Urology and Nephrology Flashcards
kidneys receive ______% cardiac output
25
functional unit of kidney
nephron
podocytes
responsible for filtering serum, must be able to dilate to achieve normal filtration
proximal tubule
80% water absorption
reabsorption of water, potassium, bicarbonate, Na, Cl, nutrients
excretion of H+ and NH3+
loop of Henle
reabsorbs more water to further concentrate urine
ascending limb: high levels of urea sit out outside to pull in water - low urea levels = medullary washout
descending limb: NaCl absorbed and water follows
distal tubule
reabsorption of NaCl, water and bicarb, excretion of K+ and H+
collecting duct
reabsorption of NaCl, urea and water
active reabsorption via ADH and aldosterone
- ADH opens aquaporins
- aldosterone opens Na channel
how does kidney maintain BP
as blood enters afferent arteriole, glomerular apparatus measures pressure
- if not enough, increases BP by producing renin –> liver (ATI) –> lungs (ATII) –> constricts arteries at kidney + stims adrenals to release aldosterone, acts on distal tubule and collecting ducts, Na reabsorption = H2O reabsorption = increased blood volume
Hormones produced by kidney
Renin - increase BP
EPO - RBC production
active vit D (1,25 dihydroxycholecalciferol) - increase Ca absorption from gut
Hormones that act on the kidney
PTH - increase Ca absorption and P excretion
ADH - open aquaporins
Aldosterone - increase Na retention
Azotemia
increase in concentration of NPN wastes in blood, can be renal, pre renal or post renal
is azotemia uremia?
no, uraemia is a clinical condition because of an increase in urea
____% nephrons are non-functional if the kidney is in failure
75%
at _____% kidneys cannot concentrate urine
66%
Renal failure
kidneys no longer able to maintain regulatory, excretory and endocrine function
metabolic acidosis
retention of nitrogenous solutes and derangements of fluid, electrolytes and acid/base status
>75% nephrons nonfunctional
Renal disease
doesn’t equal azotemia or renal failure
morphological or functional lesions in one or both kidneys regardless of extent
Uremia examples
uremic gastropathy, hyperparathyroidism (extra renal manifestations of renal failure_
Gold standard to test glomerular function
accurate and direct technique
clearance of radioisotopes with renal scintigraphy or iohexal/inulin/creatinine clearance tests
though gold standard, they are not commonly used
Indirect methods to test glomerular function
urea - subject to passive reabsorption in the tubules, clearance is not a reasonable estimate of GFR
creatinine - better indicator, produced at constant rate, dependent on muscle mass, less influenced by diet, excreted unchanged by kidneys
- better indicator of GFR but relationship is not linear
- limitations: azotemia doesn’t develop until GFR has decreased to 25%, doesn’t tell you why GFR has fallen
Azotemia doesn’t develop until GFR has decreased to _____%
25%
gold standard to measure urine concentration
osmolality (not used in practice)
Urine specific gravity
measures urine concentration with a refractometer calibrate with distilled water glucosuria falsely increases measures concentration of urine relative to plasma - renal tubular test Hyposthenuria - 1.000-1.007 Isosthenuria - 1.008-1.012 minimally concentrated - 1.013-1.030 *adequately concentrated* - dog: >1.030 - cat: >1.035
Adequately concentrated urine
Dog: >1.030
Cat: >1.035
Sediment exam of cells
big cells - transitional cells
medium cells - tubular epithelial cells
small cells - RBC and WBC
calcium oxalate crystals
square stones, small breeds predisposed
calcium mono-oxalate
antifreeze
ammonium biurate
dalmations
cysteine crystals
bulldogs
struvite crystals
any, cats predisposed
Sediment exam
in house is better
UPC proteinuria values
Dog - >0.5 = proteinuric
Cat - >0.4 = proteinuric
Partial water deprivation test
r/o hyperadrenocorticism first
maximal stim of ADH release will be present after 5% loss of BW
addition of DDAVP (vasopressin) - failure to concentrate = diabetes inspires or renal medullary washout
Fractional excretion of electrolytes - assess tubular dysfunction
fractional excretion of electrolytes
assess tubular dysfunction
fraction of electrolyte clearance relative to creatinine clearance
Na-Fractional excretion differentiates renal from pre-renal disease
if <1%, pre-renal dz
if >1%, renal dz
bladder tumor antigen test
41% specificity in dogs with UTI other than TCC
most common bacterial cause of UTI
E. coli
Hematuria
presence of blood/RBC in urine
gross or occult, or pseudohematuria (centrifuge to Ddx)
Causes: systemic disorders, renal, bladder/ureter/urethra, genital tract
where do you take a kidney biopsy from?
CORTEX NOT THE MEDULLA
Ddx between acute and chronic kidney disease
chronic look like shit, will be skinny and gross (acute haven’t had time to lose weight)
key CS of lower urinary tract disease
inappropriate urination
Normal urine production
1-2ml/kg/hr
2 exam findings on animal with a micturition disorder
oral - uremic stomatitis
rectal - prostate
when should you look at specific gravity or UPC
before giving fluids
Renal carcinoma
Dogs > cats
Unilateral renomegaly
polycythemia as paraneoplastic syndrome (decreased EPO prod)
can cause hypertrophic osteopathy as paraneoplastic syndrome
Dx w/ US
Tx by nephrectomy
Renal carcinoma
Dogs > cats
Unilateral renomegaly
polycythemia as paraneoplastic syndrome (decreased EPO prod)
can cause hypertrophic osteopathy as paraneoplastic syndrome
Dx w/ US
Tx by nephrectomy
Renal lymphoma
Cats > dogs
usually both kidneys - bilateral rnomegaly
caused by azotemia, can spread to CNS, some association with FeLV
Dx: US
Tx: multi-agent chemotherapy (COP or CHOP)
Px: good 60% in complete remission
1 non-neoplastic cause of renomegaly
acute ureteral obstruction
Non-neoplastic causes of renomegaly
renal inflammation, amyloidosis, hydronephrosis, portosystemic shunts, acute ureteral obstructions
Polycystic kidney disease
multiple cysts in both kidneys, can cause renal failure in adulthood
Persians - can genetic test
mutation in PKD-1 gene, also in bull terriers, cair terriers, WHW terriers
Renal pain
present as acute abdominal pain
Acute renal injury
mild damage to severe damage with complete anuria, infers reversibility
acute renal failure
decreased GFR, retention of nitrogenous wastes
RIFLE criteria
Risk, Injury, Failure, Loss, End-stage kidney disease
- base grades on creatinine level (but we dont know baseline in vet med = problem)
- based on proportion of serum creatinine increase + urine output decrease
Pre-renal causes of acute kidney disease
insufficient blood flow (perfusion) to kidneys
- hypoxia, ischemia, dehydration, hypovolemia, hypotension, anesthesia, surgery, shock, trauma
Na urine fractional excretion <1%
Renal causes of acute kidney disease
affect kidney itself
- hypo perfusion, obstruction, thrombosis, vasoconstriction, infectious causes, immune mediated causes, neoplasia, secondary to systemic disease
- NEPHROTOXINS
examples of nephrotoxins that can cause acute kidney disease
ethylene glycol, NSAIDs, ahminoglycosides, TMS, sulfamethoxazole, methotrexate, cyclosporine, cimetidine
- endogenous: myoglobin
Post renal causes of acute kidney disease
obstruction or urine leakage
4 phases of acute renal failure
initiation, extension, maintenance, recovery
Initiation phase of acute renal failure
aka onset phase, without CS, triggered by ischemic event
defined by decrease in urine output or increase in creatinine
intervention is necessary
Extension phase of acute renal failure
continued hypoxia and inflammation, compromised Na:k pumps, loss of brush border or apical and basal cell surfaces
increased cytosolic Ca
Maintenance phase of acute renal failure
1-3w, urine output is increased or decreased urine is ultrafiltrate
Recovery phase of acute renal failure
heralded by PU, extreme Na loss, takes weeks/months to recover
Recovery phase of acute renal failure
heralded by PU, extreme Na loss, takes weeks/months to recover
Intrinsic renal failure
acute tubular necrosis/injury
intra-renal vasoconstriction - imbalance between vasoconstrictors (endothelin) and vasodilators (NO)
ATP cannot be formed, intracellular acidosis, intracellular hypercalcemia
Tubular dysfunction = obstruction from crystals or detached RTE cells, cytoskeletal injury, loss of tight junctions, necrosis
Prevention of acute renal failure
manage risk factors (Tx shock, dehydration, avoid nephrotoxic drugs in compromised patients)
renoprotective drugs - amlodipine (Ca channel blocker), Dopamine (vasodilation), Fenoldopam (prevent vasoconstriction, EPO analogues
Prevention of acute renal failure
manage risk factors (Tx shock, dehydration, avoid nephrotoxic drugs in compromised patients) renoprotective drugs - amlodipine (Ca channel blocker), Dopamine (vasodilation), Fenoldopam (prevent vasoconstriction, EPO analogues Address BP, ensure >80mmHg, address circulatory volume, avoid hyperkalemia induced bradyarrhythmias fluid bolus (10-15ml/kg crystalloids in oliguric patients, or 2-5ml/kg colloids) to correct electrolyte abnormalities
Diagnosis of AKI
ID predisposing causes, reduced urine output, azotemia, Fex Na >1%
Renal tubular biomarkers
- GGT:Creat - can see if injury is getting better or worse
- NAG: Creat - similar to above
Treatment of Acute Renal Failure
FLUIDS FLUIDS FLUIDS
Tx shock in time he gives, calculate all the fluids, make sure to reweigh before giving. maintenance dose
Oliguria
produce <0.5ml/kg/hr
correct renal perfusion to see if it is physiological or pathological
Tx w/ fluids and drugs (mannitol, furosemide, dopamine, fenoldopam, Ca channel blockers)