Week 15 Pathology

Acute renal failure:

Pre renal causes

  • Hypovolaemia, hypotension, CCF –> poor renal perfusion–> decreased renal clearance of toxins and ischaemia of tubular cells


Intra renal causes

  • Primary Glomerulonephritis
    • Acute proliferative glomerulonephritis
      • Postinfectious (Post strep – IgG mediated)
      • Other
    • Rapidly progressive (crescentic) glomerulonephritis
    • Membranous nephropathy
    • Minimal-change disease
    • Focal segmental glomerulosclerosis
    • Membranoproliferative glomerulonephritis
    • Dense deposit disease
    • IgA nephropathy
    • Chronic glomerulonephritis
  • Systemic Diseases with Glomerular Involvement
    • HTN –> focal segmental glomerulosclerosis
    • DM –> tubulointerstitial fibrosis, hyalinizing arteriolar sclerosis, papilary necrosis.
    • immunological – SLE, good pastures, wegners, HSP (rapidly progressive, crescents), microscopic polyangitis
    • Amyloidosis
  • Hereditary Disorders
    • Alport, Fabry
  • Nephritic syndrome – haematuria, uremia, variable proteinuria, oliguria, oedema and HTN
  • Nephrotic syndrome – Proteinuria(>3.5g), hypoalbuminaemia, hyperlipidaemia, lipiduria.


  • Major Changes observed in Glomerular diseases
    • Histological changes – hypercellularity, BM thickening, Hyalinisation/sclerosis,
    • Ab-Ag complex deposit mainly subendothelially
    • antiGBM deposit in GBM
    • Heymann – antibody to ag in epithelial cell.
    • Ab –> cytotoxic injury and complement mediated injury –> epithelial cell foot process effacement and detachment–> increased leakage into urine of blood components.
Disease Pathogenesis Glomerular Pathology Most Frequent Clinical Presentation
Post strep Circulating or planted antigen IgG and C3 in GBM Acute nephritis
Good pastures Anti GBM Proliferation, cresents Rapidly progressive GN
Membranous Insitu Ab mediated Diffuse cap wall thickening Nephrotic syn
Minimal change Podocyte injury Normal, lipid in tubule Nephrotic syn
Focal segmental Unknown Focal and segmental sclerosis and hyalinosis Nephrotic syn
Membrane proliferative Immune complex Mesangial proliferation, BM thickening Nephrotic syn
Ig A nephropathy Unknown Focal proliferative GN Recurrent haematuria or proteinuria
Chronic GN Variable – mainly rapidly progressive and focal glomerulosclerosis Hyalinized glomeruli Chronic renal failure

Post renal causes (Causes of urinary obstruction) –> back flow –> renal damage and decreased function.

  • Renal Calculi
    • Types
      • Calcium oxalate and phosphate 70%
      • Struvite 15-20%
      • Uric acid 5-10%
      • Cysteine 1-2%
    • Complications.
      • Pain, infection, renal failure,
      • Ureteric stricture
  • BPH
  • Posterior urethral valves
  • Tumours
  • Inflammation – prostatitis, urethritis, retroperitoneal fibrosis
  • Sloughed pappilae/blod clots
  • Pregnancy
  • Cystocoele


Acute tubular necrosis (ATN):

From the presentation by Prof Nabil Tadros Mikhail.

From the presentation by Prof Nabil Tadros Mikhail.

  • Commonest cause of AKI – 50%
  • Destruction of tubular epithelial cells and acute renal failure
  • Causes
    • Ischaemia, hypoperfusion
    • Direct toxic injury – contrast, radiation, gentamycin
    • Acute tubulointerstitial nephritis -hypersensitivity to drugs
    • DIC
    • Urinary obstruction
  • Necrosis is more in PCT and PST in toxic type and less in ischaemic type. Both have casts from DCT to CD.
  • Clinical course
    • Initiation: 36hrs, slight decrease in UO and rise in blood urea.
    • Maintanence: sustained oliguria, rising Urea and creatinine, hyper K, metabolic acidosis, uraemia – needs supportive mangement to carry pt over this
    • Recovery: increasing UO, tubules still damaged so large amount of water and electrolytres lost – Hypo K, increase risk of infection, everything normalises eventually.


Urinary Tract Infection (UTI):

  • Causes
    • Haematologenous – Staphylococcus, E Coli
    • Ascending – E Coli, Proteus, enterobacter
  • Consequences
    • Dysuria, frequency
    • Pyelonephritis – flank pain, fever, acute renal failure.
  • Predisposing factors
    • Female – short urethra
    • Vescioureteric reflux – shallow angle of ureter insertion.
    • Instrumentation of urinary tract
    • Pregnancy
    • DM
    • Immunosuppression


Chronic renal failure:

  • HTN
  • DM
  • GN


Haemolytic-Uraemic syndrome.

  • Childhood type – associated with bloody diarrhoea  caused by intestinal infection by verocytotoxin releasing bacteria
  • Adult
    • Infection- typhoid, ecoli, shigellosis
    • Antiphospholipid Abs
    • Cx of preg and contraceptive
    • Vascular renal disease eg HTN, scleroderma
    • Chemo and immunosuppressive drugs
    • Radiation
  • Mechanism: endothelial injury–>  activation–> intravascular thrombosis–> platelet aggregation–> distal ischaemia


Thrombotic thrombocytopenic purpura (TTP):

  • Fever, neurological sx, haemolytic anaemia, thrombocytopenic purpura, thrombi in glomeruli.
  • Gene defect in ADAMTS-13–> affect cleavage of vWF –> promotion of platelet aggregation.
  • Women, younger than 40
  • Neurological sx are dominant.