lab Evaluation of the Renal System Flashcards
Approach to Assessing Kidney Function
- History and physical exam
- Anemia – yes or no?
> possible for chronic kidney disease (normocytic, normochronic, non-regenerative due to decreased erythropoietin) - Biochemical profile – urea, creatinine, phosphorus, K+, albumin
> indicators of reduced GFR
> high K with evidence of kidney injury = acute
> with chronic, electrolytes tend to balance out - Urinalysis – gross appearance, dipstick, and microscopic examination
- Bacterial culture and antimicrobial sensitivity
- Urine protein:Urine creatinine ratio
> creatinine lost at a steady state, so we can compare things to it
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- Renal function tests – fractional excretion studies – not terribly common
- Renal biopsy – not terribly common
Laboratory Tests – Diagnosis of Kidney Disease
- on serum
- Urea, creatinine & phosphorus
* Serum urea nitrogen, blood urea nitrogen (SUN, BUN) - Albumin
> high = dehydrated
> low while globulin normal = protein losing nephropathy
Laboratory Tests – Diagnosis of Kidney Disease
- on urine
- USG
- Urinalysis
- Urine protein: urine creatinine ratio
Azotemia
Increased nitrogenous waste in blood
- Urea, Creatinine, SDMA
Urea, Creatinine, SDMA - assess what?
Assess the glomerulus
- Urea, Creatinine, SDMA = GFR
> increase with decreased GFR
Proteinuria + decreased albumin (and normal globulins)
PLN
what happens to urea in the kidney? is it a good indicator of glomerular function?
40% filtered back in, 60% out
- not the best indicator of glomerular function but we still use it
> non-kidney conditions can affect levels too
Increased Urea – Prerenal reasons
- increased Protein in diet
- increased Endogenous protein catabolism
> GI bleeding, fever, infection, necrosis, hyperadrenocorticism (steroid hepatopathy)
Increased Urea – Prerenal – Ruminant specific reasons, what this means
- Ruminants – salivary & blood urea go to rumen
- Rumen microflora create amino acids from urea
> Increased urea can be caused by:
1. Rumen stasis
2. Decreased GFR - Urea not as useful an indicator of GFR in ruminants as in other species
Decreased Urea reasons
- Hepatic insufficiency (>80% loss)
- Portosystemic shunt (PSS)
- Decreased water resorption in tubules
* e.g., Osmotic diuresis
* Water resorption creates concentration gradient for urea resorption
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(4. Loss caudal GIT – horse)
(5. protein malnutrition)
creatinine - what happens to it as it enters the kidney?
- what is it?
creatinine > 100% goes into ultrafiltrate (as with everything else) and 1005 goes out into urine
- made from muscle creatine phosphate which is an energy storage molecule (produced by breakdown of muscle at steady state)
Increased Creatinine – Prerenal reasons
- increased Crt well-muscled individuals, particularly males
* Greyhounds, Belgian blue cattle
Decreased Creatinine reasons
- Young animals
- Muscle atrophy
> e.g., hyperthyroid cat, older animal, cachexia
SDMA - what happens to it in the kidney
- produced at steady state in the body, not influenced by muscle mass
- 100% comes out in urine
Symmetric Dimethylarginine – Interpretation
- what do we need?
- use?
- gold standard?
- Still need a full UA
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Early CKD – Increased SDMA, creatinine WNL - More sensitive than creatinine
- Muscle mass decreased? No problems!
- Feline CKD 17 mo before creatinine increased
- Canine CKD ~10 mo before creatinine increased
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Gold standard: use both creatinine and SDMA to stage stable CKD patients
Interpreting Azotemia and USG
- Azotemia + isosthenuria (USG 1.007 – 1.012)
* KIDNEY FAILURE
* Especially if dehydrated
<><> - Isosthenuric but NOT azotemic
* Further assessment required
> What is hydration status? Might be appropriate?
> Interference w. concentrating capacity
>If it’s not repeatable, it’s not significant
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Postrenal Azotemia
- when do we see this?
Obstruction of urinary outflow distal to nephron
* FLUTD (feline lower urinary tract disease)
* Goat urolithiasis / foal bladder rupture
> Rupture & leakage of urine into the peritoneal cavity
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* USG not helpful in determining postrenal azotemia
> USG species-appropriate… initially
* Prolonged blockage > kidney injury > kidney failure
> e.g., hydronephrosis, shock, etc.
Proteinuria - types
- Prerenal (increased protein in blood)
- Renal (glomerular & tubular)
- Postrenal (hemorrhagic / inflammatory)
Prerenal Proteinuria
- what do we see?
- reasons
Protein normal or increased on the biochemical profile
* Physiologic – e.g., fever, exercise
* Hypertension – e.g., from endocrinopathies, heart disease > increased pressure forcing proteins out
* Multiple myeloma (Bence-Jones proteinuria)
* Hemoglobinuria
* Myoglobinuria
* Post-colostral proteinuria
Renal Proteinuria - types, reasons
- what do we see?
Glomerular proteinuria
* Hypoalbuminemia noted on biochem
* Some injury to filtration barrier
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Tubular proteinuria
* Early stages, albumin normal on biochem
* Usually associated w. acute / congenital kidney diseases
> e.g., Fanconi’s syndrome, admin of gentamycin
* Proximal tubules damaged / defective – filtered proteins not resorbed
* Loss of low MW proteins and amino acids
Postrenal Proteinuria
- causes
Postrenal proteinuria (hemorrhagic / inflammatory)
* Hemorrhage into genitourinary tract
> Renal or bladder calculi, impaired hemostasis, blood vessel damage from inflammation, trauma, neoplasia, etc.
* With inflammation will often see pyuria and sometimes “sub-optimal” USG
UPCR – Interpretation
(urine protein : creatinine ratio)
- normal levels
- purpose of measurement
- what do do with results?
Normal ratio:
- Dog or cat: <0.2
Borderline:
- Dog: 0.2-0.5
- Cat: 0.2-0.4
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* Estimate quantity of urinary protein excreted / d
* Proteinuric: demonstrate persistence by re-evaluating in 2 to 4 weeks
* Borderline: re-evaluate within 2 months
* Most <0.2
* Proteinuria between 0.2 – 2.0 is tubular or glomerular
* Proteinuria >2.0 is considered glomerular
> UPCR >2, no need to demonstrate persistence = severe proteinuria
Nephrotic Syndrome – Protein-losing nephropathy leading to abdominal transudation
- what do we see?
- Glomerular disease
- Hypoalbuminemia
- Hypercholesterolemia
- Edema / abdominal transudation
* Loss of plasma oncotic pressure - Hypercoagulable state
* Loss of antithrombin
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* In Short:
When there’s Protein in the Urine
LOOK AT CHOLESTEROL & REMEMBER ANTITHROMBIN
* Animal in hypercoagulable state!
USG for cat dog, cow, horse?
- what does USG tell us?
cat: 1.035
dog: 10.30
cow, horse: 1.025
> Interpret with hydration status
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- is assessing distal collecting duct, as this is where we bring water back into the body
> if we are losing water, we have more dilute urine, if we are keeping water in the body we have more concentrated urine
> ADH receptors allow insertion of aquaporins to bring water back in
USG Isosthenuria from Kidney Disease
- USG level
- what it means
USG: 1.008 – 1.012
* 2/3 of nephrons damaged
* Kidney incapable of producing concentrated urine
* Animal polyuric
> not enough places for aquaporins to bring water back into the body
DDx Polyuria/Isosthenuria > when do we ascribe this to kidney disease?
- Acute kidney injury
- Chronic kidney disease
- NB: cats > even is chronic kidney disease, they may not be isothenuric, as they are super good at concentrating. Look for other signs. Anything less than 1.035 is bad for cats.
USG Isosthenuria – when it’s not the kidneys’ fault
- Diuresis / Endocrine / Drugs
- Pyometra / Pyelonephritis
- Medullary washout
- Hypercalcemia
- Fanconi syndrome
Hyposthenuria - what is this?
- causes?
USG <1.008 = active process
* Overhydration/Euhydration
* Central or nephrogenic diabetes insipidus
* Primary polydipsia
Acute Kidney Injury (AKI)
- how do we identify?
- what will we see?
- causes?
- prognosis?
- History… acute
- Assuming no other disease – good body condition & not anemic
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Marked decrease in GFR – oliguria / anuria - Abrupt azotemia & hyperphosphatemia
- Hyperkalemia
- Commonly associated with: toxicants, renal ischemia, or infection
> Reversible if primary insult resolves
AnQfreeze
> Death or CKD if not resolved
Diagnosing Acute Kidney Injury
USG is variable
* Urine in bladder produced prior to insult?
* Consider polyuric states and ↓ concentrating capacity
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Abrupt decrease in GFR hours – days
* Animal usually oliguric or anuric
* May have hyperkalemia & acidemia
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* May have proteinuria
* May see cellular casts on urinalysis
Chronic Kidney Disease (CKD) - signs
i. Poor body condition
ii. Anemia – decreased EPO production
iii. Polyuria, isosthenuria, azotemia & hyperphosphatemia
iv. Electrolytes stable and no A-B abnormalities until next insult
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- With further kidney injury – metabolic acidosis
> Kidneys cannot regulate body water or electrolyte balance
- May have uremia
> Neuro, GIT, CV signs, etc.
AKI / End-Stage CKD (they are similar for this)
- Acid – Base & Electrolyte Imbalances
Metabolic acidosis is noted
* increased urinary loss of HCO3-
* decreased tubular secretion of H+ ions
* Retention of K+ with oliguric / anuric kidney injury
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Hyperkalemia:
* Life-threatening in AKI or post-renal conditions associated w. oliguria or anuria
Summary – Kidney Function
1. Azotemia & concentrated urine =
2. Azotemia & dilute urine =
3. Decreased serum albumin + proteinuria generally indicates….
4. Coarse Granular Casts =
5. Isosthenuria ~ how nonfunctional
6. Azotemia ~ how nonfunctional
7. Ethylene glycol toxicosis
- Azotemia & concentrated urine = pre-renal
- Azotemia & dilute urine = renal unless some other reason can’t concentrate such as medullary washout
- Decreased serum albumin + proteinuria generally indicates glomerular damage
* Unless there’s a monoclonal gammopathy, inflammation/neoplasia/hemorrhage involving the urinary tract - Coarse Granular Casts = tubular damage
- Isosthenuria ~66% nonfunctional
- Azotemia ~75% nonfunctional
- Ethylene glycol toxicosis – clinical signs, increased AG, increased osmol gap, ethylene glycol detection kit (NB: it only detects ethylene glycol), calcium oxalate monohydrate crystals in urine
Summary – Chronic Kidney Disease vs. Acute Kidney Injury
- Duration of signs – long-standing CKD, acute AKI
- Electrolytes and acid-base balance generally WRI with CKD – until terminal CKD
- Acid-base abnormalities, and particularly increased K often noted with AKI
<><> - Speed of onset of azotemia – slower CKD, fast AKI
<><> - Amount of urine production – high CKD, low-absent AKI
<><> - Other findings: anemia CKD, no anemia with AKI, hypocalcemia end-stage CKD, hypokalemia in feline CKD patients
<><> - Body condition – poor CKD, good with AKI
<><> - ± Reversibility of AKI
<><> - Usual causes of AKI: toxicants (EG), infection, anesthesia with insufficient fluids admin ± pain meds to dehydrated animal
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for 4 and 5:
- So long as the animal didn’t have a concurrent disease causing anemia or poor body condition
