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What is the embryologic development of the kidney?
What is the function of the pronephros?
microscopically recognizable, nonfunctional
What is the function of the mesonephros?
Limited excretion function, mesonephric duct matures to vas deferens and epididymis, Paramesonephric duct matures to uterine tube
What is the function of the metanephros?
Matures into functional kidney, interplay with metanephric diverticula determines lobulation and lobule fusion
What are the species variations of kidneys?
1. Simple, reniform: rodents, dog, cat, pig, sheep, goat, horse, camelid
2. Lobulated: bovine, marine mammals, avian, reptilian, ox
What kind of structures are kidneys?
Paired retroperitoneal structures- NOT strictly bilaterally symmetrical
What can happen with the placement of kidneys in the ruminant?
Left kidney can be displaced to the right of midline by the rumen
What is normal coloration for the kidney?
Mahogany, except for cats which are tan due to lipid retention in tubule epithelium
What animal is the capsule not easy to strip off?
How much of the body’s weight is the kidney?
What is the cortex:medulla ratio?
What is the cortex demarcated from the medulla from?
What is the medulla subdivided into?
Inner and outer zones
What animals have a medullary crest?
Dog, sheep, and horses- fused medullary papillae
What are included in the lower urinary tract?
Ureters, bladder and urethra
What is the functional unit of the kidney?
How many nephrons do cats have?
How many neprhons do dogs have?
How many nephrons does an ox have?
What are the basic units of a kidney?
2. tubular component (bowmans capsule, PCT, loop of henle, DCT, CD and renal pelvis)
3. golmerular component (barely visible to the naked eye)4. interstitial component
Vessel branching in the kidney:
Reanal artery -> lobar artery -> arcuate artery -> intralobular arteries -> afferent arteriole -> glomerular capillaries -> efferent arterioles -> vasa recta -> veins
What is the only blood supply of the medulla?
What are the medullary rays?
Bundles of collecting duct
What makes up 65% of the cortical volume?
The glomerulus is aka:
What does the glomerular tuft consist of?
6-8 segments of anastomosing capillaries
What type of capillary endothelium are in the glomerulus?
Where does the filtrate enter the urinary space?
What is the structure of the glomerulus?
mesangial matrix is a mixture of:
collagen I & IV, glycoproteins, et.al.
Is the mesangium a static structure?
NO!!! dynamic state of turnover and renewal
What is the structure of the glomerular basement membrane?
precise thickness and anionic charge essential for normal function
What does the filtration barrier exclude?
filtration barrier excludes molecules >70 kilodaltons *albumen is about 70kDa so it is not filtered and stays in body
What is the function of the macula densa?
Monitor solute function- ***only 1 macula densa/nephron and vice versa
How much of the CO does the kidney receive?
How is the renal function vital to homeostasis?
What are the intrinsic hormones of the kidney?
2. Vitamin D3
What is the function of EPO?
Induces RBC stem cell proliferation
What is the function of vitamin D3?
Ca absorption from intestine
What is the kidney’s role in vitamin D3?
Adds second OH group
What is the function of rennin?
Converts angiotensinogen to angiotensin 1 (1 -> 2 2 is made in the lung)
*counteracts renal hypopersufion, inc bp
What are hormones that have direct effects on the kidney?
1. Vasopressin (ADH)
2. Parathyroid hormone (PTH)
4. Atrial natriuretic hormone
Where is vasopressin produced?
What is the function of vasopressin?
Increases water reuptake
Where is PTH produced?
Parathyroid C cells
What is the function of PTH?
Increases renal Ca absorption and inhibits renal phosphorous Reuptake
Where is aldosterone produced?
What is the function of adolsterone?
Increases sodium reuptake and increases potassium excretion
Where is ANP produced?
What is the function of ANP?
Dilates afferent arteriole and inhibits renal NaCl REuptake
What factors of fluid dynamics is the kidney involved in?
Blood flow to glomerulus and filtration
What affects the blood flow to the glomerulus?
Vascular tone of arterioles
What factors are important for filtration?
2. Oncotic Pressure
3. Fenestrations and podocyte slits4. BM- thicker = leakier
What are the PCT and DCT responsible for?
Secretion and reabsorption of solutes
What is responsible for electrolyte redistribution?
Ascending and Descending tubules, LOH, and medullary interstitium ion gradient
How much water is recovered in the kidney?
Does the kidney have reserve capacity?
Can a disconnected nephron be fixed?
No it is lost forever- healing by fibrosis results in disconnected nephrons
How much kidney can be lost before clinical recognition?
How much destruction results in renal failure?
Greater than 75%
What happens to surviving glomeruli?
What can happen IF the basement membrane is intact?
Tubule epithelium regeneration (NOT if BM is destroyed)
If the BM is “disrupted” then the neprhon is:
Severed- inflammation and fibrosis (scarring)
What are causes of developmental abnormalities?
Genetic, teratogenic or congenital
What are developmental abnormalities in the kidney?
1. Agenesis and hypoplasia
2. Fusion defects
4. Polycystic kidney disease (PKD)5. Renal dysplasia
Are agenesis and hypoplasia ommon?
RARE, can be unilateral or bilateral
Fusion defects are also known as:
Are cysts common?
Yes (cattle and pigs), clinically insignificant- tend to form in cortex, probably from disconnected tubules
What is PKD?
Innumerable, uniformly sized cysts that enlarge resulting in renal failure
What animals are predisposed to PKD?
Persian cats, carin terriers, collies and mice
What is suspected to be defective in PKD?
What are clinical signs of renal dysplasia?
Distorted shape, retention of fetal glomeruli and fetal mesenchyme, fibrous wedges, cysts, indistinction of corticomedullary junction
What is renal dysplasia due to?
Gross and microscopic evidence of disorderly growth- inherited, teratogens, unknown (idiopathic)- generally idiopathic, but known to be genetic in certain breeds of dogs, in utero viral infections can cause dysplasia (e.g., panleukopenia, BVD)
What does renal dysplasia result in?
3. Papillary necrosis4. DIC
What is an example of trauma to the vascular supply of the kidney?
Avulsion (to tear away) –(e.g., the inertial effects of hit-by-car)- rapidly fatal if renal vein or renal artery is torn, contusions, lacerations
What do less severe injury results in?
a spectrum from microscopic hematuria to hematoma.
Are renal infarcts common?
What leads to renal infarcts?
Embolic events (left hearted endocarditis), sepsis, endotoxemia, or in situ
Acute infarcts can be:
Hemorrhagic or anemic
What does the size of infarcts depend on?
Number of blood vessels and location of occlusion
Resolving infarcts have :
depressed surfaces, pallor, and peripheral vascular hyperemia
1. Dead parenchyma is removed leaving surface distortions/depressions= sunken tan
focus and distortion of reniform shape
2. Fibroplasia occurs
3. Scar retraction
4. Variable inflammatory cell residue
occlusion of arcuate artery produces:
the classic wedge-shaped infarct- apex of wedge focused on papilla, base of wedge on cortical surface
What vascular problems are cats prone to?
idiopathic polar infarcts
occlusion of intralobular arteries results in:
necrosis limited to cortex
What are medullary infarcts also called?
Papillary necrosis (akak renal crest necrosis)
Papillary necrosis is due to:
Hypoperfusion of vasa recta
What can lead to Hypoperfusion of vasa recta? *know this mechanism
1. Hypovolemia- dehydration or blood loss
2. Use of NDAIDs
3. Combination of hypovolemia and NSAIDs
**What is the mechanism of medullary infarcts?
->can be induced and exacerbated by hypovolemia or hypotension, water deprivation, blood loss, prolonged anesthesia, etc.
What are other causes of papillary necrosis:
Urine outflow obstruction, amyloid deposition in medulla, renal vein thrombosis, infectious pyelitis
papillary necrosis in humans is due to:
analgesics, especially acetaminophen- acetaminophen has a direct cumulative toxic effect on Henle’s loop
Medullary necrosis is commonly found in:
horses on high dose phenylbutazone
Does papillary necrosis lead to renal failure?
Usually not- not all nephrons have loops that go down to the medulla, so there is still plenty of renal reserve (cats are an exception)
Papillary necrosis is grossly visible as:
black, green, yellow, or orange foci in the deep medulla with necrotic tissue sloughs, leaving a visible defect
DIC is most commonly initiated by:
endotoxin from Gram negative bacteria- capillary endothelim injured, platelets consumed and thrombus formation and fibrinolysis, capillaries become leaky (also initiated by sepsis and malignant neoplasms)
DIC is grossly visible as:
Petechiation- usually seen elsewhere in the body
What are expecially vulnerable to DIC?
Prolonged postmortem interval will result in:
Fibrinolyssi of fibrin thrombin in the microvasulature
What are 3 vasculotropic infectious diseases?
1. Feline infectious Peritonisit(FIP) (coronavirus infection)
2. Malignant catarrhal fever (MCF)
3. Canine herpesvirus
Feline Infectious Peritonitis (FIP) causes:
granulomatous vasculitis in kidneys is a key diagnostic feature
Malignant Catarrhal Fever (MCF) causes:
necrotizing arteritis in kidneys is a key diagnostic feature
Polyarteritis Nodosa (PAN) causes:
Intermittent segmental inflammation of vessel walls
Hypertension results in:
What is an important principle in renal pathology?
The whole is greater than the sum of the parts
The whole is greater than the sum of the parts
What are the distribution patterns of glomerular disease?
Generalized (all glomeruli are altered) vs focal (scattered glomeruli are altered) and global (entire glomerulus tuft affected) vs segmented (a portion of the glomerulear tuft is affected)
The following are glomerular changes:
What is sclerotic/obsolete/global fibrosis?
Fibrotic or scarred (no longer working)
What is hyalinosis?
extracellular pink material (H&E stain), not necessarily collagen
What is synechia?
fibrous fusion of a segment to the Bowman’s capsule
What are types of proliferation?
1. membranous = thickened capillary walls due to thickened BM and extra matrix
2. proliferative = increased cellularity due to mesangial cells & leukocytes
3. membranoproliferative = features of both are present; a.k.a. mesangiocapillary- most common
What is atrophy?
withered or shrunken glomerular tuft
What is crescent?
proliferation of parietal (Bowman’s capsule) epithelial cells
What is lipoid cells?
accumulation of lipid-containing cells within the urinary space
What is periglomerular sclerosis?
fibrosis surrounding Bowman’s capsule
What is cystic distention?
expansion of the Bowman’s capsule, usually with tuft atrophy
What is acute episodes of glomerulitis also known as?
What do acute episodes of glomerulitis look like grossly?
may not be grossly conspicuous
What would acute glomerulitis look like grossly when it is visible?
Kidneys can be enlarged, tan-brown and soft. A section of cortex may reveal pinpoint red foci (hemorrhage into the urinary space) or white foci (microabscesses centered on the glomerulus).
What is required to diagnose glomerularnepthritis?
Microscopic confirmation is required for diagnosis- blood spilling, blood, neutrophils
What would we see grossly with chronic glomerular disease?
No marked changes unless it is in conjunction with the wider-ranging disease ->chronic glomerularnephhritis (end stage kidney disease)- see pallor- diminished blood flow through glomerulus
What are the 5 mechanisms (causes) of glomerular disease?
1. Precipitation of Ag-Ab complexes (immune mediated)
2. Autoimmune reaction against glomerulus
3. Genetically programmed dysfunction
4. Direct injury
5. Deposition of abnormal matrix
What is immune mediated glomerular disease due to?
precipitation of large antibody-antigen complexes through capillary due to antibody excess created by active infections, antiserums, vaccines
What are consequences of immune mediated golmerular disease?
1. thickens BM (membranous glomerulonephritis)
2. produces electron dense deposits ultrastructurally
3. granular pattern of immunoflourescence
4. initiates complement cascade, chemotaxins for leukocytes
Is this common?
rare in animals—results in discrete linear immunoflourescence along BM
What is the Hyperfiltration hypothesis?
How can genetics lead to glomerular disease?
numerous lab animal models have been identified or created
What are examples of Direct injury that lead to glomerular disease?
The nephrotic syndrome is the result of:
severe glomerular disease
What can cause tubulointerstitial disease? (pathologic mechanisms)
What delivers the causative agent to the kidneys?
Hametogeneously delivered bacterial and viruses- pathology is NOT focused on the glomeruli
What is seen with acute infectious tubulointerstitial disease?
Neutrophils, abscesses and necrosis
What is seen with chronic infectious tubulointerstitial disease?
Interstitial fibrosis (too many nephrons disconnected) and infiltrates of lymphocytes and plasma cells
What is this disease called in cattle?
white spot disease in cattle
What causes ATN due to Ischemia?
What can ARN due to ischemia result in?
ischemic necrosis leads to BM dissolution, precluding regeneration
What happens with ANT due to toxicity?
N.B. tubule regeneration is possible because BM remains unaltered
What does ATN look like grossly?
kidneys are grossly swollen, soft, lighter than normal coloration and the cut surface of a hemisectioned kidney bulges
What are 3 Microscopic features of ATN?
What are Regenerative changes seen with recovery from ATN?
What is acute tubular nephrosis also called?
Nephrosis (he hates this term)
What are the clinical signs of ATN (hallmark of ATN)?
What are tubular changes/abnormalities?
1. Brown pigment atrophy
4. Lipofuscinosis (xanthosis)- wear and tear pigment
5. Hyaline droplets
Lipidosis is indicative of:
severe hyperlipemia, and not really benign- (the patient will also have severe hepatic lipidosis), normal for cats
Hemosiderosis is indicative of:
hemoglobin reabsorption or RBC uptake - kidney is grossly rusty brown when severe
With Cholemic “nephrosis” the rest of the animal is:
obviously icteric, probably has a benign effect on tubule
Hyaline droplets are:
eosinophilic cytoplasmic droplets consisting of protein
Hyaline droplets are indicative of:
glomerular leakage of proteins (normal feature of male rat kidneys [a2microglobulin])
What can cause nephrotoxicity?
Diverse group of chemicals, mechanisms of toxic action vary-Many commonly used pharmaceuticals are nephrotoxic
2. heavy metals
3. Hb and myoglobin
4. ethyl glycol
6. vitamin D3
What antibiotics can cause nephrotoxicity?
What heavy metals can cause nephrotoxicity?
What is the mechanism for heavy metal nephrotoxicity?
Energy enzyme disruption
How does copper toxicity cause nephrotoxicity in sheep?
1. Chronic Copper accumulation in liver
2. Eventual overload results in hepatocellular necrosis
3. Excessive copper release
4. Hemolytic crisis
Hemoglobinuria is due to:
heme pigments are liberated from RBCs during hemolytic crisis
What is the mechanism for Hemoglobin nephrotixicity?
exact toxic mechanism is unknown
What is tubulotoxicity exacerbated by:
ischemia and hypoperfusion
causes of hemolysis include:
copper toxicity (sheep) and red maple leaf (horse)
Myoglobinuria is due to:
myoglobin is liberated from injured muscle- caused by exertional rhabdomyolysis or crushing injuries
What is the mechanism of myoglobin nephrotoxicity?
mechanism is probably identical to hemoglobin
What plants/fungi can cause nephrotoxicity?
What causes hypervitaminosis (vit D3)?
consumption of rodenticides and several plants, overzealous use of vitamin supplements
With hypervitaminosis, hypercalcemia indicates:
a grave prognosis, mineralization of basement membranes and tubule necrosis
What is the mechanism of EG nephrotoxicity?
1. alcohol dehydrogenase in liver converts EG to glycoaldehydes
2. this metabolizes glycoaldehydes to glycolic acids and oxalic acids3. These cause metabolic acidosis (potentially lethal) 4. calcium salt formed; hypocalcemia possible
5. calcium oxalate precipitates in tubules and blood vessels6. IF the animal survivesàacidosis, ATN and ARF follow
7. oxalate crystals and cellular casts obstruct nephrons
Are low level calcium oxalate dihydrate crystalluria normal for dogs?
What do we see grossly/cinically at low levels of toxicity?
There are no clinical signs of renal injury.
What do we see microscopically with low levels of toxicity?
evidence of necrosis, cast formation, as well as tubule epithelium regeneration, and/or hyperplasia will be present. Convoluted tubules are most vulnerable
What are the effects of nephrotoxicity exacerbated by?
Ischemia, hypoperfuison or obstructive casts
What are the mechanisms of neprhotoxicity?
What is pyelonephritis?
This is a special category of tubulointerstitial nephritis- Pyelonephritis is a rapidly progressing infection and a life-threatening medical emergency
What is infection in pyleonephritis due to?
due to ascending bacteria- usually occurs as a result of cystitis and catheterization
What is vulnerable to pyelonephritis?
What is usually present with pyelonephritis?
Cystitis (“Pyelo-“ means plevis, “pyo-“ means pus.)
1. pelvic exudates and necrosis
2. radiating streaks of inflammation from pelvis to cortex
3. streaks of hemorrhage and suppuration (neutrophils)
4. cortical abscesses elevate capsule (capsulitis)
What are microscopic features of acute pyelonephritis?
1. neutrophils and hemorrhage
2. bacteria visible in early stages
3. inflammatory changes fill tubule lumens and interstitium with exudate
1. loss of pelvic parenchyma
3. macrophages, lymphocytes, plasma cells
4. fibroplasia and fibrosis
5. coarse pattern of postnecrotic scarring that look similar to chronic infarcts
Why is the renal pelvis vulnerable to infection?
1. papilla has limited blood supply
2. hypertonic interstitium of inner medulla inhibits neutrophil function
3. ammonia (produced by bacteria) inhibits complement activation
Etiologic agents common to many animal species have:
What are etiologic agents of pyelonephritis?
E. coli, Staph., Enterococcus, Strep., Klebsiella, Proteus, Corynebacterium renale and Actinobaculum suis are specific for cattle and pigs
What is hydronephrosis?
A cavitating condition of the renal pelvis
What is hydronephrosis due to?
What is Amyloidosis?
a systemic condition in which the kidney can be severely affected. Except for certain breeds in which it is common, it is rarely an antemortem diagnosis. The physical presence of bulk volumes of amyloid leads to organ dysfunction
Where is the amyloid deposited and what does it lead to?
There are numerous parasites that require the urinary tract for perpetuation: (never asks these)
1. Stephanurus dentatus of pigs (severe damage to kidney and liver)
2. Dioctophyma renale of mustelids; dogs, humans (destroys entire kidney)
3. Klossiella spp of horses, guinea pigs, mice (innocuous)
4. Encephalitozoan cuniculi of rabbits and dogs (innocuous)
5. Toxacara canis of dogs (pinpoint scars)
6. Capillaria plica of dogs (egg-laying adults mature in bladder)
What are primary renal neoplasms?
most commonly reported in the dog and ox
Where is a renal carcinoma?
-neoplastic tubule epithelium
-papillary, tubular, and/or acinar patterns
-metastases go to lungs
bulbous, encapsulated, firm mass; grossly similar to lymphosarcoma
What is a nephroblastoma composed of?
complex mixture of connective tissue and primitive nephrons
neoplastic transformation of the pelvic urothelium- more commonly occurs in the lower urinary tract
What are neoplasms that commonly metastasize to the kidneys?
What do lymphsarcomas look like?
infiltrative and/or expansile tan masses
What is the most common cause for acute renal failure?
What are the clinical signs of ARF?
Anuria and oliguria due to afferent arteriole constriction, and/or occlusive casts in tubules, patients are depressed and weakened due to altered metabolism
What blood chemistry show with Azotemia?
1. SUN (BUN) > 40mg/dl (ruminants make urea as a normal rumen product)
2. creatinine > 2.0mg/dl; less subject to the effects of diet
1. prerenal due to hypoperfusion- decreased blood flow shock, heart disease, blood loss, anesthesia, etc.
2. intrarenal (intrinsic) (renal)- necrosis or cast formation- massive infarcts, nephrotoxicosis
3. postrenal due to obstruction to urine outflow
How does chronic renal failure begin?
1. polydipsia and polyuria
2. isosthenuria (inability to concentrate urine; sp.g. = 1.008 - 1.012)
3. azotemia and hyperphosphatemia
4. nephrotic syndrome
5. uremia (systemic effects of CRF)
1. wrinkled or granular surface texture
2. slightly shrunken and firm
3. pallor and firmess due to generalized fibrosis
4. minute cysts in cortical parenchyma
5. reduction in cortical mass
1. atrophic and ectatic tubules
2. regenerating tubule epithelium
3. cystic Bowman’s capsules
4. sclerotic glomeruli
5. fibrosis, periglomerular and intertubular
6. casts of various composition
7. lymphocyte and plasmacyte inflammatory cell infiltrate
8. tubule mineralization
At this stage of degeneration, all segments of the nephron are affected to varying degrees. Most examples of veterinary CRF are believed to be the result of TIN, but by the time a pathologist examines a ‘worn out’ kidney, it can......
What is azoremia?
Clinicopathologic syndrome due to prolonged azotemia- multisystemic effects
What does end stage kidney disease lead to?
2. Nephritic syndrome
What is Uremia the name for?
the extra-renal effects of renal failure.
All uremic patients are azotemic, but…
not all azotemic patients are uremic.
What are symptoms of uremia?
Uremic patients are depressed, nauseated, and uncomfortable and demonstrate one or more extrarenal manifestations of uremia.
What are some extrarenal lesions? **Know these gross pathologies
phosphate binding of Ca++ leads to parathormone (PTH) increase
elevated PTH stimulates osteocyte release of Ca++
PTH promotes tubule excretion of phosphorus (ineffectively in CRF)
What are microscopic changes?
Scar tissue, atrophic tubules, scarred glomeruli, expanded bowmans capsule, inflammatory infiltrates, casts
Have we identified a uremic toxin?
Despite years of dialysis fluid analysis, no single uremic toxin has ever been identified
What is essential for good prognosis of renal transplant?
Careful selection of recipient and donor is essential for good prognosis.
What does the donor provide?
Donor provides left kidney and entire ureter. Recipient keeps all three kidneys.
Acute postoperative complications:
Hypertension, hypoperfusion, hydronephrosis.
What medication is required for a renal transplant?
Cyclosporin is required (and immunosuppression is a complication).
What are some possible Postoperative complications?
1. Acute/chronic rejection
2. Retroperitoneal fibrosis and hyronephrosis
3. Lymphosarcoma (~%10)
What does an end stage kidney look like grossly?
2. Firm and pallor due to fibrosis
4. Reduced cortical thickness
5. Adhesion of cortex to capsule
What is the function of the ureter?
propel urine to the bladder
mucus glands in the horse
slit-like orifices are sometimes difficult to identify
What is the function of the bladder?
1. resists leakage and absorption of urine
2. highly stretchable--uroplakins in umbrella cells increase surface area
urachus is fetal tube connecting bladder to the umbilical cord, fetal urine empties into the allantoic cavity, urachus normally closes with umbilical cord separation
What is the urethral crest?
the zone between bladder and the beginning of the urethra
What are lower urinary tract anomalies?
1. Ectopic ureters
2. Persistent urachus
3. Uracal remnant
insertion at sites other than trigone, e.g., urethral crest, vagina, rectum, etc. urine dribbling and predisposition to ascending infections, relatively common
urine dribbling at umbilicus, easy route for an ascending infection relatively common in puppies and foals
What is the urachal remnant?
nipplelike to saccular outpouch at tip of the bladder, results in incomplete emptying of the bladder urine, nidus for infection and/or urolith formation, common
What are possible traumas to the bladder?
What is Ureteritis?
an extension of cystitis and pyelonephritis.
What is the defense mechanism for bacterial cystitis?
urine flow and mucosal IgA normally inhibits bacteria- leukocytes cannot function in urine
antineoplastic drugs (cyclophosphamide); cantharidin (from “blister beetles” in hay); bracken fern toxins
What is idiopathic cystitis?
hyperemia, edema, mast cells; no significant leukocyte infiltrate
What are features of cystitis?
1. neutrophils (pyuria)
3. sloughed dysplastic epithelium
5. aggregates of crystals
What are neoplasms of the bladder?
1. Transitional cell carcinoma *most common- often advance before recognition
2. Squamous cell carcinoma
4. Papilloma (benign)
plaques with infiltration of the bladder wall
Whpredilection for the trigone region
about half of all cases metastasize before being diagnosed
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