Patterns Of Disease In Kidney Flashcards by Anastasia Shumitskiy

Possible portals/routes of entry into urinary tract

Haematogenous- blood

Ascending from lower urinary tract

Epidermal (from skin)

Direct injury

How well did you know this?

Not at all

Perfectly

Haematogenous entry
-features

Localise in large renal vessel, interstitial vessel, glomerular capillary
- can lead to Infarction
– Septic
– Immune-mediated disease
– Can affect glomerulus, tubule and/or interstitium

How well did you know this?

Not at all

Perfectly

Ascending from lower urinary tract

– Females mainly
– Secondary to gastrointestinal, genital, or epidermal contamination
– Targets tubules and interstitium primarily

How well did you know this?

Not at all

Perfectly

Direct injury
-features

Substances secreted into glomerular filtrate
-e.g Formation of crystals which damage cells
-affects tubules mainly

How well did you know this?

Not at all

Perfectly

Describe the Defence mechanisms of kidney

‒ Vasculature: Basement membrane

‒ Glomerulus:
Glomerular basement membrane (GBM; filtration barrier); glomerular
mesangium (phagocytic)

‒ Tubules:
Basement membrane (provides physical
barrier and scaffolding)

‒ Interstitium:
Innate humoral and cell-mediated immune system responses

How well did you know this?

Not at all

Perfectly

Patters of disease in kidney are recognised by…

Route of infection

How well did you know this?

Not at all

Perfectly

Name the main routes of infection

– (Developmental)
– Vascular
– Glomerular
– Tubules/Tubulointerstitial – Pelvis/Ascending
– Endstagekidney (everywhere)
– Anylocation

How well did you know this?

Not at all

Perfectly

Developmental infection

How well did you know this?

Not at all

Perfectly

What is fused kidneys

How well did you know this?

Not at all

Perfectly

What are polycystic kidneys

How well did you know this?

Not at all

Perfectly

Vascular lesions
-what is this
-what is it caused by

-Blood vessels are blocked
-An infarction (inadequate blood supply)

How well did you know this?

Not at all

Perfectly

3 types of progression of vascular lesions infarction

Acute—>
Subacute—>
Chronic—>

How well did you know this?

Not at all

Perfectly

Vascular lesions- what is haemorrhage

Any systemic vascular injury (e.g.: septicaemia, vasculitis, DIC)

How well did you know this?

Not at all

Perfectly

Glomerular lesions
-3 types

• Glomerulonephritis/glomerulonephropathy
• Glomerular amyloidosis
• Glomerulosclerosis

How well did you know this?

Not at all

Perfectly

Endpoint of glomerular disease:

Protein losing nephrotrophy

How well did you know this?

Not at all

Perfectly

What can glomerular disease lead to?

Hypoproteinaemia, decreased oncotic pressure, loss of ATIII (hypercoagulability)

Nephrotic syndrome: hypoproteinaemia, proteinuria, ascites, hypercholesterolaemia

Glomerulonephritis / Glomerulonephropathy

• most common cause for this; Immune-mediated disease
—Most common is immune complex (Ag-Ab) deposition
-May be due to animal having viral or bacterial infections – FeLV, FIP, pyometra, chronic parasitism (dirofilariasis)
-May be autoimmune;
Systemic lupus erythematosus (SLE)
Neoplasia

• Results in continual damage to GBM via podocyte effacement

Glomerulonephritis: Lesions
-grossly
-histological

usually normal
May see uniform, tan/red “dots” (limited to cortex)
-so not much

Immune deposits are red “dots” along capillary loops
-should see lesions more clearly

How would you do a diagnosis of lesions

renal biopsy HE, special stains, EM, immunofluorescence

Glomerular Amyloidosis
-grossly

Can see enlarged, pale or orange, waxy kidneys
Amyloid deposition which expands mesangium

What are amyloids

– Insoluble fibrillar protein deposited in
extracellular space
– Associated with source of chronic ongoing inflammation
-Most commonly found in glomerular

Occurs in Glomerular Amyloidosis

What glomerular disease is shown in this image

Put on anki*

Glomerulosclerosis

• End-stage glomerulus = obsolescent
– Obliteration of capillary loops with increased matrix and fibrous CT
– Nonspecific response to chronic glomerular injury

• Effects on tubules (via dec flow in efferent arterioles)

• Mild, multifocal, segmental GS is COMMON in aged animals

• can lead to End-stage kidney = severe, multifocal to diffuse

What is sclerosis

= hardening of tissue (usually due to fibrosis)

Protein-losing glomerular injury—>

Name the Tubulointerstitial Diseases

• Acute tubular necrosis – Nephrotoxic vs. ischemic Oxalate nephrosis

Acute Tubular Necrosis: -caused by…

Toxins; e.g antifreeze consumption, ethylene glycol metabolites Drugs Plants; oxalate Bacterial Metals; lead mercury Miscellaneous Vitamin D Haem/myoglobin

Oxalate nephrosis -grossly

Cortex much paler Haemorrhages

Tubulointerstitial lesions -grossly -result of…

Pitted, irregular surface due to interstitial fibrosis – Palefoci= result of inflammation (lymphoplasmacytic to mixed) and fibrosis

Leptospirosis lesions -grossly -Histological

pale radiating streaks in cortex and haemorrhagic foci in cortex and medulla Histology: interstitial inflammation and tubular degeneration

Tubulointerstitial: FIP

• Systemic disease with vasculitis (phlebitis) • Pyogranulomatous to • lymphoplasmacytic nephritis Track along vasculature in FIP • Lesions can look like lymphoma

Tubulointerstitial lesions -histologically

• Tubular dilation, attenuation of epithelium • Casts • Interstitial fibrosis • Interstitial inflammation

Renal pelvis -2 types

• Hydronephrosis • Pyelonephritis

Hydronephrosis -what is this -lateral or bilateral

dilation of renal pelvis – can cause Obstruction of outflow (calculi) of urine Likely to be bilateral (affect both kidneys) Clinical significance variable

Pyelonephritis -result of… -common diseases causing this

-As a result of ascending infection in domestic animals -Impaired vesico-ureteral reflux (2ndary obstruction, cystitis) -Common: E. coli Proteus Klebsiella Staph, Strep (all species) C. renale & T. pyogenes (cattle)

Neoplasia -main ones in kidney

• Epithelial: -Renal carcinoma – most common primary – Transitional cell carcinoma (from lower urinary tract) – Nephroblastoma • Mesenchymal • Round cell: Lymphoma

End stage kidney in uraemia -hallmark of chronicity is… -grossly -histologically

• Hallmark of chronicity is FIBROSIS • Gross: pale, shrunken, pitted, firm • Histology: increased connective tissue with ectatic/atrophied tubules and sclerotic glomeruli

Sequelae / Nonrenal lesions of renal failure -2 types

• Sequelae of acute renal failure – Death due to elevated serum potassium, metabolic acidosis, and/or pulmonary oedema – Recovery • Sequelae of chronic renal failure: – Mineralisation of tissues (usually chronic) Uremic acids -Lungs, gastric mucosa, intercostal pleura, renal tubules, left atrium and great vessels -Elevated Ca x P product – Uraemia = clinical manifestation of azotaemia – Uremic ulcers (glossitis, gastritis)

Uremic acids cause…

Injury to small vessels