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
Glomerular structure
• Arterioles• Capillaries• Mesangium (“between
capillaries”)• Urinary space
surrounds glomerulus within Bowman’s capsule
• Urin sp -> prox tubule
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)
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
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
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
Complications of Acute Pyelo
• Perinephric abscess• Pyonephrosis• *Papillary necrosis• Fibrous scars, chronic
pyelonephritis
Chronic pyelonephritis
• Scars overlying distended calyces
• Chronic inflammation and fibrosis involving tubules and interstitium
• Two types– Reflux nephropathy– Chronic obstructive pyelonephritis
Reflux nephropathy
• Commoner• VUR pressure threshold• Organisms• Refluxing papillae at
upper, lower poles• Hypertension at 15-25 yrs
Chronic pyelonephritis, obstructive
• Older patients• Strictures, calculi in
ureter, renal pelvis• BPH• Tumours
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
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
Acute renal transplant rejection
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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
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)
Interstitial fibrosis and tubular atrophy in chronic renal disease correlate with progressive loss of renal function
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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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