric/phosphoric acid)
Therapeutic Options For Proteinuria
o ACE inhibitors
o Angiotensin II Receptor Blockers
o Omega-3 fatty acids
o Clopidogrel (avoid thromboembolism)
o Amlodipine (for concurrent hypertension)
Ace Inhibitors, Omega-3 Fatty Acids
Ace Inibitor
• Decreases arterial resistance
• Preferential efferent arteriole dilation
• 1st line of defense proteinuria
Omega 3 Fatty Acids
• Anti-inflammatory
• Reduces platelet activity
Angiotensin II Receptor Blockers; drugs & function
Losartan
Telmisartan
• Theoretically treats angiotensin escape that may occur when ACE inhibitors fail
Things to Examine w/ UTI
o Hooded vulva?
o Dermatitis
o Vaginal stenosis
o Discharge
o Prostate enlargement
Localizing UTI
Lower (bladder, urethra, prostate)
• Stranguria, pollakiuria
• Hematuria, pyuria, proteinuria, bactiuria
Upper (ureter & kidney)
• PU/PD
• Signs of systemic infection
• +/- leukocytosis
• Hematuria, pyuria, proteinuria, bactiuria, granular casts
Urinalysis
o USG
o Dipstick
o Urine sediment
o Culture
Urine Culture
Qualitative
• Isolation/ID of bacteria
• Not recommended
Quantitative
• CFU per unit volume
• Allows determination of significance of bacteria
UTI Predisposing Factors
o Urine retention or leakage
o Uroliths, neoplasia, polyps
o Underlying systemic dz
o Excessive perivulvular skin or ectopic ureters
o Placement of urinary catheter
Complicated Vs Uncomplicated UTIs
Uncomplicated
• Sporadic
• Healthy individual
• Lack of comorbidities
• Fewer than 3 episodes per year
• Treat 7-14 days
• Monitor clinical signs
Complicated
• Anatomic abnormality
• Functional abnormality
• Co-morbidity
• Recurrent infection
• Treatment failure
Assessing UTI w/ Ultrasound
o Bladder wall thickness
o Radiolucent uroliths
o Neoplasia (bladder, renal or other intra-abdominal causing compression)
o Dilated renal pelvises
(pyelectasia = hallmark sign of pyelonephritis, but NOT pathognemonic)
o Renal cortical and medullary tissue architecture
o Prostate
o Adrenal gland size
Reinfection Vs Relapse Vs Refractory
Reinfection
• Recurrent UTI in 6 months post successful treatment
• isolation of different organism
Relapse
• Recurrent UTI in 6 months post successful treatment
• isolation of the same organism
Refractory
• Persistently (+) culture during treatment
Subclinical Bactiuria
o presence of bacteria in the urine as determined by positive bacterial culture, in the absence of clinical and cytological evidence of UTI
o Treatment may not be necessary
o presence of multidrug-resistant bacterium does not represent, by itself, an indication for treatment
Diseases associated w/ proteinuria
o Kidney disease
o Hyperadrenocorticism
o Neoplasia
o Immune-mediated diseases
o Infectious diseases
What’s wrong with having proteinuria?
o Bad for kidneys (chicken or the egg?)
o May cause thromboembolism
o Hypertension
o Part of nephotic syndrome (proteinuria, hypoalbumenia, hypercholesterolemia, edema)
Pre-renal Proteinuria
o low-level proteinuria
o overabundant filtered load of low molecular weight proteins that overwhelm the resorptive capacity of the proximal tubule
o hemoglobin, myoglobin, and immunoglobulin in the urine
Renal Proteinuria
o all forms of functional and pathologic proteinuria
o must be an alteration in renal physiology.
pathologic renal proteinuria
• defect in glomerular filtration barrier, tubular reabsorption, or interstitial damage
• most persistent cause of proteinuria
• highest levels of protein secondary to glomerular disease
Functional renal proteinuria
• transient, mild proteinuria
• caused by heat, stress, seizure, venous congestion, fever, and extreme exercise
Post-renal Proteinuria
• protein that is deposited in the urine from any part of the urinary tract distal to the kidney
• UTIs, inflammation, and hemorrhage
• Genital infections or inflammation (vaginitis, prostatitis)
• Extraurinary post-renal proteinuria can be minimized by performing cystocentesis.
• Post-renal proteinuria is never persistent once the underlying condition is removed
Looking at Persistence & Magnitude of Proteinuria
Persistance of Proteinuria
o Compare values day to day
o Repeat urine tests 3 times 2wks apart
o Collect from different micturition episodes & pool
Magnitude of Proteinuria
o Urine dipstick
o Affected by Alkiline urine, cells in sediment
o Strip sitting in urine too long
o If + on dipstic, do UPC
When to monitor Urine Protein/Creatinine Ratio
o Non-azotemic with persistent/steady microalbuminuria
o Non-azotemic with UPC less than 0.5
When to use Diagnostics to determine where protein is coming from
o Borderline proteinuria detected -> reevaluate in 2 to 4 months.
o If proteinuria (UPC > 0.4 in a cat and > 0.5 in a dog) is repeatable on 2 or more serial urine tests with benign sediments -> workup
o Work-up: rule out infectious disease, neoplasia, endocrine disease, checking blood pressure
Acute Kidney Injury; Basics, Symptoms, Clinical Presentation
• acute reduction in kidney function
• leads to change of GFR, urine production, tubular function
Symptoms
o Inability to maintain fluid
o Electrolyte imbalance
o Acid-base balance disturbances
o Azotemia
Clinical Presentation of AKI
o good body condition
o Vomit/diarrhea
o Lethargy
o Anorexia
o Painful
Acute Kidney Injury; Pathophysiology
Initiation
• Original insult to kidney (Ischemia, Toxin, Infection, Neoplasia, Obstruction)
• Lasts hours to days
• Clinical signs often absent
• Direct damage to renal tubular cells and ischemia (proximal tubule & ascending loop of Henle)
Extension
• Amplification of initial insult
• Ongoing hypoxia
• Inflammatory response
• Duration 1-2 days
• Renal tubular cells apoptotic/ necrosis
Maintenance
• Stabilization of the GFR at its nadir
• Lasts 1-2 weeks
• Renal blood flow returns to normal, cellular repair
• Re-establishment of tubular integrity and cell polarity
Recovery
• GFR rises
• May fully recover or residual chronic kidney disease
• Cellular repair continues
• Polyuria
• Lasts weeks to months
Azotemia; Pre-renal, renal, post-renal
Pre-Renal
• Dehydration
• Hypersthenuria (USG > 1.035)
Renal
• Damage to nephrons
• ISOSTHENURIA (USG 1.008 - 1.012)
Post-renal
• Urinary outflow obstruction
ALSO
• Could be Pre-renal azotemia superimposed on an inability to concentrate urine due to some other cause
Acute Kidney Injury; Causes
Unknown (most common)
Ischemia
• Shock (cardiogenic, distributive, hypovolemic)
• Hypotension
• Thromboembolism/infarction
Toxins
• Lilies
• Ethylene glycol
• Aminoglycosides, Doxorubicin, NSAIDS, Amphotericin B, Mannitol, cisplatin
• Radiographic contrast
• Melamine
• Pigmenturia
• Chicken Jerky Treats
Infection
• Pyelonephritis
• Feline infectious peritonitis
• Leptospirosis
• Prostatitis
Neoplasia
• Lymphoma
• Adenocarcinoma
• Sarcoma
• Nephroblastoma
Obstruction
• Calculi
• Mucous plugs
• Dried blood
• Tumors
• Urethral/ureteral strictures
Acute Kidney Injury; Diagnosis
History
Blood
• Inflammatory or stress leukogram
• Anemia
• Azotemia
• Hyperphosphatemia
• Hyperkalemia
• Elevated SDMA
• Uremia (clinical signs due to nitrogen waste)
Urinalysis
• Isosthenuria
• Proteinuria
• Glucosuria
• Hematuria
• Pyuria
• Bacteriuria
• Casts
Rads
• Stones
• Normal to large kidneys
Ab US
• View obstruction/dilation
• Signs of pyelonephritis
FNA
• Diagnostic if renal lymphoma
AKI; Treatment
Fluid therapy (maintain hydration, acid-base, elctrolytes)
• Isotonic crystalloids
• Norm R, Plasmalyte, LRS, NaCl
Measure urine output
Increase urine production
• Furosemide
• Diltiazem
• Mannitol
• Fenoldopam
Anti-emetics
• Maropitant
• Dolasetron
• Metoclopramide CRI
Gastric Protectants
• Omeprazole
• Pantoprazole
Nutritional Support
• Nasoesophageal/gastric feeding tube
AKI; What to monitor
o BP every 4-6hrs
o TPR Q 4-6hrs
o Weight Q 12 hrs
o Blood gas/electrolytes Q 4-12
o CBC/Chem Q 24-48hrs
Uroliths; Pathophysiology, classification, clinical signs, diagnosis
Pathophysiology
o Precipitation of mineral ->
o Crystals aggregate ->
o Stones form
Classifying a stone
o Must be made of 70% of single mineral
o Otherwise classified as “mixed”
Clinical Signs
o Dysuria
o Hematuria
o Inappropriate urination
o Pollakiuria
Diagnosis
o Verify presence, location, #, size, density, shape w/ imaging
o Rads (best)
o Ultrasound (complimentary)
o Air/contrast material to detect radiolucent stones
o Must analyze to determine stone type
Basics of Chronic Kidney Disease
o 60% nephron loss/decrease in GFR = loss of renal concentrating ability (isosthenuria)
o 75% nephron loss/decrease in GFR = azotemia
o Any structural or functional abnormality in one or both kidneys that has been continuously present for > 3 months
o Irreversible, often progressive
o Limits quality and length of life
CKD; Clinical Presentation
o Thin and lower body condition, decreased muscle condition
o Polyuria/polydipsia
o Inappetant/hyporexia
o Pale mucous membranes
o Rubbery/soft jaw
CKD Staging (based on plasma creatinine)
At risk
• Exposure to nephrotoxic drugs
• Breed
• Infectious dz
• Age
1
• non-azotemic
• other renal symptoms
2
• Dog: 1.4 – 2.0
• Cat: 1.6 – 2.8
3
• Dog: 2.1 – 5.0
• Cat: 2.9 – 5.0
4
• >5.0
USG Values
Hypersthenuria
• Dog: 1.030 or >
• Cat: 1.035 or >
Grey Zone
• 1.013 – 1.029/1.034
Isosthenuria
• 1.008 – 1.012
Hyposthenuria
• <1.008
