Pathology of the urinary tract Flashcards
(112 cards)
1
Q
Erythropoietin - funtion
A
Produced in response to ↓ oxygen tension → stimulate maturation of erythrocytes in the bone marrow.
2
Q
Calcitriol (activated vitamin D) - function
A
Facilitates Ca absorption in the small intestine.
3
Q
pre-renal failure - causes
A
Secondary to circulatory collapse (shock, hypovolaemia) or local obstruction of vascular supply (thrombus or lodgement of embolus)
4
Q
renal failure - causes
A
Tubular necrosis - infectious agents, toxins and toxic metabolites, nephrotoxic drugs and chemicals.
Embolic disease or ascending pyelonephritis
5
Q
post-renal failure - causes
A
Ascending infection, urolithiasis or neoplasms
6
Q
acute renal failure
A
Occurs when >75% of renal functional capacity is abruptly impaired.
Failure to excrete waste products and to maintain fluid and electrolyte homeostasis
7
Q
acute renal failure effects
A
Abrupt decr in serum concentrations of urea + creatinine (azotaemia)
nitrogenous waste products of protein catabolism - indices of diminished renal function.
Retention of K+ - cardiac dysrrhythmia (& arrest).
Retention of phosphates - binds ionised calcium (hypocalcaemia) - muscular tremors & coma.
Disturbances of electrolytes and ↓ pH - metabolic acidosis.
Hypertension.
Oliguria/anuria
8
Q
chronic renal failure
A
insufficient glomerular filtration - progressive
retention of nitrogenous metabolites
failure of tubular function
9
Q
chronic renal failure - effects
A
progressive salt and water retention, metabolic acidosis, other electrolyte imbalances (esp hyperkalaemia)
decr phosphates - secretion - hyperphosphataemia & Ca2+ precipitation, decr active Vit D3 (calcitriol)
hypertension
10
Q
Chronic renal disease - clinical signs
A
Polyuria, isosthenuria, polydipsia, etc
Halitosis, dribbling, lank coat, loss of weight
older cats & dogs
11
Q
CRF - histological appearance
A
incr of interstitial connective tissue.
Renal tubules absent, atrophic or compressed.
Hyperplastic + hypertrophic tubules.
Intraluminal protein.
Thickened hyalinised basement membranes.
Calcification of vessels and basement membranes.
Multiple acquired cysts.
Glomerulosclerosis.
Foci of interstitial lymphocytes and plasma cells
12
Q
end stage renal failure - kidney appearance
A
replacement of renal parenchyma with mature fibrous tissue
Kidneys are firm and distorted.
Distortion due to contraction of mature fibrous tissue (scarring)
13
Q
uraemia - define
A
urea in the blood
14
Q
4 stages of developing uraemia
A
- decr renal reserve, GFR 50% asymptomatic
- Renal insufficiency, GFR is 20-50% azotaemia + polyuria
- Renal failure, GFR 20-25% , kidneys can not maintain
homeostasis, uraemia (GI, cv, respiratory and skeletal
complications). - End-stage renal disease, GFR <5% terminal uremia.
15
Q
Systemic Effects of Uraemia
A
retention of nitrogenous metabolites.
NaCl and water retention, metabolic acidosis, other electrolyte imbalances (esp hyperkalaemia).
Plasma protein loss (oedema).
Hyperphosphataemia and secondary renal hyperparathyroidism.
↓ Production of erythropoietin → ↓ stimulation of erythropoietic maturation → non-regenerative anaemia.
Hypertension.
16
Q
Secondary Renal Hyperparathyroidism due to uraemia - chain of events
A
GFR <25% phosphate is no longer adequately secreted by the kidneys.
Hyperphosphataemia precipitates ionised calcium conc in serum.
decr calcitriol - decr intestinal absorption of calcium.
decr ionised serum Ca stimulates PTH secretion - Ca
release via osteoclastic bone resorption.
try to incr renal excretion of phosphate + reabsorption of Ca.
Parathyroid chief cell hyperplasia - renal secondary
hyperparathyroidism.
17
Q
Secondary Renal Hyperparathyroidism - effects - kidneys
A
Fibrous osteodystrophy and mineralisation of soft tissues.
Renal disease made worse by nephrocalcinosis - calcification of tubular BMs, Bowman’s capsules and necrotic tubular epithelium
18
Q
Secondary Renal Hyperparathyroidism - effects - non-renal
A
Endothelial degeneration and necrosis - vasculitis with
secondary thrombosis and infarction
mineralisation
ulcers
19
Q
examples of non-renal lesions due to Secondary Renal Hyperparathyroidism
A
Caustic injury to epithelium of the oral cavity and stomach (ulceration) Ulcerative glossitis and stomatitis Ulcerative and haemorrhagic colitis Ulcerative and haemorrhagic gastritis Uraemic encephalopathy Uraemic pneumonitis + Pulmonary calcification Intercostal mineralisation Fibrinous pericarditis Arteritis
20
Q
portals of entry to the kidney
A
haematogenous
glomerular infiltrate
ascending from the ureter
direct penetration
21
Q
main Diseases of the Glomeruli
A
Immune mediated glomeruolonephritis.
Glomerular Amyloidosis
Acute suppurative glomerulitis
Glomerulosclerosis
22
Q
Causes of glomerular damage
A
Damage tofiltration barrier - deposition of immune complexes. thromboemboli and bacterial emboli. Direct viral or bacterial infection Damage to other parts of the nephron. Reduced blood flow. Chronic loss of tubular function. Amyloid deposition.
23
Q
Functions of the glomerulus affected
A
Plasma ultrafiltration. Blood pressure regulation. Peritubular blood flow regulation. Tubular metabolism regulation. Circulating macromolecule removal
24
Q
Protein losing nephropathy
A
albumin leaks into filtrate - too much protein to be absorbed in PCT
high protein filtrate in dilated tubular lumina - proteinuria and hypoproteinaemia
renal protein loss - decr plasma colloid osmotic pressure + loss of antithrombin III - nephrotic syndrome
25
nephrotic syndrome
generalised oedema, ascites, pleural effusion, hypercoagulability and hypercholesterolaemia
26
Responses of glomeruli to injury
```
Necrosis.
Proliferation of cells and membranes.
Infiltration of leukocytes.
decr vascular perfusion.
Incr vascular permeability
```
27
response of glomeruli to continued/severe injury
atrophy and fibrosis of the glomerular tuft (sclerosis) and secondarily atrophy of renal tubules
28
Immune mediated glomerulonephritis - how it happens
Circulating immune complexes in subepithelial,
subendothelial or mesangial locations.
antibodies against entrapped nonspecific antigens or
antigens within the GBM.
release of proteineases and oxygen derived free
radicals - damage the basement membrane.
Activation of both glomerular epithelial cells and mesangial cells to produce damaging mediators such as oxidants and proteases
29
Immune mediated glomerulonephritis - causative diseases
persistent infections
Specific viral infections → FeLV and FIP.
Chronic bacterial infection → pyometra or pyoderma.
Chronic parasitism.
Autoimmune diseases such as SLE.
Neoplasia
Transient infection
Continual exposure of glomeruli to soluble IC
30
Immune mediated glomerulonephritis - diagnosis
IF or IHC of immunoglobulin + complement components in the glomerular tufts.
specific causative antigen often hard to identify
electron dense deposits in mesangial, subepithelial
or subendothelial locations by EM
31
Immune mediated glomerulonephritis - gross appearance on kidneys
Glomeruli visible as pinpoint red/pale dots on the cut surface of the cortex.
Fine granularity to the cortical surface.
Capsule may be adherent.
32
Immune mediated glomerulonephritis - histopathology
↑ cellularity + proliferation of glomerular cells.
Dilated renal tubules filled with homogenous proteinaceous fluid.
Interstitial and periglomerular fibrosis.
Foci of interstitial lymphocytes & plasma cells.
Glomerulosclerosis.
33
Glomerular Amyloidosis
associated with chronic inflammatory disorders, systemic infectious disease or neoplasia.
deposits - fragments of a serum acute phase reactant protein.
Glomeruli are the most common renal sites for deposition
of amyloid.
Idiopathic.
34
Glomerular Amyloidosis - consequences
PLN and the nephrotic syndrome
decr RBF through the glomeruli and the vasa recta
tubular atrophy, degeneration and fibrosis. In severe cases
renal papillary necrosis.
Medullary amyloidosis is usually asymptomatic unless papillary necrosis.
35
Glomerular Amyloidosis - gross appearance on kidneys
Enlarged, pale, smooth to finely granular capsular surface
Amyloid laden glomeruli may be visible as fine glistening dots on the cut surface of the cortex.
Brown staining of glomeruli after treatment with iodine.
Medullary amyloidosis not grossly visible
36
Glomerular Amyloidosis - histopathology
Glomerular amyloid in mesangium and subendothelium.
Acellular eosinophilic homogenous to fibrillar material.
tubules - dilated and contain proteinaceous and cellular casts
stains with Congo red - amyloid deposits have
apple green birefringence under polarised light
37
Acute suppurative glomerulitis - cause
bacterial or embolic nephritis.
Bacteraemia - bacteria in glomerular and interstitial capillaries
formation of microabscesses in cortex.
glomeruli are targeted but manifestation of renal vascular disease
Produce toxic by products → damage endothelium →
localised vasculitis and colonisation → embolic nephritis
38
Acute suppurative glomerulitis - bacterial causes
Actinobacillus equuli in foals.
Erysipelothrix rhusiopathiae in pigs.
Corynebacterium pseudotuberculosis in sheep and goats.
Arcanobacterium pyogenes in cattle
39
Acute suppurative glomerulitis - gross appearance on kidneys
Multifocal random raised tan pinpoint foci - subcapsular and cut surface of renal cortex.
40
Acute suppurative glomerulitis - histopathology
Glomerular capillaries - bacterial colonies admixed with necrotic debris and neutrophils.
Glomerular or interstitial haemorrhage.
Can persist as focal residual abscesses
or progressively replaced by chronic
inflammation and coalescing scars.
41
Glomerulosclerosis
↓ in the no. of functional glomeruli.
Loss of glomerular capillaries + replacement of mesangial matrix and Bowman’s space by FCT.
↓ blood flow through the vasa recta from glomerular efferent arteriole.
hypoxia → tubular epithelial degeneration and loss.
Chronic proteinuria.
42
Diseases of the Tubules
Inherited Abnormalities, Acute Tubular Necrosis
43
Causes of tubular disease
```
Blood borne infections
Ascending infections (intratubular pathogens).
Direct damage from toxins (intratubular effects).
Ischemia.
Infarction.
Tubular obstruction.
Interstitial fibrosis.
External compression
```
44
Responses of the tubules to injury
Degeneration, necrosis, apoptosis and/or atrophy → PCT most vulnerable.
Cells slough into the lumen to form cellular casts.
compensatory hypertrophy → attempt to maintain overall renal function
no regeneration of nephrons
45
Responses of the tubular basement membrane to injury
retained more consistently after toxic rather than ischemic results.
if it remains intact → repair by proliferation of the remaining viable epithelial cells.
Severe damage to or loss of tubular basement membranes → necrosis, failure of functional repair and replacement by fibrosis.
46
Primary renal glycosuria
Inherited disorder
decr reabsorbtion of glucose by tubular epithelial cells
no gross or histological findings.
Predisposes to bacterial infections of LUT
47
Fanconi syndrome
hereditary defect in tubular reabsorption of protein, glucose, phosphate, amino acids.
Can develop progressive renal insufficiency & associated renal fibrosis.
48
cystinuria
Sex linked inherited tubular defect in male dogs
| predisposes to calculus formation and obstruction of the LUT.
49
acute tubular necrosis - effect
decr renal perfusion → ↓ GRF & activation of arteriolar vasoconstriction → prolonged ischemia
50
Nephrotoxic pigments - Haemoglobinuric nephrosis - causes
chronic copper toxicity in sheep, babesiosis in
| cattle, red maple toxicity in horses and AIHA in dogs.
51
Nephrotoxic pigments - Myoglobinuric nephrosis
extensive muscle necrosis
azoturia of horses, capture myopathy of exotic or wild
animals and severe trauma.
52
Acute Tubular Necrosis - Heavy metals
Lead → membrane/mitochondrial damage in the PCT cells
Acid fast IN inclusions present in the PCT epithelium
specific metal can't be identified by renal lesions alone
53
Acute Tubular Necrosis - oak poisoning in cattle
toxic substances are metabolites of tannins.
Target endothelial cells → vascular leakage.
Perirenal oedema.
54
Acute Tubular Necrosis - oxalate containing plants - cattle + sheep
Calcium oxalates precipitate in BVs or within
renal tubules.
obstruction and epithelial cell necrosis.
Neuromuscular dysfunction → hypocalcaemia
55
Acute Tubular Necrosis - Ethylene glycol (antifreeze)
Dogs, cats and occasionally pigs.
Readily absorbed from GIT.
Oxidised by hepatic alcohol dehydrogenase to toxic metabolites - glycolic acid and oxalate.
Filtered by the glomeruli.
Direct toxic effect on tubules.
Calcium oxalate crystals precipitate in renal tubular lumens → intrarenal obstruction.
56
Acute Tubular Necrosis - bacterial toxins
Clostridium perfringens type D → epsilon toxin
| Pulpy kidney → acute tubular degeneration and/or necrosis, interstitial oedema + haemorrhage
57
Diseases of the Interstitium
Interstitial nephritis
58
renal interstitium - define
fibrovascular stroma that surrounds the nephron
59
Diseases of the Interstitium - Caused by
Ascending infection → pyelonephritis.
Haematogenous infection of tubules and interstitium → E-coli and Leptospira spp, Canine adenovirus.
Secondary to injury of the vasculature or tubules or glomeruli.
60
Responses of the interstitium to injury
Oedema.
Haemorrhage.
Inflammation.
Fibrosis.
61
Diseases of the Interstitium - gross appearance
grey foci on the capsular and cut surface.
62
Diseases of the Interstitium - Histopathology
```
Initially oedema, haemorrhage and neutrophilic infiltration.
Later lymphocytes and plasma cells.
Tubular epithelial degeneration.
Vascular compromise.
Fibrosis
```
63
Diseases of the Interstitium - E-coli septicaemia
E-coli septicaemia:
‘White spotted kidney’
Embolic nephritis or nonsuppurative interstitial nephritis.
Microabscess replaced by lymphocytes, plasma cells and
macrophages.
64
Diseases of the Interstitium - Equine arteritis virus or PRRS
Multifocal lymphohistiocytic tubulointerstitial nephritis with
interstitial oedema.
Vasculitis - fibrinoid necrosis and lymphohistiocytic infiltrates.
Virus can be found in the endothelium and macrophages
65
Diseases of the Interstitium - Canine adenovirus infection
viral glomerulitis
Transient immune complex GN.
virus leaves glomeruli - reappears in tubular epithelial cells
Basophilic intranuclear viral inclusions.
Persistence of virus in tubular epithelium for weeks to months.
Viral induced cytolysis → tubular epithelial necrosis → production of chronic lymphoplasmacytic and less commonly histiocytic interstitial nephritis.
66
Diseases of the Interstitium - Leptospirosis - pathophysiology
Bacterial tubulointerstitial nephritis.
organisms localise in renal interstitial capillaries.
Migrate through vascular endothelium → persist in the interstitial spaces.
Migrate into renal tubular lumina.
Degeneration and necrosis of tubular epithelial cells.
Infiltrate of macrophages, lymphocytes and plasma cells in the interstitium and neutrophils can be present in tubular lumina
67
Diseases of the Interstitium - Feline infectious peritonitis
Granulomatous necrotising vasculitis.
Interstitial pyogranulomas.
other causes of granulomatous interstitial nephritis - Mycobacteria, Fungi, Parasites.
68
Responses of the vasculature to injury
```
Hyperaemia and congestion.
Haemorrhage and thrombosis.
Infarction.
Papillary (medullary crest) necrosis.
Embolic nephritis.
```
69
causes of haemorrhage in the kidney
Direct trauma.
Coagulopathies.
Septicaemia - erysipelas, streptoccocal infections.
Embolic bacterial diseases → Actinobacillus equuli.
Vasculitis - FIP.
Vascular necrosis → Canine herpesvirus.
DIC.
70
Disseminated intravascular coagulation
abnormal coagulation → generation of excess thrombin
Diffuse vascular damage → endotoxin induced → exposure of tissue factor → induced activation of extrinsic coagulation to produce thrombin.
Formation of widespread fibrin thrombi in the renal
microcirculation → platelet and coagulation factor consumption → widespread haemorrhages.
Not primary disease but a potential complication of any
condition associated with widespread activation of thrombin.
Results in cortical infarction and ischemic (coagulative) necrosis
71
Sources of renal emboli
Cardiac mural or valvular thrombi.
Endarteritis in parasitic diseases such equine strongylosis.
Neoplastic cell emboli.
Bacterial or septic emboli → Arcanobacterium pyogenes
in cattle, Erysipelas rhusiopathie in pigs and Staphylococcus aureus in dogs.
72
Neoplasia of the kidney
<1% of total neoplasms reported.
Usually unilateral.
Primary renal tumours - highly malignant and metastatic disease is common
73
Epithelial tumours -
Renal adenomas - usually incidental at necropsy.
74
Epithelial tumours - Renal carcinomas
Large with foci of haemorrhage, necrosis and cystic degeneration, occupy and obliterate one pole of the kidney.
Paraneoplastic condition -polycythaemia - overexpression of erythropoietin
75
Epithelial tumours - Transitional cell papillomas and
| carcinomas
Arise in the renal pelvis and LUT.
Can obstruct urinary outflow.
Can invade into the kidney
76
Metastatic tumours
Carcinomas and sarcomas arising in other organs can metastasise to the kidneys.
Randomly scattered multiple nodules.
Usually involving both kidneys.
Renal lymphoma - cats and cattle
77
Diseases of the renal pelvis - Hydronephrosis
Dilation of the renal pelvis d/t obstruction of urine outflow → incr pelvic pressure - atrophy of renal parenchyma.
interstitial vessels collapse + renal blood flow decr - hypoxia and ischemic necrosis - tubular atrophy and interstitial fibrosis.
if bacteria enter hydronephrosis kidney → becomes filled with pus → pyonephrosis
78
Diseases of the renal pelvis - Hydronephrosis - causes
```
Congenital malformation.
Ureteral/urethral blockage due to urinary calculi.
chronic inflammation.
Ureteral/urethral neoplasia.
Neurogenic functional disorders.
```
79
Diseases of the renal pelvis - Hydronephrosis - unilateral
hydronephrosis can be become notable
continual urine production and pooling of urine into the
expanding pelvis.
80
Diseases of the renal pelvis - Hydronephrosis - Bilateral
uraemia occurs before pelvic enlargement becomes extensive.
81
Pyelonephritis
Bacterial infection of the pelvis with extension into the renal tubules and concomitant interstitial inflammation.
form of suppurative tubulointerstitial disease.
frequently bilateral and recurrent infections common.
Associated with parturition, service and catheter use
82
Pyelonephritis - Bacteria involved
Corynebacterium spp, E coli, Staphylococcus
spp, Streptococcus spp, Pseudomonas aeruginosa and
Arcanobacterium pyogenes.
83
pyelonephritis - Competency of vesicoureteral valve is
| compromised
causes incr reflux
when pressure is incr in the urinary bladder - urethral obstruction.
Infl of the bladder wall - cystitis.
Endotoxin from G-ve bacteria - inhibit ureteral peristalsis.
84
Pyelonephritis - gross
Ureters distended with suppurative exudate.
Exudate in the pelvis and medulla.
May extend into cortex
olar scars.
Infl can extend through the surface of the kidneys - peritonitis.
85
Pyelonephritis - Histopathology
Transitional epithelium is necrotic and sloughed.
Necrotic debris, fibrin, neutrophils + bacterial adhere to denuded surface and accumulate in tubular lumina.
Interstitial infl, haemorrhage + oedema.
If vasa recta are obstructed - papillary necrosis.
Extend radially into the cortical tubules.
Lymphocytes, plasma cells macrophages and fibrosis.
86
Primary papillary necrosis
Prolonged treatment or overdose with NSAIDs - damage to medullary interstitial cells.
decr PG synthesis (vasodilator) - decr blood flow - ischemic necrosis of the inner medulla
87
Secondary papillary necrosis - causes
decr vasa recta blood flow - glomerular amyloidosis or
glomerulosclerosis.
Compression of the vasa recta within the medulla -
interstitial oedema or fibrosis.
Compression of the renal papilla - pelvic calculi, LUT obstruction, pyelonephritis and vesiculoureteral reflux
88
papilary necrosis - effects on kidney
Sharply delineated coagulative necrosis of the inner medulla.
Eventually sloughs - detached fragment in the pelvis.
Large fragments could obstruct the ureter - hydronephrosis.
formation of calculi
Rarely lead to progressive renal damage + failure.
89
disease of the LUT - causes
```
Infection:
Neoplasia.
Toxins/poisons.
Congenital defects.
Physical trauma → urolith.
Obstruction
```
90
defense mechanisms of the LUT
Flushing action of urine minimises risk of ascension of bacteria.
Peristalsis acts to eliminate bacteria with adhesion capabilities.
Inhospitable environment for bacterial growth controlled by urine pH.
Protective urothelial mucus coating.
Innate, humoral and cellular immune responses.
91
LUT response to injury
Dilation and pressure necrosis caused by obstruction.
Inflammation.
Neoplastic transformation
92
ectopic ureters
Empty into the urethra, vagina or bladder neck.
Predisposed to obstruction or infection.
Present clinically with urinary continence.
93
patent urachus
Foals.
Foetal urachus fails to close → direct channel between the bladder and the umbilicus.
Underlying omphalitis or congenital urethral obstruction.
↑ Bladder pressure → due to obstruction → forces urine out into the urachus.
Dribble urine from umbilicus.
94
acquired causes of obstruction of the LUT
```
Calculi.
Neoplasia.
Trauma and inflammation.
Circumferential fibrosis.
Bladder paralysis.
Vaginal and/or uterine prolapse.
Feline urologic syndrome - fine struvite crystals in a mucoid protein matrix fill the urethra
```
95
Consequences of obstruction of LUT
```
Distended/ruptured bladder.
Transmural ecchymotic haemorrhages.
Mucosal ulceration and haemorrhages.
peritonitis.
Infl
```
96
acute cystitis - clinical signs
Dysuria, stranguria and haematuria
97
acute cystitis - causes
Bacterial infection most common cause.
Uropathogenic E coli in many spp, Corynebacterium renale in cattle and Eubacterium suis in pigs.
Hydrolysis of urea by urease producing bacteria C renale and E suis in pigs - release excessive ammonia damage mucosa & urine pH
98
acute cystitis - affect of LUT
Denuded oedematous mucosa, adherent neutrophils, bacterial colonies, hyperaemia and haemorrhage
99
acute cystitis - predisposing factors
```
Urinary stasis.
Infrequent urination
Calculi.
Catheterisation.
Prolonged antibiotic use
```
100
Chronic Cystitis - difuse
Thickened mucosa infiltrated with mononuclear infl cells
Submucosal fibrosis.
Hypertrophy of the muscularis.
101
Chronic Cystitis - follicular
Multiple small red nodules on the mucosal surface.
Hyperplastic lymphoid cells surrounded by hyperaemia and haemorrhage.
Associated with uroliths
102
Chronic Cystitis - polypoid
Multiple masses of proliferative nodules of connective tissue (polyps).
Lymphocytes and neutrophils
103
Emphysematous cystitis
Glycosuria enhances bacterial growth.
Glucose split by bacteria - E coli, Clostridium perfringens
release of CO2 into the bladder lumen.
Absorption of gas into the bladder lymphatics - emphysema
104
Toxic cystitis
Chronic ingestion of bracken fern - enzootic haematuria -
haemorrhage, chronic cystitis or bladder neoplasia.
Active metabolites of cyclophosphamide used to treat neoplasia and IMD
105
epithelial tumours
Transitional cell papillomas or carcinomas
SCC & adenocarcinomas can arise from transitional epithelium
Metastasis regional lymph nodes, lungs and kidney
106
Mesenchymal tumours:
Leiomyomas
Fibromas from the lamina propria.
Lymphoma.
Rhabdomyosarcomas
107
Developmental Disorders - Renal aplasia
failure of one or both kidneys to develop.
108
Developmental Disorders - Hypoplasia
incomplete development of one or both kidneys
| fewer than normal nephrons.
109
Developmental Disorders - Ectopic kidneys
pelvic canal or inguinal position
histological structure and function usually normal but malposition of the ureters predisposes then to
obstruction - secondary hydronephrosis.
110
Developmental Disorders - Fused kidneys
fusion of cranial or caudal poles
horseshoe shape
structurally and functionally normal.
111
Developmental Disorders - Dysplasia
abnormal differentiation in one or both kidneys
112
Developmental Disorders - Progressive juvenile
| nephropathy
Severe bilateral renal fibrosis.
Shrunken pale kidneys with a pitted surface.
Foetal glomeruli, interstitial infl, fibrosis and tubular dilation
