1. ultrafiltration of plasma by glomerulus
2. selective tubular reabsorption of water and solutes
3. selective tubular secretion of solutes

• Glycogen storage
• Renin production
• Acid-Base balance
• Toxin and drug excretion
• Erythropoietin production
• activation of vitamin D to calcitriol

azotemia- the buildup of nitrogenous wastes such as BUN and/or creatinine. 

uremia-the clinical signs associated with renal failure (loss of appetite, vomiting, oral ulceration, oral bleeding, uremic breath)

pollakiuria

polyuria

1.  daily water consumption (general volume)
2. volume of urine passed
3. time taken to urinate
4. frequency of urination (and when/where)
5. force and color of urine stream

smaller animal= more water per unit weight requirement

Water consumption depends on nature of diet (dry vs wet), salt intake, enviro humidity and temp, exercise, fecal characteristics

polyuria-increased frequency AND volume of urine

if SG>1.025 in a dog or >1.035 in a cat, polyuria is UNlikely. nocturia can be a clue

oliguria-reduced urine production

<0.27-1.0mL/kg/hr or <6.5ml/kg/day

lack of urine production

 <0.1ml/kg/hour or <2ml/kg/day

• nuclear scintigraphy
• Iohexol clearance test
• creatinine clearance test
• inulin clearance test
• Cystatin C

1. be freely filtered across the glomerular capillary
2. not be reabsorbed or secreted into the tubular lumen
3. not be stored, metabolized, or synthesized by the kidney

serum creatinine

from muscle, consistent from day to day because dependent on muscle mass, excreted by kidneys via glomerular filtration alone.

can be affected by tying up or crush injury "rhabdomyolysis", and cachectic animals may have decreased serum creatinine 

• urea synthesized in liver from dietary ammonia, amino acids, and catabolism of endogenous protein. 
• dietary protein, body energy balance, and magnitude of fluid turnover can change daily. 
• dogs with GI hemorrhage can have disproportionately increased BUN

• 75%
• 60%

lower urinary tract disease

upper urinary tract disease

dog 1.030-1.045

cat 1.045-1.065

the SG of isosthenuric urine is_____

and the normal pH range of urine is ______

1.008-1.012

5.5-7.5

• proteins added to urine in tubules
• no, dipstick primarily detects albumin
• very alkaline urine may give a false elevated proteinuria
• sulfosalicylic acid turbidometric (SSA) test

• urine protein/creatinine ratio
• done on single sample to estimate 24 hour protein excretion.
• should be <0.5 in the dog, <0.4 in the cat, not meaningful in the face of gross hematuria or pyuria

anything. 

increased glomerular permeability, decreased tubular reabsorption, inflammation anywhere, bleeding into the urinary tract, DM, hypertension, hyperadrenocorticism, strenuous exercise, seizures, fever

• DM
• hyperadrenocorticism
• fluid therapy (iatrogenic)
• epinephrine secretion/admin
• stressed cats
• pheochromocytoma

• impaired tubular reabsorption
• congenital tubular defect
• acute renal failure w/severe tubular damage
• fanconi syndrome
• false positive (drugs)

acetoacetic acid. (20%)

beta-hydroxybutyric acid NOT detected (78%)

(acetone is remaining 2%)

free hemoglobin

high vitamin C

old strips

where do the following originate and what are their significance?

a. caudate cells

b. squamous cells

c. renal tubular cells

d. transitional cells

a. renal pelvis (unknown)

b. vagina, prepuce, distal urethra (no significance)

c. renal tubules (tubular inflammation as in tubular necrosis, pyelonephritis, or glomerulonephritis)

d. urethra, bladder, ureters (traumatic catheterization, inflammation, neoplasia

hemolysis

hepatocellular disease

bile duct obstruction

conjugated. 

dogs.

• bacterial infection
• urolithiasis
• neoplasia
• idiopathic
• hemorrhage 

1. uric acid
2. ammonium urate
3. amorphous urates
4. cystine
5. calcium oxalate

1. struvite
2. amorphous phosphates
3. calcium phosphate
4. calcium carbonate

stress

fever

exercise

white blood cell casts indicate _______.

red blood cell casts indicate _________.

waxy casts indicate ________________.

1. pyogenic process in kidney
2. glomerulonephritis
3. nephrotic syndrome

• few- relatively unimportant
• cellular inclusions- active ongoing renal disease
• absence-does not rule out possibility of active renal disease
• can be an early sign of aminoglycoside toxicity

Dioctophyma renale eggs

Capillaria plica eggs

renal size on VD radiographs should be:

and other things to evaluate include:

2.5-3.5x L2 in dogs

2.4-3.0x L2 in cats

size and position of bladder, prostate

mineralization of prostate

presence of uterus

sublumbar lymph node enlargement

lysis of ventral L6-L7

intravenous urography-severe, primary renal failure will not take up contrast agent. PU/PD will dilute. dehydration can lead to acute renal failure

negative contrast cystography- air can cause embolism in patients with hematuria. requires sedation

positive contrast cystography (for bladder integrity)-requires sedation

double contrast cystography-not used for rupture, requires sedation

retrograde urethrogram-requires anesthesia (females), sedation (males)

vaginourethrogram-requires anesthesia

US guided pyelography

1. motility for retrograde migration
2. adhesion molecules
3. bacterial capsular Ag to inhibit phagocytosis and complement-mediated lysis
4. bacterial urease leading to ammonia formation to damage the uroepithelium
5. production of hemolysins and iron-chelating agents that enable bacteria to scavenge iron

1. normal micturition
2. normal anatomic structures in the urethra and ureters
3. mucosal defense barriers
4. antimicrobial properties of urine

1. adequate urine flow
2. frequent voiding
3. completeness of emptying

1. urethral length
2. urethral high pressure zone
3. urethral peristalsis
4. ureterovesical flap valve and ureteral peristalsis

1. intact mucosa
2. Ab production (IgG and IgA)
3. surface glycosaminoglycan layer
4. cell exfoliation
5. commensal bacteria

1. hi or low pH
2. concentration
3. urea
4. diet-derived organic acids

excretory urography-small and irregular with pelvic dilatation. 

diverticula have irregular borders

US-guided pyelocentesis with culture to prove bacterical pyelonephritis

NOTstranguria, pollakiuria, discolored urine as in normal patients. 

maybe still: strong odor, pain upon palpation, thickened bladder (chronic)

you MUST culture and sensitivity

o   Variable and non-specific

o   Anorexia, lethargy

o   “Back pain”

o   PU/PD (chronic)

o   Depressed

o   Fever

o   Pain on palpation of T-L area

o   Pollakiuria

o   Stranguira

o   Hematuria

o   Strong odor

o   Normal attitude, appetite unless prostate involved

o   Pain on palpation of caudal abdomen

o   Thickened bladder (chronic, small dogs and cats)

o   Palpation may stim stranguria

o   Remainder of exam normal (with uncomplicated infection)

§  positive culture w/o signs
§  Cushing’s and chemo patients
§  Usually treated to prevent pyelonephritis
§  Do not treat if resistant bacteria and antibiotics are toxic

-not common because you're not looking for it. 

•  No predisposing factors/concurrent abnormalities 
•  Typical lower UTI clinical signs
•  Usually young female, otherwise normal
• dysuria, pollakiuria, urgency without fever or systemic signs

• Predisposing factors: ectopic ureters, neuro, neoplasia, foreign objects, urine retention, DM, Cushing's, chronic renal disease)
• Unlikely to cure w/o correcting underlying problem
• Pyelonephritis is usually the result of a complicated UTI

o   Cure

§  Eradication of microorganisms

§  Resolution of clinical signs

§  Proven by negative culture

o   Persistence

§  Failure to eradicate

§  Demonstrated by positive culture 3-5 days after initiation of Abx therapy

§  R/O inappropriate drug, inadequate dose, frequency, owner/patient compliance

o   Relapse

§  Positive culture 7-14 days after discontinuation of Abx (same strain)

§  Similar R/O as persistence

§  Or deeper seeded infection, mixed infection, formation of drug resistance

o   Reinfection

§  May be difficult to distinguish from relapse or persistence

§  Culture different organism

§  Re-eval for predisposing cause

                                Base therapy on new culture and sensitivity

staph, strep, and proteus can be treated with:

E-coli and anything can be treated with:

pseudomonas and anything can be treated with:

penicillins

TMS or amoxicillin

treat the other, then also give tetracycline

o   10-14 days for uncomplicated bacterial cystitis

o   4-6 weeks for complicated UTI including pyelonephritis and prostatitis

o   Mixed infection

§  Treat with single Abx that both are sensitive to

§  Treat with 2 different Abx based on C&S (owner compliance)

§  Treat predominant pathogen. Culture during therapy and treat second pathogen if still present. 

• the prostate gland is involved.
• Many drugs do not penetrate prostate-blood barrier without inflammation, so chronic cases may take up to or longer than 8 weeks treatment
• treatment for chronic prostatitis is similar to pyelonephritis
• effective drugs include TMS, chloramphenicol, quinolones, erythromycin, clindamycin

• Methenamine
• Urinary antiseptic (not antibiotic)
• Converted to formaldehyde
• Requires acidic urine pH<6 (dietary urinary acidifiers, may promote vomiting)
•   Every 6 hours for dogs, every 12 hours for cats
• need to clear current infection first

1. young to middle age neutered female
2. has not had these signs previously
3. had dysuria/stranguria, pollakiuria, with/without hematuria
4. does not have history of recent antibiotic use

cephalexin, amoxicillin, clavamox

10-14 days

• IMHA
• DIC
• transfusion reaction
• heat stroke
• splenic torsion
• caval syndrome of HW
• coral snake envenomation

the differential diagnoses of upper urinary tract macroscopic hematuria include:

• renal neoplasia
• trauma

the differential diagnoses of lower urinary tract macroscopic hematuria include:

• infection
• inflammation
• calculi in bladder or urethra
• neoplasia
• trauma
• benign prostatic hyperplasia, prostatic cyst, paraprostatic cyst
• pro-estrus, estrus, subinvolution of placental sites

1. glomerulonephritis
2. chronic bacterial pyelonephritis
3. cystic renal disease
4. strenuous exercise
5. renal neoplasia (macroscopic upper UT)
6. trauma (macroscopic upper UT)

what does microscopic hematuria and proteinuria suggest, especially with hypoproteinemia and hypoalbuminemia?

what test is done to determine significance of protein loss?

glomerulonephropathy

UPC (not valid in gross hematuria due to leakage of albumin)

• peripheral blood leukocytosis
• azotemia
• systemic disease (fever, vomiting, inappetance, lethargy, back pain)
• not persistent hematuria, but occasional
• active urine sediment
• positive urine culture

• hematuria
• renal/perirenal pain if obstructed
• hematuria
• UTI signs
• possible hydronephrosis, hydronephrosis, hydroureter

gross hematuria without stranguria

blood red or coffee colored

back pain

polycythemia (inc. renal erythropoietin)

• hematuria
• other signs related to kidney not seen
• v/d, pain
• may have no signs in older patients, incidental finding during US

• due to renal hemangioectasia
• early middle age
• no dysuria or pollakiuria
• breed, hx, PE, UA, IVP, renal arteriography, renal biopsy

• similar to hematuria of Welsh corgis
• bleeding so severe that anemia produced
• frank bleeding without inflammatory cells in UA
• bleeding from one or both kidneys

• younger cats, with decreasing severity with age
• extremely common
• element of obstruction
• acute onset of lower UT signs for 2-7 days, 50% will have recurrence of signs
• urine, UT, or UT response to urine problem OR systemic issue with bladder signs
• diagnosis of exclusion
• hematuria  +/- pyuria with negative culture
• thick bladder on radiograph
• cystoscopy- glomerulations (small hemorrhagic lesions)

1. decrease risk of obstruction
2. reduce severity of signs
3. decrease frequency of episodes
4. do nothing with self-limiting cases
5. increase water consumption
6. decrease stress (Feliway)
7. amitriptyline
8. GAGs
9. analgesics
10. no antibiotics

• sudden onset of hemodynamic, filtration, and excretory failure of kidneys with subsequent accumulation of metabolic toxins and dysregulation of fluid, electrolyte, and acid-base balance
• rapid onset of primary renal azotemia over hours to days
• pathologic oliguria of less than a day

• sudden onset renal parenchymal injury
• mild changes in serum creatinine, urine output, other biomarkers

• degeneration of renal tubular epithelium due to hypoxic/ischemic or toxic causes.
•  hi blood flow, hi metab, and conc mech make kidneys susceptible
• can be iatrogenic

o   Endogenous: calcium, myoglobin, uric acid, hemoglobin

o   Exogenous: ethylene glycol, aminoglycosides, easter lily, monensin, radiographic contrast agents, chemo agents

what are the ischemic or vascular causes of AKI?

• dehydration
• hemorrhage
• shock
• hypotension
• hypertension
• sepsis
• trauma
• heart failure, cardiac arrest, arrhythmia
• vasculitis
• thromboembolism
• DIC
• anesthesia
• NSAIDS
• ACE inhibitors

pyelonephritis

interstitial nephritis (lepto)

glomerulonephritis (SLE, tick-borne dz)

o   Induction phase (hrs to days)

§  Hard to test, must recognize potential sources of insult

§  Best time to treat and prevent progression (e.g. known ethylene glycol ingestion, treat NOW)

o   Maintenance phase (days to weeks)

§  Tubular lesions established

§  Low BRF and GFR perpetuated by intra-renal mechanisms

§  Mechanisms of perpetuation

·         Afferent arteriolar vasoconstriction

·          decreased glomerular capillary surface area and permeability

·         Efferent arteriolar vasodilation

·         Obstruction of tubular lumens

·         Backleak of filtrate

o   Recovery phase (weeks to months)

§  Compensatory hypertrophy (not really recovery)

§  Nephron repair

·         Requires intact basement membrane and viable epithelial cells

§  Improvement in renal function

·          increased GFR, decreased BUN/Creat

§  Degree of recovery dependent on severity and extent of injury 

• Depressed, anorexic, vomiting, dehydration, anorexia, known/suspected toxic exposure
• Detection of azotemia with inappropriate USG
• Increasing serum Creatinine (0.3 increase in 24 hours)
• Urine vol may be increased, decreased, or normal ********
• Assume azotemia is due to AKI until proven otherwise
• Identify life threatening complications, aka Hyperkalemia, acidosis, dehydration, sepsis
• Localize pre, ren, postrenal (Hx, PE, UA, imaging)
• o   Determine urine production rate after rapid rehydration
• §  Oliguric <1mL/kg/hr, <2 with IV fluids
• o   Culture it
• Discriminate between AKI and Chronic kidney disease
• §  Chronic unlikely has oliguria/anuria (only at the very end)
• §  Small kidneys and weight loss/poor BCS is usually chronic
• §  Nonregenerative anemia is chronic
• §  Hyperkalemia is acute
• §  Renal osteodystrophy is acute

• inc P exceeds inc in creat
• mild to mod decrease in Ca
• inc in K propotional to inc in creat
• dec in HCO3 roughly proportional to degree of renal failure
• inc in anion gap due to accumulation or organic acids
• glucosuria in absense of inc in blood glucose = dysfunction of proximal tubule
• proteinuria may be indicator of glomerular or tubular damage
• casts indicate active renal tubular pathology

o   Negative prognostic factors

§  Oliguria

§  Pre-existing renal or non-renal disease

§  Systemic infection

§  Older age

o   Positive prognostic factors

§  Local infection

§  Toxins (OTHER than ethylene glycol and lilies)

·         More likely to have intact tubular basement membrane

§  Hyperkalemia >8mg/dl or EKG abnormalities
·         IV fluids
·         Glucose and insulin
·         Calcium gluconate (cardio protective)
·         NaHCO3
·         Furosemide
·         Potassium binding agents (oral, rectal)
§  Metabolic acidosis pH<7.1 or HCO3<12
·         IV fluids
·         NaHCO3
o   Not a benign treatment!
o   Slowly give ½ calculated deficit
o   Reassess frequently!!!
o   can -->decrease Ca, paradoxic CSF acidosis, cerebral edema, death

§  Additional fluid volume expansion

§  Dextrose, mannitol

§  Furosemide

§  Dopamine, dobutamine

§  Diltiazem

fenoldopam (still controversial)

§  ***these do not reverse the disease, only aide in excretion of metabolic waste/toxins

§  If not converted or over-hydrated, then keep going.

• §  Must be rehydrated
• §  Does not increase GFR, generally no decrease in azotemia
• §  Goal is to increase urine volume
• §  Furosemide-avoid when dealing with AG toxicity
• §  Dextrose-osmotic diuretic, little use.
• §  Mannitol-osmostic, avoid if over-hydrated

1. conservative management of fluid, electrolytes, acid-base, uremic symptoms
2. dialysis

• control gastric-mediated gastritis (decreased GFR= serum levels increased, increased acid production and ulceration)
• histamine H2 blockers (famotidine)
• proton pump blocerks (omeprazole)
• cytoprotective agents (sucralfate)
• control vomiting with antiemetics
• metoclopramide (not concurrent with dopamine)
• chlorpromazine
• ondansetron
• control nitrogenous waste products by reducing amino acid content of parenteral/enteral feeding

• weight loss
• abnormal urination
• decreased performance
• incontinence
• abdominal distention and colic
• peripheral or ventral edema

40-60ml/kg/day water intake (20-40L)

Urine output 5-20ml/kg/day (5-15L)

in a transrectal, what is palpable in a horse vs a cow?

how are small ruminants palpated?

• Horse: kidneys (both only if pathologic), bladder, ureters (if path), urethra
• Cow: dorsal midline lobulated left kidney, ureters(if path), bladder, urethra
• sheep/goats: digital, transabdominal, perineal urethra, inspect urethral process

• horse: will urinate in their stall if clean. catheterization-avoid xylazine (induce glucosuria), avoid furosemide (alters UA)
• cow/swine-stroke perineum or use wet brush on prepuce
• small ruminants-hold nose

in a horse with chronic renal failure, what is seen on lab tests?

what about acute renal failure?

• CRF-profound hypercalcemia, hypophosphatemia
• ARF- hypocalcemia and hyperphosphatemia

o   In LA, can be altered by many things. (including profuse sweating)

o   Ruminant and hindgut fermenters can use urea, so levels can be falsely normal

o   Exceptions: hi protein diet, anorexia, neonate

high producing dairy cattle will be low normal

suckling neonates will be hyposthenuric

[U(x)/P(x)] x [P(Cr)/U(Cr)] x 100

low sodium FC is dehydration (distinguishes prerenal or renal)

hi P or K FC indicates tubular damage, diet, acid-base

o   Glucosuria and hyperglycemia=systemic disease

o   Glucosuria and euglycemia=tubular disease

serum GGT- liver and pancreas 

urine GGT- brush border enzyme of proximal tubule epithelial cells, only indicates active destruction

• kidneys (glomerulonephritis, amyloidosis, acute interstitial nephritis, pyelonephritis) 
• or from exudative processes affecting ureters, urinary bladder, or urethra

CaCO3 

straw colored, slightly turbid

• equine metabolic syndrome
• pituitary parts intermedia dysfunction
• corticosteroid therapy
• intense exercise
• pain 
• shock

• severe hypotension
• prolonged anesthesia
• GI fluid losses
• acute blood loss
• endotoxemia
• exercise-associated sweat loss
• volume redistribution (third spacing)

• ischemia (vasomotor nephropathy) (ace in hypotensive)
• aminoglycoside antibiotics
• other antimicrobials
• NSAIDS (phenylbutazone, flunixin)
• pigment nephropathy (Mb, Hb)
• heavy metals (arsenic, mercury, lead, cadmium)
• vitamin D (supplement or plant source)
• vitamin K3
• leptospirosis

put the following in decreasing order of nephrotoxicity

a. streptomycin

b. kanamycin

c. amikacin

d. gentamicin

e. neomycin

1. neomycin
2. kanamycin
3. gentamicin
4. amikacin
5. streptomycin

• bind to phospholipase on brush border of proximal tubules
• accumulate in renal cortex and interfere with lysosomal, mitochondrial, and Na/K/ATPase function
• renal vasoconstriction
• saturable binding, so prolonged exposure is worse
• serum creatinine should be monitored every 3-5 days, also GGT, proteinuria, glucosuria

• COX inhibitors which inhibit prostaglandins which are needed for vasodilation
• especially hypovolemic patients
• renal medullary crest or papillary necrosis is classic lesion due to lower blood flow

• pigments cause vasoconstriction leading to ischemia
• tubular obstruction by heme casts
• reduction of ferrous iron compounds forms increased hydroxyl radicals causing cellular damage

• hematuria, eosinophilia, eosinophiluria 
• immune-mediated caused by delayed cell-mediated hypersensitivity or Ab against tubular basement membranes
• prognosis grave

1. get a urine sample.
2.  give fluid therapy
3. pre-renal will 50% or greater reduction in magnitude of azotemia within 24 hours. renal patients will respond slower

1. discontinue nephrotoxics/ treat underlying
2. admin fluids and correct electrolytes/acid-base (LRS, Normosol-R, Plasmalyte 148)
3. observe for urination within 12-24 hours. edema in conjunctiva will develop in oliguric patients
4. if oliguric, admin furosemide, mannitol, or dopamine
5. peritoneal and hemodialysis

more common in colts than fillies

1. bladder
2. urethral (perineal, preputial)
3. urachal (SC edema around umbilicus
4. ureteral (retroperitoneal)

• lethargy, colic, abdominal distention, stranguria, pollakiuria, depression, anorexia
• post-renal azotemia, hyponatremia, hypochloremia, hyperkalemia
• peritoneal creatinine >2x serum creatinine

• 0.9%NaCl, 5% dextrose
• Ca gluconate, bicarb
• drainage

• uremia
• chronic weight loss with anorexia
• rough hair coat
• poor athletic performance/lethargy due to anemia due to decreased erythropoietin
• PU/PD
• ventral edema
• nephrotic syndrome
• tartar buildup and oral lesions and halitosis

persistent isosthenuria

increased creatinine

ration of BUN:Cr>10:1

mild nonregenerative normocytic normochromic anemia

hypoalbuminemia

hypercalcemia

hyponatremia, hypochloremia, hypokalemia, hypophosphatemia

kidney small firm and irregular

1. IV fluids 
2. discontinue nephrotoxics
3. Antibiotics in pyelonephritis
4. give good grass hay and carbs instead of hi protein and Ca
5. salt supplementation if hyponatremic/chloremic
6. omega-3 fatty acids as antioxidant

uroliths in horses are most common in (location, age, etc.)________

and form by _______

lower urinary tract

geldings and adults

bladder, urethra, kidney, ureter (in that order)

urine stasis and nidus like desquamated epithelial cells or necrotic debris

what drug may be associated with uroliths in horses?

what dietary change can help prevent future uroliths?

phenylbutazone

cut out alfalfa and other hi Ca foods

• males-pararectal cystotomy, perineal urethrostomy, cystotomy
• flank-nephrectomy, ureterotomy
• lithotripsy
• medical-bladder lavage, anti-inflam, antimicrobials, inc water consumption, eliminate alfalfa, urinary acidifiers unproven

• at level of ischial arch at dorsocaudal aspect
• hemospermia, hematuria at end of urination
• no pollakiuria or dysuria
• affects quarterhorse geldings
• blowout of corpus spongiosum into urethra
• can diagnose via endoscopy
• tx: nothing, subischial/perineal urethrotomy, buccal mucosal graft

• hematuria, weight loss, colic
• unilateral
• azotemia
• nephrectomy

accumulation of crystalloid urine sediment secondary to incomplete bladder emptying

weight stretches detrusor muscle, further disrupting normal urination

incontinence, hindlimb weakness, ataxia

tx: bladder lavage, broad spec antibiotics, bethanechol

• ectopic ureter, bladder paralysis, bacteremia, nephrolithiasis
• Actinobacillus, Strep equi, R equi, Salmonella

• UMN- increased urethral resistance
•      pollakiuria, sporadic dribbling
•      spinal cord lesions
• LMN-relaxed bladder and sphincter
•      continuous dribbling, neuro deficits
•      cauda equina syndrome
•      EHV-1 myelitis
•      Sorghum/sudan grass toxicity

• neurogenic- dec vasopressin secretion
• nephrogenic- collecting duct insensitive to vasopressin

• impingement of hypothalamus and posterior pituitary
• cortisol antagonism of vasopressin
• hyperglycemia and osmotic diuresis

• blister beetle found in alfalfa hay
• irritates lower UT, causing hemorrhagic cystitis
• also affects GI and CV systems
• severe hypocalcemia, hypomagneaemia, azotemia, metabolic acidosis, hypoproteinemia

type 2

proximal

other signs collectively known as Fanconi syndrome

o   Post-parturient hemoglobinuria

§  Older dairy cows 5-8 y

§  1-4 week post-partum

§  Low intracellular P

§  Tx: blood, fluid, P

o   Copper toxicity in sheep

o   Bacillary hemoglobinura (very fast)

§  Clostridium novyi type D

§  Hemolysis and liver failure

o   Water intox

o   Salt poisoning

o   Selenium deficiency

o   White muscle disease (vit E, Se def)

§  Small ruminants susceptible

§  Neonates can be affected in utero

o   Cassia occidentalis (wild coffee)

§  Common in FL and TX

§  Causes muscle degeneration

§  Toxin contained within fruit

• Cestrum diurnum-vitamin D toxicosis
• Cassia occidentalis (wild coffee)-myoglobin nephropathy
• Oak-tannins hydrolyzed in rumen to gallic acid   (NOT in sheep and goats bc they have tanninase)(melena, tenesmus, bloody diarrhea, weight loss, bitter milk)
• Pigweed (Amaranthus)-oxalates chelate calcium (weakness, ataxia, ascites, 5-7 days after turnout)

·         Leptospira interrogans

o   Hardjo, Pomona, grippo

o   Pathophys

§  Renal vasc endo damage

§  Hypoxia

§  Hemoglobinuria

§  Interstitial nephritis

o   Young animals exposed to stagnant water

o   Fever, abortion, mastitis, meningitis

o   Diagnosis

§  Paired titers

§  Urine PCR, fluorescent Ab, dark field microscopy

o   Tx: tetracycline (also nephrotoxic, use if Creatinine is normal), penicillin, ampicillin

o   Inflam dz-->serum amyloid A-->deposition in kidney, GI, liver, adrenal-->disrupt glomerulus-->PLN

o   Diarrhea, wt loss, edema

o   Severe proteinuria, hypoalbuminemia

o   Renal or pulmonary thrombosis

o   Biopsy, prognosis poor

what are the causes of acute and chronic glomerulonephritis in ruminants?

what are the signs?

o   Acute

§  Pregnancy toxemia in small ruminants

o   Chronic

§  BVD, hog cholera, African swine fever (latter two reportable)

§  Inherited in finnish landrace lambs (higher number of lambs, higher risk)

o   Poor productivity, diarrhea, edema

o   Proteinuria

o   Corynebacterium renale

§  Contagious in cattle, host-adapted

§  Transmission

·         Direct, venereal, iatrogenic

§  Subclinical carriers possible

o   E. coli

§  Ascending

o   C. pseudotuberculosis, A. pyogenes, Salmonella, S. aureus

§  Hematogenous

o   Signs

§  Colic, arched back, treading, tail swishing

§  Fever, depression, inappetance, decreased milk yield

§  Blood, pus, crystals on vulva

o   Diagnosis

§  Enlarged, painful kidney, dilation of pelvis

§  ↑white count, fibrinogen, globulin

§  +/-azotemia

§  Hematuria, proteinuria, bacteriuria, leukocyte casts

§  Culture

o   Treatment

§  G+: penicillin

§  G-: ceftiofur

§  >3 weeks (more longterm for good penetration)

§  Quarantine infected animals (coryne renale)

nematode inhabiting perirenal tissues

signs: production lossis, ascites, skin nodules, paresis

tx: fenbendazole or ivermectin at 4 month intervals

§  Hi conc, pelleted diet

·         Feedlot, pet

§  High silicate grass

§  Decreased water consumption

·         Supersaturation

§  Estrogenic substances

·         Nidus

§  Vitamin A deficiency

§  Males castrated early and urethra doesn't develop as much 

§  legumes-->calcium carbonate

§  fescue in cattle or apples, sweet potato, pigweed in sheep-->oxalate calculi

§  grain diets-->struvite and calcium phosphate

what are the signs of urethral obstruction in ruminants?

where do they block?

o   Restlessness, treading, tail-swishing, teeth grinding

o   Vocalization

o   Stranguria

o   Rectal prolapse

o   Small ruminants block at urethral process

o   Feedlot steer-sigmoid flexure

o   Other: Neck of bladder, ischial arch

o   Urethral rupture-“water belly”

o   Bladder rupture

§  Abdominal distension

§  Anorexia

§  colic

§  Azotemia

§  Hemoconcentration

§  hypoNa, hypoCl

§  hyperP, hyperK, hperMg

§  abdominocentesis

·         peritoneal: serum Cr>2:1

§  PE: pulsing on abdominal palp (trying to urinate)

§  US: measure bladder, look at kidneys

o   Medical tx: fluid/electrolyte therapy, Walpole’s solution pH 4.5, >30% recurrence, US-guided cystocentesis to relieve pressure

§  amputate urethral process

·         Temporarily restores patency in 66%

·         Catheterize and flush retrograde

o   Sx:

§  Perineal/ischial urethrostomy

·         Stricture in <1yr

·         Good in feedlot steer

§  Tube cystotomy

·         44% recurrence in 12-60 months

§  Bladder marsupialization

§  Determine composition of stone

§  ensure dietary Ca:P >2:1

§  Mg <0.2%

§  More forage, avoid legumes

§  Acidify urine

·         Ammonium chloride

·         Decrease dietary cation:anoin difference

·         Variable effects

·         Systemic academia

o   Bracken fern

§  Chronic ingestion (herd problem?)

·         Hematuria in several animals

·         Bladder neoplasms

·         Dysuria, pollakiuria, death

§  Acute toxicity

·         Bone marrow suppression

§  Pathology 

·         Irritant

·         Immunosuppression

o   Recrudescence of BPV-2

·         Mutagenic, carcinogenic

§  Treatment=prevention

·         Ulcerative posthitis and vulvitis

o   Caused by Corynebacterium renale

§  Proliferates in hi urinary urea/excess protein in diet

§  Hydrolyzes urea to ammonia causing ulceration

§  Contagious

§  Moist ulcers

§  May progress to internal form

·         Adhesions, distorted vulvar conformation

§  Dysuria, vocalization, weight loss

§  Isolate affected

§  Reduce protein

§  Systemic and topical antimicrobials

o   Patient with historical, clinical, lab kidney dz

§  Biomarker

§  Glucosuria

§  Cylinduria

§  Inflammatory sediment

§  Microalbuminuria

o   Patients with imaging evidence of AKI that are non azotemic

o   Patients whose clinical presentation is readily fluid-therapy responsive

o   Also includes animals with progressive (hourly or daily) increases in serum creatinine of 0.3 within the nonazotemic range during a 48 hour interval

o   Kidney damage for >3 months, defined by struc/func abnormalities of kidney with or without decreased GFR

§  Path abnorm

§  Markers of kidney damage including  comp of blood/urine/imaging

§  GFR-not measured as much in vetmed

o   Mild renal insufficiency

§  Up to 60% loss of function

§  Minimal symptoms

§  PU/PD, anorexia, vomiting

§  Minimal treatment, mostly preventative

o   Moderate renal insufficiency

§  Azotemia

§  Anorexia, wt loss, anemia, metabolic acidosis, hyperparathyroidism, +/-systemic hypertension

§  Progressively more intensive treatment, tailored to indiv problems

o   Severe renal insufficiency

§  Past 80% func loss

§  Severe azotemia

§  Anorexia, vomiting, wt loss, anemia, metabolic acidosis, hyperparathyroidism, hyperphosphatemia, systemic hypertension

§  Intensive treatment limits of conventional treatment

o   Hypogastric nerve

§  sympathetic efferent synapse on β receptors in bladder (detrusor muscle)

§  also on α receptors on internal urethral sphincter

o   Pelvic nerve

§  Parasympathetic synapse on bladder wall (Ach)

o   Pudendal nerve

§  Carries somatic efferent to skeletal external sphincter muscle

o   Storage phase

§  Sympathetic dominance

§  Hypogastric nerve- allows relaxation of bladder, inc tone of internal sphincter

§  Pudendal nerve- maintains external urethral sphincter tone

o   Voiding phase

§  Sensory

·         Distensionàpelvic nerveà brain

·         Painà hypogastric nerveàbrain

§  Motor

·         Voluntary voiding

o   Ponsà reticulospinal tractà pelvic nerve

·         Voiding phase

o   Bladder contraction

§  Ach release from pelvic nerve

o   Urethral relaxation

§  Inhibition of hypogastric (internal) and pudendal nerve (external striated)

with/without organ complications

also "not taken" as in fractious animals

§  Brain (rare)

·         Cerebrum

o   Loss of voluntary control

o   Nocturia/unconscious urination

o   Mentation changes

youth, dementia, tumor

emptying complete

• Lesion cranial to S1, look around L5
• Voluntary bladder function loss
• Sphincter intact, so difficult to express, no inhibition
• Interneurons stimulated over time, can inhibit pudendal nerve to an extent, but not coordinated, and internal urethral sphincter not inhibited.
• ·         Tetra or paraparesis/paralysis
• ·         Hyperreflexia
• ·         CP deficits
• ·         Differentials
• o   IVD
• o   Trauma
• o   neoplasia

• ·         Sacral lesion
• o   Pelvic/pudendal nerve
• ·         Distended, flaccid bladder
• ·         Paraparesis/paralysis
• ·         dec anal tone and dec perineal reflex
• ·         Differentials
• o   Trauma
• o   Cauda equine syndrome
• o   Congenital
• bladder easily expressed

• if detrusor is intact, then no signs
• as detrusor function is lost, more frequent urination and bladder emptying incomplete

• voiding disorders (increased residual volume)
• detrusor atony
• urolithiasis
• neoplasia
• stricture
• prostatic disease
• dyssynergia
• storage disorders (normal residual volume)
• ectopic ureter
• chronic inflammation
• neoplasia
• hormone responsive urethral incompetence

•  Enhance relaxation (all have anticholinergic activity)
• o   Propantheline (anticholinergic)
• o   Amytryptyline (tricyclic antidepressant)
• o   oxybutynin (antimuscarinic) 

§  Keep bladder small

§  Stim detrusor

§  Bethanechol

·         Parasympathomimetic

§  smooth muscle relaxation-α antagonist 

·         prazosin

·         phenoxybenzamine

·         tamsulosin- NOT IN CATS

§  striated muscle relaxation -anticholinergic

·         diazepam

·         acepromazine

• ·         DES (diethylstilbesterol) or premarin NOT IN CATS
• o   Dogs only, after spay
• o   Low risk of blood dyscrasias
• o   ↑sensitivity and density of α receptors in trigone and urethra
• o   Careful of aplastic anemia, dose low
• ·         Phenylpropanolamine
• o   α adrenergic
• o   most commonly used in dogs
• o   dose is per/cat not per/kg

1. supersaturated solution
2. nucleation initiates precipitation
3. direct growth
4. aggregation

1. treat hyperkalemia and acidosis via IV fluids 
2. sedation/anesthesia
3. pass largest catheter possible
4. apply digital pressure rectally proximal to obstruction, then release once pressure has built up from flushing
5. can do decompressive cystocentesis
6. tube cystotomy or surgery if necessary

• reduce protein, phosphorus, and magnesium
• inhibits urease-producing bacteria from increasing ammonium levels and thereby phosphate ion availability, and supersaturation event
• Pt will have reduced urine SG, urine pH, and BUN

• no specific supersaturation event
• causes: genetic risk or lack of alternative ions available for binding
• not amenable to dissolution therapy
• minimize calciuria and oxaluria
• keep urinary SG low, avoid aciduria
• hydrochlorothiazide diuretics (dec calciuria)
• potassium citrate (urine pH mod and alternate binding for Ca)
• vitamin supplementation does not work and can exacerbate

• common in dalmatians or patients with hepatic dysfunction (PSS)
• amenable to dissolution
• decrease urine urate and ammonium
• reduce protein and nucleic acid in diet
• neutral or alkaline urine pH targeted
• Rx: Allopurinol (not in hepatic disease patients)

•   Struvite F>>M
• Calcium oxalate F=M
•  

• weight loss with reduced appetite
• vomiting, dark tarry stools
• inc water consumption and urine output
• nocturia
• skin dry
• easily dehydratable esp when stressed
• systemic hypertension
• pallor due to anemia
• oral ulcers
• immature animals-bone disease due to secondary hyperparathyroidism
• thick maxilla, rubber-jaw, loose teeth
• depression
• coarse tremors, tonic-clonic seizures

1. reduced RBC production (reduced erythropoietin)
2. reduced RBC lifespan (Na/K/ATPase pump affected)
3. blood loss (GI ulceration, dec gastrin production)

secondary hyperparathyroidism

inc P retention

dec Vit D and dec Ca GI absorption and inc PTH

renal osteodystrophy

metastatic calcification

• dogs-start with ACE inhibitor like enalapril (efferent), double, then amlodipine (Ca channel blocker)
• cats-start with amlodipine (afferent), double, then try ACE inhibitor like enalapril or beta blocker like propranolol or atenolol

• limit stress
• control anorexia, vomiting, azotemia, hyperphosphatemia, hyperparathyroidism, metabolic acidosis, anemia, and hypertension
• free access to fresh, clean water
• diet 70-110kcal/kg BW/day of metabolizable energy
• limit sodium intake to help with hypertension
• maintain serum bicarb >20mEq/L
• transfusion, EPO, or Darbepoietin

1. treat underlying
2. consider kidney biopsy
3. ACEI plus dietary plus dietary protein reduction
4. low-dose acetylsalicylic acid if serum albumin is <2.0 g/dl
5. monitor

• sudden onset, life threatening
• can have multiple episodes
•  no systemic illness
• more than 50% of Arabians
• no age, sec predisposition
• blood clots from one or both kidneys
• usually not azotemic since only one kidney affected
• treat with supportive care (transfusion, hemostasis), unilateral nephrectomy, but will eventually affect other kidney

• further reduce phosphate (3&4)
• dietary protein reduction (3&4)
• treat anemia if affecting quality of life (3&4)
• treat v/d/nausea with H2 blockers (3&4)
• fluids to treat hydration (3&4)
• dialysis (4)

(i) Hyperparathyroidism

1. inc PTH

a. Kidneys

inc Ca

dec  P

b. Bones

inc Ca resorp

inc P resorp

c. Calcitriol

inc Ca absorp

inc P absorp

pre-renal: elevated SG

renal: reduced SG or isosthenuric, but not hyposthenuric usually

post-renal: hyperK, hypoNa, poss hi BUN/hi Creat and low protein in abdominal fluid