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Kidney pathology 2010.1

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Kidney pathology 2010.1. Tubular & interstitial diseases. Kidney - cut surface. Outer cortex (Co) Inner medulla composed of pyramids * Cortical columns of Bertini (B) between pyramids* Urine first collects in calyces, pelvis. Co. *. *. B. Calyx. Pelvis. - PowerPoint PPT Presentation
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Kidney pathology 2010.1 Tubular & interstitial diseases
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Page 1: Kidney pathology 2010.1

Kidney pathology 2010.1

Tubular & interstitial diseases

Page 2: Kidney pathology 2010.1

Kidney - cut surface

• Outer cortex (Co)• Inner medulla

composed of pyramids *

• Cortical columns of Bertini (B) between pyramids*

• Urine first collects in calyces, pelvis

*Co

B

Calyx

*

Pelvis

Page 3: Kidney pathology 2010.1

Malpighi and Malpighian “corpuscles”

(glomeruli)

Page 4: Kidney pathology 2010.1

Glomerular structure

• Arterioles• Capillaries• Mesangium (“between

capillaries”)• Urinary space

surrounds glomerulus within Bowman’s capsule

• Urin sp -> prox tubule

Page 5: Kidney pathology 2010.1

Normal renal tubules

Page 6: Kidney pathology 2010.1

Acute pyelonephritis

• Most severe end of spectrum of UTI

• Acute bacterial inflammation of kidney

• E coli, Proteus, Enterobacter, Klebsiella …

• Abscesses in cortex, medulla

• Polymorphs in tubules; glomeruli spared• (CMV, polyoma virus in immunocompromised)

Page 7: Kidney pathology 2010.1

Acute pyelonephritis

Page 8: Kidney pathology 2010.1

Acute pyelonephritis

Page 9: Kidney pathology 2010.1

Acute pyelonephritis - clinical

• M < 1yr and over 40 yrs; F 1 - 40 yrs

• Sudden onset tenderness in costo-phrenic angle

• Temp, rigors, cystitis

• Most resolve quickly

• May recur, become chronic

• Complications

Page 10: Kidney pathology 2010.1

Pathogenesis of acute pyelonephritis

• (Haematogenous spread)• Bacterial adhesins, colonisation, ascending

infection• Cystitis• Vesico-Ureteric Reflux & Intrarenal Reflux,

congenital or acquired– VUR: Urine, bacteria -> ureter– Inrarenal reflux: Urine enters kidney papillae

Page 11: Kidney pathology 2010.1

Predisposing factors

• Short female urethra• Obstruction (pregnancy, congenital, stones,

tumours, BPH)• Bladder dysfunction• Diabetes• Catheters, cystoscopy, other• Vesico-Ureteric Reflux & Intrarenal Reflux

– If no reflux, infection only in bladder

Page 12: Kidney pathology 2010.1

Complications of Acute Pyelo

• Perinephric abscess• Pyonephrosis• *Papillary necrosis• Fibrous scars, chronic

pyelonephritis

Page 13: Kidney pathology 2010.1

Chronic pyelonephritis

• Scars overlying distended calyces

• Chronic inflammation and fibrosis involving tubules and interstitium

• Two types– Reflux nephropathy– Chronic obstructive pyelonephritis

Page 14: Kidney pathology 2010.1

Reflux nephropathy

• Commoner• VUR pressure threshold• Organisms• Refluxing papillae at

upper, lower poles• Hypertension at 15-25 yrs

Page 15: Kidney pathology 2010.1

Chronic pyelonephritis (reflux)

Page 16: Kidney pathology 2010.1

Chronic pyelonephritis - reflux type

Page 17: Kidney pathology 2010.1

Chronic pyelonephritis, obstructive

• Older patients• Strictures, calculi in

ureter, renal pelvis• BPH• Tumours

Page 18: Kidney pathology 2010.1

Chronic pyelonephritis - clinical

• Chronic renal failure, hypertension

• UTI (but often negative urine cultures)

• Interstitial fibrosis, tubular atrophy, thyroidization of tubules, thick arteries, FSGS

• Accounts for 10 - 20% of patients on dialysis

• Other types of pyelonephritis

Page 19: Kidney pathology 2010.1

TB (L) & Xanthogranulomatous PN (R)

Page 20: Kidney pathology 2010.1

Non-bacterial inflammation of renal tubules, interstitium

• Drugs/toxins: penicillins, rifampicin, NSAIDs…..

– Immune injury (types I, IV); direct, unknown

– Fever, oliguria in 50%, rash

– Micro; inflammatory cells, inc eosinophils

• Analgesic nephropathy - phenacetin, +/- aspirin, codeine

• Assoc with glomerular disease e.g. SLE, renal vasculitis

• Gout, multiple myeloma

• Renal allograft rejection

Page 21: Kidney pathology 2010.1

Acute interstitial nephritis

Page 22: Kidney pathology 2010.1

Eosinophils in drug induced interstitial nephritis

Page 23: Kidney pathology 2010.1

Acute renal transplant rejection

QuickTime™ and aPhoto - JPEG decompressor

are needed to see this picture.

Page 24: Kidney pathology 2010.1

Acute renal failure

• Sudden onset of oliguria (<400ml) – Raised serum Creatinine

• Cause determines symptoms, prognosis • Overall mortality is 40%

– Drugs, toxins

– Crescentic glomerulonephritis e.g. ANCA+ vasculitis

– Genitourinary obstruction

– Shock, ischaemia

Page 25: Kidney pathology 2010.1

Acute renal failure - pathology

• Most patients have a microscopic lesion - Acute Tubular Necrosis (necrosis of tubular epithelial cells is a “marker” of acute loss of renal function)

• Renal tubular epithelium sensitive to toxins, ischaemia

• Vasoconstriction -> hypoxia in outer medulla

• Two types of ATN:

• ATN due to drugs, toxins - PCT cells (95% survival)

• ATN due to ischaemia, shock or sepsis - granular casts (20-50% survival)

Page 26: Kidney pathology 2010.1

Normal tubules (L) and drug-induced ATN* (R)

*

Page 27: Kidney pathology 2010.1

ATN, drug-induced

Page 28: Kidney pathology 2010.1

ATN due to toxin

Page 29: Kidney pathology 2010.1

ATN due to Sepsis/Ischaemia

Page 30: Kidney pathology 2010.1

Interstitial fibrosis and tubular atrophy in chronic renal disease correlate with progressive loss of renal function

QuickTime™ and aPhoto - JPEG decompressor

are needed to see this picture.

Page 31: Kidney pathology 2010.1

Chronic renal failure

• Progressive and irreversible loss of renal tissue

• Chronic GN, chronic PN, hypertensive nephrosclerosis, diabetes, adult type PCKD

• Symptoms - anaemia, dehydration, nausea, metabolic bone disease, etc

• Asymptomatic renal insufficiency present prior to this while kidneys’ intact nephrons compensate

• Dialysis, transplant or death within 1 year of onset of CRF


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