Urinary System Flashcards
AKI diagnostic findings
LABS
- azotemia
- hyperphosphatemia
- hypocalcemia
- hyper or hypokalemia
- metabolic acidosis
- anemia if GI bleed
- isosthenuria or minimally concentrated urine (<1.035)
- proteinuria
- glucosuria
- casts = ongoing renal damage
- RBC/WBC/bacteria = UTI
- calcium oxalate crystals = ethylene glycol toxicity
- UMIC r/o bacterial pyelonephritis
AXR
- normal to enlarged kidneys
- +/- neproliths/ureteroliths
AUS
- normal to enlarged kidneys
– ethylene glycol tox = hyperechoic kidneys
– perirenal fluid = lepto (dogs); lymphoma (cats)
– hydronephrosis = obstruction or pyelonephritis
– mild ureteral dilation (minimally past renal pelvis) = supportive of pyelonephritis
CT
- +/- ureteral obstruction
AKI Treatment Goals/Therapy
GOALS
- limit further renal damage
THERAPY
- traditional fluid therapy = diuresis via aggressive IVFT rates
- reverse fluid therapy approach =
1. Acute fluid resuscitation
2. Maintenance of intravascular volume homeostasis
3. Fluid removal during convalescence to remove unnecessary volume
- balance polyionic solutions (P-Lyte, Norm-R, LRS)
- treatment of oliguria/anuria
—>oliguria = <1.0 ml/kg/hr UOP in well-perfused pet, 1-2 ml/kg/hr considered relative oliguria during diuresis
—> diuretics = increase in UOP from diuretic use may allow increased volume allowance for meds/nutrition
—> mannitol = despite theoretical advantages, trials = no better response
—> loop diuretics (furosemide) = can increase UOP w/o increasing GFR despite increase in UOP, loop diuretics do not improve outcome
RENAL REPLACEMENT THERAPY
- dialytic therapy has no established time line, but intractable hyperkalemia, life-threatening volume overload, and persistent uremic C/S are universally accepted.
—> early institution of dialysis = more favorable outcomes
- renal transplant NOT emergent, but can be considered if renal function doesn’t recover
- peritoneal dialysis = more available than hemodialysis, removes toxins by diffusion from peritoneal membrane into abdominal dialysate, then drained
- intermittent hemodialysis (IHD) = rapid blood flow and rapid dialysate flow for efficient removal of uremic toxins and fluid
- continuous renal replacement therapy = slower than IHD
- extracorporeal renal replacement therapy (ERRT) = intermittent hemodialysis AND continuous renal replacement therapy
TREATMENT OF URETERAL OBSTRUCTION
- relatively common cause of AKI
- if not resolved w/in 7d, renal function reduced by 1/2 permanently; NO return of renal function after 40d
- treatment of hyperkalemia
1. hyperkalemia more likely w/ oliguria or anuric AKI than polyuric
increased extra cellular K+ changes electrical potential of excitable cells, ECG changes include tall, spiked T waves, shortened QT intervals, wide QRS complexes, and a small, wide, or absent P wave
2. severe hyperkalemia = V.Fib or standstill, muscle weakness possible if >8 mEq/L calcium gluconate to restore cardiac membrane excitability, but DOES NOT decrease K+
3. regular insulin (given w/ dextrose) move K+ from extra- to intracellular space.
4. dextrose induces endogenous insulin release in NON DIABETIC patients, can be used w/out insulin for mild-mod hyperK+
5. Na bicarb to treat K+ moved from intra- to extracellular space caused by metabolic acidosis
6. albuterol moves K+ from extra- to intracellular space
7. Kayexalate, Kionex (cation exchange resin polystyrene sulfonate) PO or enema = bind K+ in GIT, release Na; takes several hours to act, usually temporary unless urine produced
ELECTROLYTE CHANGES
- hypokalemia = usually due to excessive loss 2nd to PU; treat w/ KCl in IVFT +/- PO supplementation
- sodium = hypernatremia prior to IVFT due to excessive free water loss; hyponatremia possibly excessive loss 2nd to PU/GI loss or transient dilution after mannitol/hypertonic NaCl/colloid solutions
- phosphorus = dietary PO4 readily absorbed from GIT —> excreted by kidneys; decreased excretion = hyperphosphatemia; IVFT may partially control PO4, PO4 binders prevent absorption from food
AKI Overview
- defined as rapid loss of renal function leading to the accumulation of nitrogenous waste, fluid imbalances, and electrolyte disturbances
- approximately 75% of renal function must be altered to increase serum creatinine
- AKI (unlike CKD) possibly reversible by resolution of injury, adaptation of the kidney (via hypertrophy), or both
- azotemia can be categorized as prerenal, renal, or postrenal (with possibility of overlap)
CKD Overview
- defined as renal damage or decreased renal function that has persisted for at least 3 months
- previous terminologies: kidney disease, kidney failure, renal insufficiency, azotemia, uremia
- generally considered an irreversible and progressive loss of function; patients have sustained permanent injury and exceeded maximal amount of compensatory glomerular hypertrophy
- azotemia = blood work changes (BUN and creatinine)
- uremia = clinical signs associated with declining renal function
- C/S: vomiting, lethargy, anorexia, weight loss, halitosis, neurological abnormalities
IRIS STAGING
- based on serum creatinine
- should only be performed on fasted, well-hydrated patients, based on a minimum of two values of a period of several weeks
1. non-azotemic
2. mildly azotemic usually only PU/PD, +/- wt loss/selective appetite, +/- pyelonephritis/nephrolithiasis, +/- proteinuria/hypertension
3. moderately azotemic more consistent clinical signs as listed above
4. severely azotemic uremic
UPCR AND ARTERIAL BP SUBSTAGING
- UA/UMIC and sediment analysis should be performed to r/o urinary causes of proteinuria (UTI, hemorrhage, inflammation)
- UPC should be rechecked several times over two weeks, unless markedly elevated or <0.2
- samples collected at home show lower UPCR than those collected in hospital
- BP should be determined several times over several weeks
- BP performed prior to PE or collecting lab samples
- 5-10 readings with minimal restrain and o’ present (document with HR and perceived anxiety level)
CKD Diagnostic Findings
LABS
- metabolic acidosis (severe acidosis in advanced CKD)
- azotemia (elevated BUN and creatinine)
- hyperphosphatemia
- hyper- or hypocalcemia
- hypermagnesemia
- hypokalemia
- anemia (non regenerative)
- elevated SDMA
- isosthenuria
- proteinuria
- cylinduria
- bacteriuria/pyuria/hematuria
- glucosuria
- cystinuria
AXR
- enlarged or small kidneys
- renal mineralization/nephroliths/ureteroliths
- abnormal renal shape
- absent kidney
AUS
- all listed in AXR
- abnormal renal echo texture
CKD Treatment Goals and Therapy
GOALS
- conservative medical management
- supportive/symptomatic therapy designed to ameliorate C/S, correct fluid deficits or excesses and electrolyte, acid-base, endocrine, and nutritional balances
THERAPY
- dietary = phosphate binders (stages II-IV), modified protein (stages III-IV), O3FA + antioxidants to reduce oxidative stress, introduction of renal diet in stage I-II may help with acceptance prior to clinical signs
- SCF = when signs of chronic or recurrent dehydration; balanced electrolyte solution (LRS) q 1-3d; excess Na (NaCl) should be avoided, as excess Na may harm the kidneys
- GI signs of uremia = nausea/vomiting common; H2-blockers (famotidine, ranitidine), PPI (omeprazole, pantoprazole, esomeprazole), sucralfate recommended for dogs with inappetence, nausea/vomiting; antiemetics (maropitant, ondansetron) help reduce fluid loss via vomiting, ondansetron SC more bioavailable than PO
- appetite stimulation = mirtazapine +/- cyproheptadine, Elura (capromorelin) newly approved for CKD cats
- esophagostomy tubes beneficial for p’ with progressively declining body weight despite efforts to improve nutrition less effective once severely uremic
- metabolic acidosis = common in stage IV (less common in stage III); alkalizing agents considered when plasma bicarb below 15mmol/L (parenteral intervention if pH <7.10 until >7.20); renal diets, K citrate, and Na bicarb all oral options
- hypokalemia = CATS: common in stage II-III, less common in stage IV; common with hypertension; total body K depletion more likely than hypokalemia; poss due to inadequate intake, increased loss (urinary), enhanced activation of RAAS 2nd to chronic dehydration +/- dietary salt restriction; amlodipine may contribute; uncommon in dogs; oral supplementation preferred, parenteral reserved for emergent replacement needs (up to 30mEq/L can be added to SCF)
- hyperkalemia = uncommon in CKD, but may develop in advanced stage IV; usually 2nd to adequate caloric intake via e-tube, or with ACE inhibitors (enalipril, benazepril) or angiotensin receptor blockers (telmisartan); reduce dietary K+ or prevent GI uptake (Na polystyrene sulfonate - Kayexolate, Kionex)
- hypertension = treat to prevent end-organ injury (eyes, kidney, brain, heart); mild (160-179 mmHg), severe (>180mmHg), emergent (>200mmHg); ACE-i (enalipril, benazepril), Ca channel blocker (amlodipine), ARB (telmisartan) txt with ACE-i AND ARB at higher risk for hyperkalemia
- anemia = progressive CKD can develop nonregenerative anemia 2nd to inadequate production of erythropoietin (EPO); txt with darbepoetin alfa, epoetin alfa, epoetin beta, recent approval of oral therapy molidustat (Varenzin-CA1); EPO stimulating agents (ESA) have been linked to production of anti-EPO Abs and pure red cell aplasia (PRCA), routine monitoring and reduction of dose are essential
- iron deficiency = increasing RBCs requires iron, supplementation should be given early with ESA therapy; iron dextran IM preferred over PO administration
- calcitriol = most active/bioavailable form of vitamin D; txt for renal secondary hyperparathyroidism, shown to increase PTH levels in dogs and cats with CKD; DOGS: stage III-IV +/- stage II to slow progressive deterioration in renal function, use in cats remains speculative; overdose induces hypercalcemia w/ poss renal injury, routine monitoring crucial
Renal Anesthetic Considerations
- Avoid or reduce dose of drugs metabolized/excreted primarily by the urinary tract
- Urethral or ureteral obstruction leads to impaired excretory capabilities
- PLN —> reduced serum proteins —> sensitive to highly protein bound drugs
- Crucial to maintain appropriate BP under anesthesia
- Multi-modal anesthesia helps prevent dose-dependent vasodilation caused by inhalants
Amyloidosis
- serum Amyloid A (SAA)
- renal amyloidosis = beta-pleated sheets of amyloid A protein deposited in the kidney (primarily glomerulus) —> leads to profound proteinuria —> leads to glomerular dz and PLN
- heritable dz (Abyssinians and Shar Peis): amyloid A deposited primarily in the interstitium, dz manifest earlier in life as CKD, but proteinuria is typically lacking
- though to be a result of chronic inflammation, chronic infection, or neoplasia
- PLN: weight loss, hypertension (may lead to retinal detachment), thromboembolic dz is most severe/life-threatening complication of glomerulonephritis (clots to brain or lungs) specifically when serum albumin under 1.5 g/dL
- PE = unremarkable in early stages; then muscle wasting, weight loss, dull/thin hair coat, retinal hemorrhage or detachment; then pale MM, pitting edema, and ascites in severe cases
Polycystic Kidney Disease (PKD)
- DOGS: Bull Terrier, Cairn Terrier, Westies; genetic mutation of PKD1 gene; Bull Terriers have decreased renal function in the first years of life (cysts limited to kidneys), Cairn Terriers and Westies within the first months of life (cysts in kidneys and liver)
- CATS: Persians; renal, hepatic, and occasionally pancreatic cysts; mutation in PKD1 gene
- txt: as with CKD
Renal Dysplasia
- congenital, kidneys appear as those with advanced CKD
- histopath = inappropriate differentiation (fetal nephrons alongside normal nephrons); functioning nephrons undergo hypertrophy; persistent immature mesenchyme, persistent metanephric ducts, atypical tubular epithelial proliferation, dysontogenic metaplasia
- txt: as with CKD
Glomerulonephritis
- characterized by inflammation of the glomeruli, often involves deposition of immune complexes within the glomerular capillary walls —> leads to proliferation and thickening of the glomerulus —> eventually glomerular cell death
- proteinuria early in dz process —> may progress to CKD if enough glomeruli are lost
- immune complexes thought to be a result of chronic inflammation, chronic infection, or neoplasia
- heritable form: Dobermans, Samoyeds, Rottweilers, Greyhounds, Bernese Mountain Dogs, English Cocker Spaniels, Soft-Coated Wheaton Terriers
Pyelonephritis
- defined as an infection of the renal pelvis
- results in more severe signs when compared to simple lower UTI, treatment is more complicated
- generally from ascending bladder infection, but hematogenous spread possible with discospondylitis or sepsis; E. coli most common
- predisposing diseases: HAC, DM, CKD
- acute pyelonephritis: high fever, abdominal pain/hunched posture, lethargy, vomiting; foul-smelling urine, inappropriate urination, PU/PD (not pollakiuric as with lower UTI), enlarged/painful kidneys
- advanced/severe pyelonephritis: oliguria/anuria
- chronic pyelonephritis: range from no C/S to presentation similar to CKD, kidneys palpate normal or small/irregular
Protein Losing Nephropathy (PLN)
- variety of disorders affecting the nephrons
- glomerulus, renal tubule, and interstitium most commonly affected
- normal kidney: serum proteins are readily absorbed as urine is passed through the nephron
- in PLN: serum proteins leak into urine, due to either an insufficiency of absorption or impaired filtration
- albumin is primary protein found in the urine of PLN cats and dogs
- prolonged PLN can lead to CKD
Ectopic Ureters
- defined as a ureter that opens in any location other than the trigone of the bladder
- females>males (longer urethra and urethral sphincter likely reduce clinical signs and diagnosis in males)
- intramural ectopic ureter: enter the bladder trigone on external surface, but tunnel through bladder wall to exit at more distal locations (urethra, vagina, uterus)
- extramural ectopic ureter: completely bypass the urinary bladder and directly insert at a more distal location
- urinary sphincter mechanism incompetence (USMI) common w/ intramural ectopic ureters (due to disruption of sphincter by tunneling ectopic ureter)
- Huskies, Labs, Goldens, Westies, Fox Terriers, Skye Terriers, mini and toy poodles
- C/S: intermittent or continuous dribbling of urine, incontinence when asleep or awake
- dx: excretory urography (can underdiagnose), AUS (can underdiagnose), CT, fluoroscopy, cystoscopy, contrast-enhanced CT best for identifying type and location of ectopic ureters
- txt: historically surgical, now laser ablation is minimally invasive option for intramural ectopic ureters; urethral sphincter may be compromised with either option —> urethral collagen injections may help maintain continence
Renin-Angiotensin-Aldosterone System (RAAS)
- RAAS plays vital role in regulating salt, blood volume, and systemic vascular resistance —> together influence cardiac output and arterial pressure
- RENIN: proteolytic enzyme secreted exclusively by juxtaglomerular cells in walls of renal afferent arterioles; synthesized as an inactive zymogen called prorenin; juxtaglomerular cells capable of secreting both prorenin and renin
- renin is released by sympathetic nerve activation (via beta adrenoceptors), renal artery hypotension (from systemic hypotension or renal artery stenosis), or decreased Na delivery to distal tubules of kidney; inhibition of renin secretion is regulated by a negative feedback loop (angiotensin II, high BP, high plasma Na, and volume overload all contributing factors)
- ANGIOTENSIN II: when renin released into bloodstream angiotensinogen cleaves to form angiotensin I in the liver —> vascular endothelium (lungs) has ACE enzyme which cleaves two amino acids from angiotensin I to form angiotensin II; important functions of angiotensin II include constriction of resistance vessels (increasing SVR and systemic arterial pressure), acts on adrenal cortex to release aldosterone, stimulates release of vasopressin (ADH) from posterior pituitary (increasing fluid retention by the kidneys) stimulates thirst center in brain and facilitates release of norepi reuptake (enhancing sympathetic adrenergic function)
- ALDOSTERONE: released by adrenal cortex (when stimulated by angiotensin II) —> acts on kidneys to increase sodium and water retention, promotes urinary excretion of potassium and protons
- RAAS pathway regulated by renin release, and also modulated by natriuretic peptides (ANP and BNP) released by the heart which act as an important counter regulatory system
- manipulation of RAAS important in treatment of hypertension, heart failure, renal disease (especially glomerulonephritis) ex) ACE-i, angiotensin II and aldosterone receptor blockers (ARB) used to decreased arterial pressure, ventricular afterload, blood volume (and hence ventricular preload), as well as inhibit and reverse cardiac and vascular hypertrophy in patients with cardiac disease
