Nephrology/Urology

Question 1

List the clinical signs associated with renal amyloidosis in cattle.

Answer 1

Mature animals with:- Chronic diarrhoea.- Weight loss.- Poor productivity.- +/- Generalised or ventral oedema.- +/- Enlargement of the left kidney on rectal (non-painful).- +/- stable foam on urine.

Question 2

What clinical pathology abnormalities will be seen in cattle with renal amyloidosis?

Answer 2

• Marked proteinuria.- Marked hypoalbuminaemia.- Advanced dz: azotemia.- Chronic, active dz: hyperfibrinogenaemia, hyperglobulinaemia.

Question 3

What two diseases cause prolonged proteinuria in cattle? How would you differentiate between the two in the live animal?

Answer 3

• Renal amyloidosis and glomerulonephritis.- Renal biopsy.

Question 4

Describe the pathophysiology of renal amyloidosis in cattle.

Answer 4

• Chronic inflammatory disease e.g. TRP, mastitis –> circulating serum amyloid A; abnormal catabolism of SAA or inherent abnormality in SAA –> misfolding of SAA and deposition of amyloid fibrils which are resistant to proteolysis in glomerulus –> sustained albuminuria.- Dxa: GIT wall oedema or amyloid deposition in GIT.- Renal or pulmonary thrombosis: loss of low-molecular weight anticoagulant proteins through the compromised kidney.

Question 5

Described the gross and histopathology of kidneys of cattle with amyloidosis.

Answer 5

• Gross: large, yellow-tan to white kidney, waxy quality of renal parenchyma; generalised oedema.- Histo: amyloid deposition in glomerulus, interstitium and tubule lumen (congo red –> light pink or bright green under polarised light).

Question 6

What is the prognosis associated with renal amyloidosis?

Answer 6

Hopeless.

Question 7

What is the common common route of infection in cattle with pyelonephritis and what are the two most common aetiologic agents?

Answer 7

• Ascending infection from the lower urinary tract e.g. urogenital trauma during calving, abnormal vulvar conformation, urine retention, catheterisation.- Corynbacterium renale - contagious; adhere to urinary tract epithelium via pH-mediated pili i.e. adherence enhanced in alkaline urine and dec in acidic urine.- Escherichia coli - faecal contamination.

Question 8

List bacteria that have been implicated in causing pyelonephritis of haematogenous origin in cattle.

Answer 8

Salmonella, Staphylococcus, Streptococcus, P. aeruginosa and T. pyogenes.{Corynbacterium pseudotuberculosis (small ruminants)}.

Question 9

List the clinical signs of acute pyelonephritis in cattle.

Answer 9

• Sudden reduction in feed intake.- Sudden reduction in milk production.- Fever.- Tachycardia.- Tachypnoea.- Dehydration.- Rumen stasis, mild colic.- Scleral injection.- +/- signs of cystitis: dribbling urine, swishing tail, arched stance after urinating, discharge on distal vulva.- +/- L kidney large, painful, smooth on rectal palpation.

Question 10

List the clinical signs of chronic pyelonephritis in cattle.

Answer 10

• Vague clinical signs: weight loss, muscle wasting, poor growth, anorexia, diarrhoea, reduced milk production.- Pale mucous membranes due to anaemia.- There may be no abnormal behaviour or posturing during urination.- +/- loss of lobulation in L kidney on rectal (may not be pain or enlargement).

Question 11

Describe ultrasound findings in acute pyelonephritis.

Answer 11

• R kidney in 12th ICS and R paralumbar fossa.- L kidney: L paralumbar fossa or per rectum.- Renal enlargement, abnormal kidney shape, dilated renal calyces, flocculent echogenic material in the renal pelvis and ureter.

Question 12

Describe clinicopathologic abnormalities in cattle with pyelonephritis.

Answer 12

• Neutrophilic leukocytosis w hyperfibrinogenaemia.- If more chronic expect hyperglobulinaemia and hypoalbuminaemia (renal loss).- Chronic: anaemia (dec EPO and renal loss).- Bilateral pyelonephritis –> azotemia and isosthenuria = poor Px.- Haematuria, proteinuria, bacteria; USG 1/005-1.020.

Question 13

Describe the epidemiology of pyelonephritis in cattle.

Answer 13

• Israeli study: prevalence 0.3-2.7%.- Female predisposed due to short urethra and potential contamination and trauma from breeding/parturition.- Majority of cases w/in 90d of calving.- C. renale is difficult to eliminated on a herd level once established.

Question 14

List necropsy findings in cattle that have died from pyelonephritis.

Answer 14

• Bladder has evidence of haemorrhage, ulceration and fibrin deposition of epithelial surfaces; may extend through urethra.- Polypoid growths may develop with chronicity.- Ureters may be enlarged and filled w purulent debris.- Kidney(s) enlarged, may have grey, odourless exudate in renal pelvis, medulla and cortex (acute) or abscess (chronic).

Question 15

Describe the treatment of pyelonephritis in cattle

Answer 15

• Agressive and long-term ABs: penicillin; if coliform infection and no response after 96h gent, ceftiofur, TMPS.- Diuresis with oral or IV fluids to remove necrotic debris and bacteria from the UT.- Nephrectomy if unilateral pyelonephritis that is unresponsive to medical therapy.- Perform urinalysis and urine culture 1wk after stopping therapy to confirm efficacy.

Question 16

What is the prognosis for cattle with pyelonephritis?

Answer 16

• Treatment more efficacious if instituted early.- Case fatality/cull rates of 18-47% reported.- Recrudescence rate of 9.4% reported.

Question 17

Describe the pathophysiology of glomerulonephritis in cattle.

Answer 17

• Immune-mediated damage to the glomerulus.- Reported w acute septic dz, cattle w BVD and fascioliasis, mesangiocapillary GN in landrace lambs, preg tox in ewes.- Ab may be directed against host or foreign Ag in the vascular endothelium, mesangial cells or BM of the glomerulus or Ag-Ab complexes may deposit –> complement activation, chemotaxis of leukocytes –> glomerular injury –> inc glomerular permeability.

Question 18

List clinical signs displayed by ruminants with glomerulonephritis.

Answer 18

• Weight loss or poor productivity.- Chronic diarrhoea.- Lethargy.- Generalised oedema.- Kidneys maybe mildly enlarged, non-painful on rectal.- Signs of concurrent dz: BVD, fascioliasis, preg tox.- Mesangiocapillary GN of Landrace lambs: 1d-3mo old, dull, ataxic, appear blinds, seizures, fine muscle tremors, colic.

Question 19

Describe clinicopathologic abnormalities in ruminants with glomerulonephritis.

Answer 19

• Heavy proteinuria.- Mild anaemia.- Hypoalbuminaemia.

Question 20

Describe prognosis for ruminants with glomerulonephritis.

Answer 20

• Treatment not described.- Prognosis poor.- Mesangiocapillary GN of Landrace lambs not invariably lethal; some lambs may survive to adulthood.

Question 21

Describe congenital defects of the kidneys reported in ruminants.

Answer 21

• Renal cysts: common in cattle; no clinical significance unless multiple (polycystic kidney dz).- Renal agenesis: most common renal defect in lambs.- Renal oxalosis: inherited in Beefmaster calves –> weakness, lethargy, anorexia, dehydration, dxa, alopecia w/in wks of birth due to accum of Ca oxalate crystals.- Extopic ureter: rare in ruminants.

Question 22

Describe urinary tract neoplasias (not related to bracken fern ingestion) in ruminants.

Answer 22

• Primary bladder tumours reported in 0.05% cattle in Nth Am abattoirs = adenomas, papillomas, TCCs.- Fibropapillomas and SCC of genitalia may impinge upon urethra.- Renal carcinoma has been reported in cattle.- Nephroblastoma has been reported in a ewe and a lamb.- Urinary tract involvement occ seen w lymphosarcoma.

Question 23

Haemolytic uraemic syndrome occurs in people following ingestion of E. coli O157:H7. It has been reported in 4 horses and 2 cattle. Describe the pathophysiology and clinical findings in cattle with HUS.

Answer 23

• Thrombotic microangiopathy disorder charac by microangiopathic haemolytic anaemia, thrombocytopaenia and renal failure; normal clotting times.- Cattle CSx: severe progressive anuric renal failure, acute haemolytic anaemia and consumptive thrombocytopaenia; haemolysis and tendency to bleed.- Necropsy: renomegaly, renal infarcts, scattered petechial and ecchymotic haemorrhage w/in renal parenchyma, ATN, fibrin thrombi in glomerular capillaries.

Question 24

List aetiologic agents of acute renal failure in ruminants.

Answer 24

• Aminoglycosides.- Tetracycline.- Ionophores.- Ethylene glycol.- Oxalate-containing plants.- Vitamin C or D overdose.- Oak, acorns, pigweed, Easter lily, phildendron, ponderosa pine, cocklebur, jessamine.- Myoglobin.- Haemoglobin, methaemoglobin.- Arsenic, mercury, cadmium, chromium, lead, zinc.

Question 25

List clinical signs of acute renal failure in ruminants.

Answer 25

• Non-specific; freq presented for poor appetite, diarrhoea or epistaxis.- May be anuric, oliguric or polyuric.- Depression, nasal discharge, ileus, melena and mild free-gas bloat may be present.- If concurrent septic dz: fever, scleral inj, tachycardia.- Acid-base, elec, fluid imbalances –> weakness.- Uraemia –> saliva w ammonia smell, enceph signs.

Question 26

List clinicopathologic abnormalities in cattle with acute renal failure.

Answer 26

• CBC: if inflammatory condition affecting renal tubules: neutropaenia or left shift.- Azotemia: elevated BUN (maybe as influenced by rumen physiology); elevated creatinine.- HypoNa, hypoCl, variable K +/- hyperMg, hyperPO4, hypoCa.- Metabolic alkalosis (acidosis in calves w concurrent dxa).- Urinalysis: proteinuria, haematuria, granular casts, FE sodium >4%.

Question 27

Describe the pathophysiology of acute renal failure in ruminants.

Answer 27

1. Reduced blood flow/ischaemia in kidneys: secondary to blood loss, septicaemia, endotoxaemia, severe dehydration from mastitis, metritis, enteritis, rumen acidosis or intestinal accidents, heat stress (lambs) –> infarction of renal cortex, renal v thrombosis, damage to tubular BM.2. Bacterial infection: bilateral pyelonephritis –> destruction of nephrons by bacterial toxins and host inflam resp.3. Pigment nephrosis: haemoglobin/myoglobin –> renal vasoconstriction and tubular obstruction from protein coagulation.4. Toxic nephropathies: various mech e.g. sulphonamides –> deposition of insoluble precipitates in renal tubules, NSAIDs –> dec Pg synth and medullary crest necrosis, aminoglyc –> cell death of tubules thru mitochond inj.

Question 28

Outline the treatment of acute renal failure in ruminants.

Answer 28

• Remove offending toxin or source: rumenotomy, activated charcoal, heavy metal chelators.- Promote diuresis through IVFT (IV, oral or rumen) and diuretic meds (furosemide or mannitol until urinating).- Correct acid-base and electrolyte derangements.- Additional therapy if indicated in specific cases: broad-spectrum ABs, plasma, PPN or transfaunation.

Question 29

Describe leptosira bacterial structure and transmission.

Answer 29

• Motile, gram-negative, obligate aerobic, tightly coiled spirochetes 0.1-0.3um diam and 6-20um length.- Persist in chronic infections of renal tubules of maint host –> little or no dz.- Transmitted to incidental host through urine from maint host (directly or contam feed/enviro).- Causes multi-organ dz in incidental hosts e.g. abortions, repro failure, kidney, liver or CNS dz.- Survives in warm, moist enviro for 6mo; survives short period if dry and cold; doesn’t survive freezing.- Seasonal incidence higher in Summer/Autumn in temperature regions or rainy season in warm climates.

Question 30

Describe epidemiology of leptospirosis in cattle.

Answer 30

• Cattle are primary maintenance host reservoir of L. interrogans serovar hardjo type hardjopragitno (UK) and L. borgpetersenii servo hardjo type hardjobovis (worldwide).- Also maint or incidental host for L. interrogans serovar pomona and L. interrogans serovar grippotyphosa.- Serovars hardjo, pomona and grypotyphosa most often implicated in renal infection in cattle; renal dz caused by lepto in small ruminants rare but may serve as carriers.- Urine/renal/seroprev varies in US from 2-47%.- Infection w host-adapted serovar hardjo –> mild dz; overt losses attrib to effects on reproduction.- Incidental infection w non-host adapted strains –> acute severe renal dz (particularly in calves).

Question 31

Describe clinical presentation of host-adapted Leptospira serovar hardjo infection in cattle.

Answer 31

• Asymptomatic.- Chronic interstitial nephritis; renal dys rarely observed.- Infertility, stillbirth, abortion and birth of weak calves.- Milk-drop syndrome/flabby udder: fever, agalactia, mastitis, milk yellow/red-tinged and thick; udder soft.

Question 32

Describe clinical presentation of non-host-adapted Leptospira serovars infection in cattle.

Answer 32

• Severe systemic disease in calves > adult cattle.- Haemolytic anaemia (some L. serovars prod haemolysins), hepatitis, interstitial nephritis, tubular nephrosis, fever, anorexia, lethargy, dec milk prod, petechiation.- Agalactica and mastitis in lactating cows; +/- abortion.- Renal lesions result from damage to vascular endothelium, pigement nephropathy, interstitial nephritis –> azotemia, proteinuria, pyuria, granular casts, +/- haemoglobinuria.

Question 33

Describe the pathophysiology of leptospirosis in cattle.

Answer 33

• Leptospires ingested or penetrate external mucosa surfaces and scarified skin, mutliply, enter bloodstream thru lymphatics or direct penetration of blood vessels.- Bacteraemia 4-7d –> infection multiple organisms.- Leptospires become localised in mammary gland, kidney or genital tract; appear to be protected from IR.- Leptospires cleared from body OR chronic infection of renal prox tubules/repro tract occurs –> shedding for wks to months (non-adpated) or years (host-adapted).- Virulence factors: toxin effect of lipopolysaccharide, adhesion to cells and extracellular matrix, bacterial motility, haemolysins and iron sequestration.

Question 34

How is leptospirosis diagnosed in cattle?

Answer 34

• Microscopic agglutination test (MAT) is most widely-used serologic test: detects ABs to specific serovars, but cross-reactivity occurs b/w related serovars.- Acute infection: four fold inc b/w acute and convalescent sample or conversion from -ve titre to titre >100.- Chronic infection: titres may be -ve, inc, dec, static.- L. shedding in urine or semen can be assessed via culture (often unrewarding), PCR, phase-contrast or dark-field microscopy, FA, nucleic acid hybridisation or immunblot.- Urine testing: admin furosemide, discard first sample, clean vulva of gross debris, collect and test 2nd sample.- Histo renal tissue: Warthrin-Starry or Levaditi stains.

Question 35

Outline treatment of leptospirosis in cattle.

Answer 35

• Oxytetracycline for 5-7d (reported clinically effect but not proven); PPG/ampicillin (efficacy in cattle unproven).- IV or oral fluids, blood transfusions, diuresis if ARF.- Oxytet, ceftiofur, tilmicosin and tulathromycin have been shown effective in clearing renal shedding in herds.

Question 36

What is the prognosis associated with leptospirosis in cattle?

Answer 36

• Varies w virulence of serovar involved, host immunity, extent of renal lesions.- Guarded prognosis in azotemic cattle as >75% nephrons affected in such cases, therefore even if acute dz tx, may –> chronic interstitial nephritis and fibrosis.

Question 37

Outline strategies to prevent leptospirosis in cattle herds.

Answer 37

• Draining or fencing off standing water.- Maintaining a dry, clean environment.- Limiting rodent and wildlife contact with cattle and their feed and water.- For host-adapted strains, eliminate renal carrier state.- Vaccination (pentavalent vacc) is considered effective at preventing losses but may not consistently prevent renal colonisation w host adapted hardjobovis.- Recommended at a young age followed by annual boosters to prevent initial renal colonisation.

Question 38

Describe the aetiology of enzootic haematuria of ruminants.

Answer 38

• Chronic (1-3 mo) ingestion of bracken fern (Pteridium aquilinum).- Toxins in plant –> haemorrhagic cystitis –> chronic or intermittent haematuria.- Chronic ingestion + bladder infection w BPV-2 –> bladder neoplasm of epithelial, mesenchymal or mixed origin.- NB distinct from acute Bracken Fern toxicity –> acute coagulopathy or fulminant septicaemic crisis assoc w severe bone marrow suppression.

Question 39

Outline clinical signs of enzootic haematuria in ruminants.

Answer 39

• Group of animals grazing same pasture or cutting of hay.- First CSx is protracted, poss intermittent haematuria +/- blood clots in urine.- Chronic blood loss –> tachycardia, tachypnoea, exercise intol, pale MM, dec productivity and body condition.- May palpate bladder wall thickening per rectum.- +/- dysuria, pollakiuria, obstr of bladder trigone (tumour) or urethra (clot).

Question 40

Describe diagnostic test findings in cattle with enzootic haematuria.

Answer 40

• Ultrasound: bladder thickening, irregularly shaped bladder wall.- CBC: severe anaemia; may see low platelet, seg neut and lymphocyte counts.- Urinalysis: haematuria, proteinuria, +/- pyuria.

Question 41

Describe the pathophysiology of enzootic haematuria in ruminants.

Answer 41

• All parts of the plants are toxic to sheep and cattle.- Several compounds in bracken fern possess irritant, mutagenic, immunosuppressive or carcinogenic activities incl ptaquiloside, quercetin and alpha-ecdysone.- May cause recrudescence of latent BPV-2 through immunosuppression.- Mutagenic compounds interact w BPV-2 in bladder to induce local neoplasia.- Bladder carcinomas from cows w enzootic haematuria express COX-1 and COX-2 at a high level compared to normal controls.

Question 42

Describe the epidemiology of enzootic haematuria in ruminants.

Answer 42

• Described in America, UK, Aus, Europe.- Occurs most in US in Pacific Northwest and upper Midwest.- Plant grows best in well-drained, fertile coils and is often localised in open areas of forests; poisoning occurs in ruminants grazing pasture itself or hay w bracken fern.- Primarily adult sheep and cattle; haematuria seen in cattle 2-3yo, neoplasia 3-7y after grazing commences.- Up to 90% adult cattle affected in endemic areas.

Question 43

Describe the necropsy findings in ruminants with enzootic haematuria.

Answer 43

• Tissue pallor from anaemia.- Bladder wall thick and mucosa haemorrhagic and ulcerated.- Histo bladder wall: capillary engorgement, intramural haemorrhage, metaplasia of bladder epi, several type of bladder tumours.- Metastasis of epi neoplasms to regional LNs or other organs can occur.

Question 44

Describe the treatment and prevention of enzootic haematuria in ruminants.

Answer 44

• Tx limited to reduction or elim of bracken fern in diet.- Haematuria will cease if bracken feeding is discontinued before onset of tumour formation.- Early culling may help prevent low productivity from anaemia and neoplasia.

Question 45

Describe the clinical signs of ulcerative posthitis and vulvitis of small ruminants (‘Pizzle Rot’).

Answer 45

• Begins as a moist ulcer at/near mucocutaneous junction of the prepuce, covered by a scab, focal swelling, painful.- Spreads along mucosal surface inside the prepuce –> entire prepuce swollen, dysuria, vocalise during urination.- May progress to fibrous adhesions between penis and prepuce, restriction of urine egress due to swelling of glans penis or impairment of breeding soundness (blood/exudate in ejaculate, penis adhesions, scarring prepucial orifice, suppuratives urethritis.- Weight loss in chronic cases.- Ewes/does: ulcerative lesions on vulva and perineum, gross vulvar enlargement, dysuria.- Ddx: orf, ulcerative dermatosis (poxvirus), urolithiasis, caprine hervesvirus-1.

Question 46

Describe the pathophysiology of ulcerative posthitis and vulvitis in small ruminants.

Answer 46

• Corynebacterium renale: aerobic, gram-positive, pleomorphic, club-shaped bacteria; normal flora of skin and external genitalia.- Bacteria contains enzyme urease.- High-protein diet –> inc ammonia in rumen –> urea elim thru kidneys –> C. renale proliferate in alkaline urine and urease hydrolyses urea to ammonia –> chemical irritation and ulceration of prepuce and surrounding skin.

Question 47

Describe the epidemiology of ulcerative posthitis and vulvitis in small ruminants.

Answer 47

• Males > females.- Risk factors: inc/excessive dietary protein (>16%, as low as 12%) e.g. alfalfa hay or lush legume pastures.- Inc plane of nutrition in intact males prior to breeding.- Breeds w dense wool or hair e.g. Merino, Angora.- Organism persists in wool, hair and scabs for up to 6mo and can survive freezing in scabs/exudative material.- Can occur in single or multiple animals; venereal transmission reported.- Causes losses from debilitation caused by pain, incapacitation of breeding animals, loss of breeding soundness, deformation of external genitalia.

Question 48

Outline the treatment of ulcerative posthitis and vulvitis in small ruminants.

Answer 48

• Reduction of protein and non-protein nitrogen intake.- Isolate affected animals.- Clip hair around affected region and apply topical ABs.- Systemic ABs in severe cases e.g. penicillin, oxytet.- NSAIDs if required for pain/inflammation.- Sx of severe strictures to allow normal urine flow.

Question 49

Describe the prognosis associated with ulcerative posthitis and vulvitis in small ruminants.

Answer 49

• Response to tx optimal early in infection before deformation of prepuce or vulva as a result of fibrosis.- Changes for full recovery poor if dietary protein not restricted.- Complete recovery of breeding soundness unlikely if internal ulcerative posthitis.

Question 50

Describe the common signalment of ruminants with urolithiasis.

Answer 50

• Common metabolic dz in all livestock spp.- Castrated small ruminants at greatest risk.- Dx in single animal suggests whole herd is at risk due to important of diet/enviro factors in pathogenesis.- Can occur as epidemics or indv disorder.

Question 51

Describe the clinical presentation of acute urethral obstruction secondary to urolithiasis in ruminants.

Answer 51

• Impacted calculi –> urethral trauma and bladder distension –> stranguria and abdo pain.- CSx: restless, swish tail, grind teeth, stranguria, vocalise, tachycardia, tachypnoea, mild bloat sec to rumen stasis.- Stranguria may result in rectal prolapse.- Visible dilation or palpable pulse in urethra at midline of perineum proximal to obs may occur.- Anuria or urine dribbling.- May see blood or crystals on prepuce.- Distended bladder on abdo/rectal palpation.- Most common site of obstruction = sigmoid flexure in cattle and urethral process in sheep and goats.- NB always ultrasound kidneys as hydronephrosis –> poor Px.

Question 52

Describe the clinical presentation of chronic urethral obstruction secondary to urolithiasis in ruminants.

Answer 52

• Uncommon, but may occur if calculi cause partial obstruction of urethra and still allow for urine flow.- CSx: slow/intermittent urine flow during voiding, lethargy, dec appetite, thin BCS if renal failure has developed.- Rectal may reveal small bladder with thick wall.- DDx for urine dribbling: neuro dz, previous urethral trauma –> stricture formation, congenital anomalies of urogenital tract, infection, neoplasia, internal ulcerative posthitis.

Question 53

Describe the clinical presentation of urethral rupture secondary to urolithiasis in ruminants.

Answer 53

• Common complication of urethral obstruction.- Wall of urethra undergoes pressure necrosis –> leakage of urine into s/c tissue of perineum and ventral abdo.- Sequelae: cellulitis, penile adhesions, urethral fistula formation, urethral stricture, erection failure.- CSx: depression, inappetence, bilaterally symmetric pitting oedema in ventral perineum, inguinal region, prepuce and ventral abdo, may –> gangrenous necrosis.

Question 54

Describe the clinical presentation of urinary bladder rupture secondary to urolithiasis in ruminants.

Answer 54

• Prolonged bladder distension secondary to urethral obs –> pinpoint perforations, tears or necrosis of large areas of bladder wall.- Most common location for rupture is dorsum of the bladder fundus.- Rupture –> relief of stranguria.- CSx 1-2d post-rupture: abdo distension, depression, anorexia, weakness, dehydration, shock; breath may smell of ammonia; may ballot fluid wave in abdo; death.- U/s –> free fluid w collapsed or partially filled bladder.- Abdominocentesis: larve vol blood-tinged fluid.

Question 55

Describe the clinical presentation of ureterolithiasis and nephrolithiasis in ruminants.

Answer 55

• Acute ureteral obs may present w severe colic if obs is complete, or absent/milder colic.- Enlarged ureter/L kidney may be palpated rectally.- Rectal/transabdo u/s may aid dx.- May see evidence on u/s of pyelonephritis (necrotic debris/calculi may be released into ureter from infected renal pelvis) or ureteral or renal rupture.- If no signs of colic may be see non-specific signs of illness –> serum chem/urinalysis/ultrasound for definitive dx.

Question 56

Describe the procedure of examination of the urethral process for stones/sand-like grit in small ruminants.

Answer 56

• Sedation: diazepam or acepromazine +/- butorphanol; recomm to avoid xylazine as inc urine production.- Can admin epidural instead of/as adjunct to sedation; 1ml/15kg 2% lignocaine, no more than 15ml.- Prop sheep/goat on rump w spine perpendicular to floor.- Apply lidocaine jelly to prepuce, exteriorise penis by pushing sigmoid flexure cranially from base of scrotum and pull sheath caudally.- Inspect/palpate urethral process and amputate w scalpel blade if stones/grit palpated.

Question 57

Describe clinicopathologic findings in ruminants with acute and chronic urethral obstruction.

Answer 57

• CBC/chem may be WNL if acute.- May see hyperglycaemia and stress leukogram.- Dec water intake –> haemoconc and azotemia.- Chronic obst: hypoNa, hypoCl, hypoCa, hyperP, severe azotemia w isosthenuria.- Haematuria and proteinuria are consistent abnormalities; crystalluria is variable finding; +/- pyuria.

Question 58

Describe clinicopathologic findings in ruminants with bladder rupture.

Answer 58

• HypoNa, hypoCl, hyperP, uraemia, haemoconc.- K+ conc is variable, depending on appetite and time prior to dx; bladder rupture usually –> hyperK in animals but in ruminants K is usually low or normal due to anorexia, salivary potassium excretion and aldosterone release.- Peritoneal fluid:serum creat 2:1 or greater.- May see leukocytosis and hyperfibrinogenaemia secondary to peritoneal inflammation.

Question 59

Describe clinicopathologic findings in ruminants with ureterolithiasis and nephrolithiasis.

Answer 59

• Azotemia and secondary hydronephrosis most severe if condition is bilateral.- Chronic: hypoNa, hypoCl, hypoCa, hyperP, severe azotemia w isosthenuria.- Pyuria present w traumatic urethritis, cystitis or secondary bacterial infection.

Question 60

Describe the pathophysiology of urolithiasis in ruminants.

Answer 60

• Mucopolysaccharides, ions, organic acids in urine act as intrinsic inhibitors of crystallisation of calculogenic ions.- Calculus formation initiated if supersaturation of urine w crystalloids exceeds capabilites of these inhibitors –> crystalloids rendered insoluble and precipitate out of urine.- Dietary, enviro, management factors interact to determine degree of supersat of urine w calculogenic minerals.- pH: struvite (Mg amm phos), Ca phos, Ca carb less soluble in alkaline urine; Ca ox not affected by pH, silica debatable.- Rare cause and rare consequence of UTIs in ruminants.- Vit A defic may create nidus for calculi formation through desquamation of epi cells/altered cell surface charac.- Ad lib feeding may dec calculi formation, as 1-2 feedings/day –> ADH release after feed –> urine conc.- Water hardness may be sig, partic Mg content.

Question 61

Describe factors influencing development of phosphatic urinary calculi in ruminants.

Answer 61

• High phosphorus (grain-based) diet –> struvite (Mg amm phos) or apatite (Ca phos) calculi.- Ca:Phos outbreaks of urolithiasis.- Struvite dev primarily affected by Mg content in diet; Mg > 0.6% DM.- High dietary K+ alters DCAD –> inc risk uroliths.- Pelleted rations –> inc risk phosphatic uroliths; dec saliva prod w pellets –> dec GI phos loss –> inc renal excr.- Struvite uroliths: white or grey, smooth, radiopaque, easily broken; single stone or sand-like debris.

Question 62

Describe factors influencing development of silica urinary calculi in ruminants.

Answer 62

• Ruminants grazing native rangeland grasses of western North America; silica content higher in mature grass.- Periods of water deprivation –> water and Na resorption by kidneys –> highly conc urine –> silic acid conc and polymerises to polysilicic acid –> binds to urinary mucoproteins and becomes insoluble.- Incidence may be inc by dietary defic of Cu and Zn and high dietary Ca:PO4 content > 2.8:1 (opp to struvite!).- Silica uroliths are hard, smooth, white to brown, radiopaque, often layered; 20% mucoprotein, 75% silicon dioxide and variable amounts Ca ox and Ca carb.

Question 63

Describe factors influencing development of calcium-based urinary calculi in ruminants.

Answer 63

• Two main types: Ca oxalate and Ca carbonate.- Ca carb common in small ruminants grazing lush, rapidly growing clover pastures or fed alfalfa hay, high in Ca, low in PO4 and Mg, high oxalate content.- Oxalate binds GI Ca –> inc urinary Ca excretion; ruminal bacteria metabolises oxalate to bicarb –> alkaline urine; both factors –> inc Ca carbonate calculogenesis.- High oxalates, low Ca in diet and dec water intake –> inc risk of Ca oxalate uroliths.- Ca carb uroliths: round, smooth shape, golden colour.- Ca oxalate uroliths: dense, hard, white to yellow, smooth or jagged.

Question 64

Describe the epidemiology of urolithiasis in ruminants.

Answer 64

• Gender: obs urolithiasis almost exclusively dz of males; testosterone –> inc urethral diameter, therefore castration (esp prior to puberty) = risk factor. - Season: inc incidence in late Autumn and Winter: limited water avail, inc silica content, higher number of young, growing male animals; higher risk in arid months of year in warmer climates.- Age: tendency in younger ruminants, maybe due to management factors e.g. high grain rations.- Other: inherent indv diff in animals’ mineral metabolism or urinary tract health.- Breed: higher risk in African Pygmy goats; truley higher risk or management facts due to pet status?

Question 65

List surgical treatment options for management of urolithiasis in ruminants.

Answer 65

• Amputation of obstructed urethral process.- Perineal urethrostomy.- Prepubic urethrostomy.- Urethrotomy.- Cystotomy.- Tube cystotomy.- Bladder marsupialisation.

Question 66

Describe medical management options for treatment of urolithiasis in ruminants.

Answer 66

• Tranquillisers: antispodic effect on urethra and relaxation of retractor penis muscle –> relaxation of sigmoid flexure (NB low success of NSAIDs, IVF, tranquillisers alone).- Percutaneous drainage of bladder prior to Sx or as adjunct to medical therapy.- Percutaneous inj of Walpoles soln into the bladder –> dec urine pH to 4-5 to dissolve uroliths in bladder/urethra.- Pre-operative stabilisation of hypovol and correction of electrolyte abnorm e.g. hypertonic followed by 0.9% NaCl.- If hyperK can give IV dextrose, sodium bicarb or insulin to move K into cells.- Slow drainage of urine from abdo cavity to reduce pressure on diaphragm and slow progression of metabolic derangements. - Peri-operative ABs to prevent UTIs.

Question 67

Describe factors of management which can prevent or decrease the risk of urolithiasis in ruminants.

Answer 67

• Perform ration and urolith analysis to ID dietary factors.- Goal: dilution of urine to reduce urinary concentration of calculogenic mineral ions.- Dietary management of phosphotic calculi:– Ca:P 2:1 or greater; dec grain (high phos), inc Ca w alfalfa or other legumes.– 0 mEq DCAD diet w ammonium Cl –> urine pH 6-6.5.– Inc long-stemmed forage –> inc saliva –> inc P excr.- Dietary management of silica calculi:– Cannot change silica content or range grasses.– Can only add salt to inc water intake; up to 15% DM NaCl or 1% NH4Cl.– Dec Ca:P from 2:1 to 1:1 –> trend towards less calculi.- Dietary management of Ca carb uroliths:– Supplement hay w grass hay instead of alfalfa alone.– Salt grass hay to inc water intake.– NH4Cl to inc water intake and acidify urine.- Water management: clean feeders, in shade in Summer, warmed in Winter, multiple sites, check regularly.

Question 68

Can serum creatinine concentration at presentation be used to predict survival in horses with renal failure?

Answer 68

• Yes.- Non-survivors (mean = 9.4mg/dL) had higher creatinine concentrations than survivors (mean = 6.1mg/dL).Ref: J. Vet. Intern. Med. 2011; 25(6):1426–1430.

Question 69

Are serum calcium concentrations different in horses with acute renal failure and chronic renal failure?

Answer 69

• Mean serum calcium concentration was significantly higher in horses with CRF than ARF.- Cases of ARF were more likely to be normocalcaemic or hypocalcaemic, whereas CRF cases were more likely to be normocalcaemic or hypercalcaemic.Ref: J. Vet. Intern. Med. 2011; 25(6):1426–1430.

Question 70

What is the complication rate associated with renal biopsies in horses? What complications are seen?

Answer 70

• Study of 151 biopsies in horses 48h-30y old.- 11.3% had complications (9% minor, 2.3% major).- 0.7% mortality rate (fatal haemorrhage).- Haemorrhage (7/17).- Colic (6/17).- Macrohaematuria (4/17)- Microhaematuria (2/17).- Pyrexia (2/17).- Abortion (1/17 - no evidence linking directly to biopsy).- Death (1/17).Ref: J. Vet. Intern. Med. 2011; 25(3):532-539.

Question 71

List risk factors for complications when performing renal biopsies in horses.

Answer 71

• Biopsy of left kidney.- Diagnosis of neoplasia.- Low urine specific gravity.- NB No association with complications was found for age, sex, breed, institution, presenting complaint, other initial clinicopathologic data, biopsy instrument, needle size, or use of ultrasonographic guidance.Ref: J. Vet. Intern. Med. 2011; 25(3):532-539.

Question 72

What is the likelihood of obtaining a diagnostic sample following renal biopsy in horses? What is the agreement of diagnosis from biopsy with that at necropsy?

Answer 72

• Biopsy specimens yielded sufficient tissue for a histopathologic diagnosis in most cases (94%).- Dx had only fair (72%) agreement with PM findings.Ref: J. Vet. Intern. Med. 2011; 25(3):532-539.

Question 73

Is renal replacement therapy safe and efficacious in adult horses?

Answer 73

• Study performed with horses in stocks for 6h, connected via a commercial renal replacement machine with blood flow rate 250 mL/min; dialysate rate 3,000 mL/h; prefilter replacement pump 3,000 mL/h; and postfilter replacement pump rate 2,000 mL/h. Balanced electrolyte solution was used as dialysate and replacement fluid.- Renal replacement therapy was successfully performed in horses, resulting in a mean creatinine clearance of 0.127 mL/kg/min (68.9 mL/min) and urea reduction ratio of 24%. - No adverse effects were detected although a significant decrease in rectal temperature was observed (P .007). A significant increase in serum phosphorus (P .001) and decrease in BUN (P .04).Ref: J. Vet. Intern. Med. 2013; 27(2):308-316.

Question 74

Describe the risk factors for development of calcium carbonate urolithiasis in goats.

Answer 74

• The breed with the highest odds of developing calcium carbonate uroliths was Nigerian Dwarf.- Breeds with the lowest risk of developing calcium carbonate uroliths included mixed, Anglo-Nubian or Nubian, and Toggenburg. - Goats of African descent (Pygmy, Nigerian Dwarf, Boer) had significantly higher odds of developing calcium carbonate uroliths than did those of non-African descent.- Goats that were > 4 yo.- Males were approx 196 times as likely to develop calcium carbonate uroliths as were females.- Calcium carbonate uroliths were sig more likely to be collected in Autumn, Summer and Winter than in Spring.Ref: J Am Vet Med Assoc 2015;247(3):293–299.

Question 75

What are the conventional treatment principals of acute renal failure (ARF) therapy?

Answer 75

• Reversal of inciting or underlying cause.- Judicious administration of IV fluids.- Correction of electrolyte and acid-base abnormalities.Ref: JVIM 2013; 27: 308-316.

Question 76

When should renal replacement therapy (RRT) be instituted in cases of ARF?

Answer 76

• If ARF remains refractory to conventional treatment.- Renal indications: reduced GFR –> solute imbalance; oliguria –> ECF overload.- Non-renal indications: facilitating clearance of drugs, toxins, toxic metabolites or inflammatory cytokines.Ref: JVIM 2013; 27: 308-316.

Question 77

Describe the way in which continuous renal replacement therapy (CRRT) purifies the blood.

Answer 77

Blood is passed through thousands of semipermeable membranes and blood is purified via diffusion, convection (solvent drag) and adsorption (adhesion).Ref: JVIM 2013; 27: 308-316.

Question 78

List the advantages of CRRT over haemodialysis.

Answer 78

• Slow, continual process allows for better control of blood pressure, electrolyte and acid-base balance.- Convective process allows for more effective removal of larger molecules with limited diffusibility.- Ability to use pre-packaged sterile fluids vs pure dialysate.Ref: JVIM 2013; 27: 308-316.

Question 79

Describe the reported procedure for CRRT in the horse.

Answer 79

1. Sedation: initial bolus followed by CRI of detomidine.2. Anti-coagulation: initial bolus followed by CRI of heparin.3. Fluids: double lumen dialysis catheter in jugular vein; CRRT extracorporeal circuit with 1.5m2 filter was connected to the horse for 6h removing 250ml/min blood and dialysate rate set at 3000ml/h; dialysate and replacement fluid = Plasmalyte.4. Free choice access to feed and water throughout.Ref: JVIM 2013; 27: 308-316.

Question 80

Outline the reported side effects of CRRT in horses.

Answer 80

• Hypothermia: progressive decrease in rectal temperature over 6h; due to cool IV fluids and/or detomidine CRI.- Mild dec in HR/RR.- Occasional transient arrhythmias: proposed due to detomidine CRI not CRRT.- Thrombocytopaenia: due to heparin admin.- Haematoma formation at catheter sites: due to heparin admin.- Hyperphosphataemia: mechanism unknown.Ref: JVIM 2013; 27: 308-316.

Question 81

Compare the creatinine clearance rate achieved in CRRT with that achieved by peritoneal dialysis and that of the healthy horse.

Answer 81

• CRRT: 0.127mg/kg/min.- Peritoneal dialysis: 0.0322 mL/kg/min (intermittent) to 0.1054 mL/kg/min (continuous).- Normal horse: 1.7-2.7ml/kg/min.Ref: JVIM 2013; 27: 308-316.