3. DEFINITION
• An abrupt decrease in the glomerular filtration rate (GFR)
or the more clinically available index of renal function,
creatinine clearance (CLcr).
• This results in an accumulation of nitrogenous waste
products and other toxins.
3
13. Causes of intra-renal failure
I. Acute tubular necrosis
II. Immune and inflammatory renal disease
I. Acute tubular necrosis :
ATN is a diagnosis made by renal biopsy;
the findings include:
damage to the proximal tubule and
the ascending limb of the loop of Henle,
interstitial oedema and sparse infiltrating inflammatory
cells.
13
14. These may arise exogenously from :
drugs or chemical poisons,
or from endogenous sources such as haemoglobin,
myoglobin, crystals (uric acid, phosphate) and
toxic products from sepsis or tumours
Some endogenous toxins maybe released as a direct
consequence of drug exposure
For example, myoglobin may be released (rhabdomyolosis)
following muscle injury or necrosis, hypoxia, infection or
following drug treatment.
for example, with fibrates and statins, particularly when
both are used in combination.
14
19. • Anti-neutrophil cytoplasmic antibodies (ANCA) refer to the
presence of circulating antibodies that are targeted against
primary neutrophil cytoplasmic antigens (proteins including
proteinase 3 and myeloperoxidase).
• The two main types of anti-neutrophil cytoplasmic
antibodyassociated SVV are Wegener's granulomatosis and
microsopic polyangiitis
19
20. Interstitial nephritis
• Interstitial nephritis is thought to be nephrotoxin-induced
hypersensitivity reaction associated with infiltration of
inflammatory cells into the interstitium with secondary
involvement of the tubules.
• The nephrotoxins involved are usually drugs and/or the toxic
products of infection.
• Drugs that have been most commonly shown to be responsible
include
NSAIDs,
antibiotics (especially penicillins, cephalosporins and
quinolones),
proton pump inhibitors such as omeprazole,
furosemide, allopurinol and azathioprine, 20
21. Post-renal acute kidney injury
• Post-renal AKI results from obstruction of the urinary tract
(the renal pelvis to the urethral orifice )by a variety of
mechanisms.
• these can be divided into causes :
within the ureters (e.g. calculi or clots),
a problem within the wall of ureter (malignancies, benign
strictures) and
external compression (e.g. retroperitoneal tumours).
• It is extremely unusual for drugs to be responsible for
postrenal AKI.
• Practololinduced retroperitoneal fibrosis resulting in
bilateral ureteric obstruction is a rare example.
21
