Revise Notes Renal Flashcards by Sanjana Sathyan

Haemolytic-Uraemic Syndrome

Clinical Features

A syndrome characterised by a triad of:

Haemolytic anaemia
Thrombocytopenia
Acute renal failure (increased creatinine/urea)

Aetiology

Occurs most commonly post-dysentery (Shiga toxin producing E.Coli 0157: H7)
Management

Supportive care
Plasma exchange

How well did you know this?

Not at all

Perfectly

Renal Papillary Necrosis

Causes

Sickle cell disease
NSAIDs

Clinical Features

Loin pain
Haematuria
Proteinuria
Diagnosis

IV Urogram: Cup + Spill appearance

How well did you know this?

Not at all

Perfectly

Acute tubular necrosis

The most common cause of renal/intrinsic AKI

Pathology

Necrosis of the tubular epithelial cells results in impaired renal function
Histopathology: loss of nuclei, detachment from basement membrane

Causes

Ischaemia - shock or sepsis (a prolonged ‘pre-renal’ insult will eventually causing ischaemic injury due to hypoperfusion)
Nephrotoxins

Lead
Myoglobin (e.g. rhabdomyolysis)
Drugs - NSAIDs
Contrast

Biochemical/Clinical Characteristics

Urine Na+ > 40 - necrosed cells are unable to reabsorb Na+
Urine Osm < 350

Urea: Creatinine ratio - normal (urea less elevated than pre-renal)

Urinalysis: muddy brown casts
Fluid challenge: Poor response

Phases of ATN: oliguria –> polyuria –> recovery

How well did you know this?

Not at all

Perfectly

Pre-renal AKI

Causes

Hypovolaemia (e.g. dehydration, haemorrhage)
Reduced cardiac output - CCF, sepsis
Drugs (reduced BP or renal perfusion)

ACEi/ARBs - impair renal perfusion
NSAIDs
Diuretics/MRAs

Biochemical/Clinical Characteristics

Urine Na+ < 20 mmol/L (kidneys are ‘holding on to Na+’ to preserve fluid volume)

Urine Osm > 500 - concentrated urine as kidneys reabsorb H2O

Urea: Creatinine ratio - urea is significantly elevated

Urine dip: often normal
Fluid challenge: good response

How well did you know this?

Not at all

Perfectly

Acute Kidney Injury
Background

AKI is a clinical syndrome characterised by an acute decline in renal function over hours to days, which can result in the failure of homeostasis of electrolytes/fluid/acid-base balance.

AKI is defined by KDIGO as:

Increase in serum creatinine by 26.5 umol/L within 48hrs

Increase in serum creatinine to 1.5 x baseline

Urine output < 0.5 ml/kg/hr for 6 hours

KDIGO stages AKI according to the extent of serum creatinine rise/urine output.

How well did you know this?

Not at all

Perfectly

The causes of AKI are vast, and are typically divided into 3 categories (as outlined below):

Pre-renal - due to renal hypoperfusion with consequently reduced glomerular filtration rate
Intra-renal - structural damage to the kidney itself (e.g. tubules/glomeruli etc)

Confusingly, may result from prolonged ‘pre-renal’ hypoperfusion (causing ischaemia) or post-renal causes (e.g. due to pressure)

Post-renal - caused by obstruction of urine flow, resulting in increased intratubular pressure

How well did you know this?

Not at all

Perfectly

Alport Syndrome
Alport syndrome is a genetic disorder characterised by progressive renal disease, sensorineural hearing loss, and ocular abnormalities, resulting from mutations in the genes coding for type 4 collagen.

It typically follows an X-linked dominant inheritance pattern but can also present as autosomal recessive or autosomal dominant.

Bloods and Investigation Findings

Urinalysis: Microscopic haematuria, proteinuria.

Renal biopsy: Electron microscopy reveals thickened and laminated GBM with a “basket weave” appearance.

Genetic testing: Identification of mutations in COL4A3, COL4A4, or COL4A5 genes.

Management

Renal: ACE inhibitors or ARBs to reduce proteinuria and slow progression to renal failure. Dialysis and renal transplantation in advanced stages.

Hearing: Hearing aids or cochlear implants for severe hearing loss.

Ocular: Regular ophthalmologic monitoring, corrective lenses, and surgical intervention for lenticonus if necessary.

How well did you know this?

Not at all

Perfectly

Alports syndrome

Pathophysiology

X-linked dominant inheritance.
Mutations in COL4A3, COL4A4, and COL4A5 genes lead to defective type IV collagen synthesis.

This compromises the structural integrity of the glomerular basement membrane (GBM), cochlea, and ocular lens capsule.

This results in progressive glomerulonephritis, sensorineural deafness, and ocular abnormalities.

Clinical Features

Renal: Haematuria, proteinuria, progressing to chronic kidney disease and ESRF.

Auditory: Bilateral sensorineural hearing loss, usually manifesting in late childhood or adolescence.

Ocular: Anterior lenticonus, retinal flecks, and corneal erosions.

How well did you know this?

Not at all

Perfectly

Autosomal Recessive PKD

Much rarer than it’s dominant counterpart

Mutation: CHROMOSOME 6
Diagnosis: Prenatal USS

Clinical features:
Abdominal masses
Renal failure during childhood
Associated conditions: Liver fibrosis

How well did you know this?

Not at all

Perfectly

Autosomal Dominant Polcystic Kidney Disease (ADPKD)

The most common inherited cause of CKD, characterised by the development of renal cysts, amongst other extra-renal manifestations.

More than half of patients with ADPKD will develop ESRF, requiring RRT.

ADPKD Type 1

Accounts for the majority of cases - approx. 85%
Mutation: Chromosome 16, PKD1 gene encoding polycystin 1 protein

ADPKD Type 2

15% cases
Mutation: Chromosome 4, PKD2 gene encoding polycystin 2 protein

Clinical Features

Abdominal/loin pain
Hypertension
Haematuria
O/E: Ballotable kidneys

Extra-renal manifestations

Intracranial aneurysms - subarachnoid haemorrhage
Liver and pancreatic cystic disease

Valvular heart disease - Mitral regurgitation/prolapse

How well did you know this?

Not at all

Perfectly

Autosomal Dominant Polcystic Kidney Disease (ADPKD)

The most common inherited cause of CKD, characterised by the development of renal cysts, amongst other extra-renal manifestations.

More than half of patients with ADPKD will develop ESRF, requiring RRT.

Diagnosis

1st Line: (if positive FHx of ADPKD) - Abdominal USS

US must be performed after 20 years of age (or risk of false negatives)

Associated complications

Mitral valve prolapse - regular echocardiogram screening

Diverticular disease - Barium enema screening

Management

Tolvaptan may be indicated to slow progression of renal disease (normally in patients with CKD 2/3 with evidence of rapid deterioration in renal function)

How well did you know this?

Not at all

Perfectly

Complications of CKD

Electrolyte derangement - Hypocalcaemia & Hyperphosphataemia

Reduced renal synthesis of 1,25-dihydroxyvitamin D (from 25-OH Vit D) - Hypocalcaemia
The most common cause of secondary/tertiary hyperparathyroidism

Reduced phosphate excretion results in co-existent hyperphosphatemia

Renal bone disease
Secondary/Tertiary Hyperparathyroid bone disease – osteitis fibrosa cystica

Osteomalacia (low Vit D)

Suggested by a raised ALP in the context of hypocalcaemia/low Vit D

How well did you know this?

Not at all

Perfectly

Peritoneal Dialysis

Continuous ambulatory peritoneal dialysis is the most common form – commonly 2 Litres, 4 x per day

Complications: SBP – staphylococcus epidermis is the most common cause

How well did you know this?

Not at all

Perfectly

Calciphylaxis

Pathology

Calciphylaxis describes calcific uraemic arteriopathy which occurs as a complication of ESRF

Arteriolar calcification causes occlusion which can result in painful purpura and bleeding within the affected area.

Note - warfarin can trigger calciphylaxis
Management

Medical/dietary measures to reduce calcium and phosphate levels

How well did you know this?

Not at all

Perfectly

Anaemia in CKD

Pathophysiology: Reduced renal production of EPO in CKD leads to anaemia

Management:
1st Step: Check ferritin – correct iron deficiency first! (target ferritin > 200)

2nd Step: If patient remains anaemic, consider EPO: Target Hb 10-12 after 4 months of EPO

Adverse effects of EPO include:

Hypertension with risk of hypertensive crisis

EPO induced seizures

Thrombosis (due to increased haematocrit)

How well did you know this?

Not at all

Perfectly

Proteinuria in CKD

Diagnosis

1st line: Urine ACR (ideally of a first pass morning specimen)

Management of Proteinuria

1st Line: ACE inhibitors are mainstay of Mx (or ARB)

Indications:
CKD and diabetes with ACR > 3mg/mmol
ACR > 70mg/mmol

Hypertension - ACEi 1st line regardless of age/ethnicity
Additional Mx: SGLT2-inhibitors

NICE recommend dapagliflozin in patients with CKD with an eGFR of 25-75 at the time of commencing treatment, and have either:

Or urine ACR > 22.6 mg/mmol OR
T2DM
It must be used as an add-on to highest tolerated dose of ACEi/ARB

How well did you know this?

Not at all

Perfectly

Chronic Kidney Disease
CKD is a broad term, describing a chronic, irreversible decline in renal function

. Diabetes and hypertension are the commonest causes.

Diabetic Nephropathy

The commonest cause of end-stage renal failure (ESRF) in the Western world.

Pathophysiology involves

Increased Glomerular capillary pressures
Basement membrane glycosylation

Histology

Basement membrane thickening
Kimmelstiel-Wilson nodules

How well did you know this?

Not at all

Perfectly

Chronic Kidney Disease
CKD is a broad term, describing a chronic, irreversible decline in renal function

. Diabetes and hypertension are the commonest causes.

Diabetic Nephropathy

The commonest cause of end-stage renal failure (ESRF) in the Western world.

Pathophysiology involves

Increased Glomerular capillary pressures
Basement membrane glycosylation

Histology

Basement membrane thickening
Kimmelstiel-Wilson nodules

How well did you know this?

Not at all

Perfectly

Nephrotic Syndrome
A renal syndrome resulting from damage to the glomerular basement membrane, endothelial surface or podocytes.

Clinical Features

Nephrotic syndrome - a triad of:

Proteinuria (>3g/24hrs)
Hypoalbuminaemia (albumin < 30)
Oedema

Additional features may include:

Increased risk of thrombosis - due to renal loss of AT3/protein C/S

May present with DVT/PE or renal vein thrombosis (pain, haematuria)

Hypercholesterolaemia

Infection
Immunosuppressed due to urinary loss of immunoglobulins

How well did you know this?

Not at all

Perfectly

Causes of nephrotic syndrome

Causes of Nephrotic Syndrome

There are 3 main causes of nephrotic syndrome:

Glomerulonephritis - most common (80%)

Minimal change disease – Children

Membranous glomerulonephropathy - Adults

Focal segmental glomerulosclerosis - patients with HIV, heroin users

Systemic disease - SLE, amyloidosis (AA)
Drugs - gold, penicillamine

How well did you know this?

Not at all

Perfectly

Nephritic Syndrome
Another important renal syndrome presenting with a triad of:

Haematuria
Hypertension
Proteinuria (subnephrotic), oedema

Plus acute renal failure (oliguria/elevated creatinine etc)

Causes of nephritic syndrome

Systemic causes

-Post-streptococcal glomerulonephritis
-Hepatitis C
-IgA vasculitis
-malaria
-sle

Renal causes

-Membranoproliferative glomerulonephritis

-IgA Nephropathy (Berger’s disease)

-Rapidly progressive (crescentic) glomerulonephritis
1.Goodpasture’s disease
2.ANCA positive vasculitis – e.g. GPA

How well did you know this?

Not at all

Perfectly

Glomerulonephritis

Inflammation of the glomerulus (blood vessel network within Bowman’s capsule).

There are multiple causes of glomerulonephritis (below), each classically presenting with either nephrotic or nephritic syndrome

Glomerulonephritis Presenting with Nephrotic Syndrome

Membranous glomerulonephropathy - Typically adults - Treat with ACEi
Minimal change disease - Typically children - Treat with steroids
Focal segmental glomerulosclerosis

How well did you know this?

Not at all

Perfectly

Membranous Glomerulonephritis

The commonest cause of GN in adults

Question with nephrotic syndrome in an adult? Suspect membranous glomerulonephritis!

Causes

Idiopathic, hepatitis B, malaria, cancer

Key features

Nephrotic syndrome

Antiphospholipase A2 antibodies are often positive

Renal biopsy
Electron microscopy - spike and dome appearance with a thickened basement membrane

Management

ACE inhibitor / ARB indicated for ALL patients - to reduce proteinuria

If severe, consider steroids/ cyclophosphamide

Minimal change disease

Pathophysiology

T-cell mediated damage to the GBM results in loss of anions, reducing the electrostatic charge of the GBM –> increased glomerular permeability –> proteinuria

The commonest cause of glomerulonephritis in children

Question with nephrotic syndrome in a child? - Suspect minimal change disease!

Causes

Idiopathic, Hodgkins lymphoma, EBV, NSAIDs
Biopsy

Normal glomeruli (hence “minimal change”) seen on light microscopy
Electron microscopy: podocyte fusion

Management

STEROIDS –– 80% of patients are steroid responsive
Steroid resistant patients – consider cyclophosphamide

3. Focal Segmental Glomerulosclerosis Presentation: Nephrotic syndrome

Causes: HIV, HEROIN USE, Alport’s syndrome Biopsy: Focal segmental sclerosis with hyalinosis Management: Steroids/ immunosuppressants Complications: High recurrence rate following treatment or even after renal transplantation

Glomerulonephritis with Mixed Nephrotic/Nephritic Picture A mixed picture (nephritic/nephrotic) can occur with: membranoproliferative glomerulonephritis diffuse proliferative glomerulonephritis (SLE)

1. Membranoproliferative (mesangiocapillary) Glomerulonephritis Causes: cryoglobulinaemia, Hep C, partial lipodystrophy Bloods: C4 level is low Management: Steroids 2. Diffuse proliferative glomerulonephritis – Lupus Nephritis A distinct type of glomerulonephritis which is associated with systemic inflammatory diseases, most commonly SLE – LUPUS NEPHRITIS Histology: Immune complex despoition with a wire loop appearance

Glomerulonephritis Presenting with Nephritic Syndrome

1. IgA nephropathy (Berger's disease) Young adults with haematuria post URTI (may have associated HSP) 2. Rapidly progressive / crescentic glomerulonephritis Causes: Goodpasture's / ANCA positive vasculitis Results in rapidly progressive acute renal failure

1. IgA Nephropathy (Berger’s disease) Pathophysiology Immune complex (IgA+C3) mediated damage to the basement membrane results in haematuria and renal insufficiency Hence often develops immediately after or during an immune response ( URTI/GI infection)

Clinical Features Macroscopic haematuria in young adult 1-2 DAYS after an URTI Timing is an important differentiator vs post-strep GN which presents 1-2 weeks post URTI Subnephrotic proteinuria Management ACEi/ARB if significant proteinuria Steroids considered if deteriorating renal function

Rapidly Progressive (Crescentic) Glomerulonephritis (RPGN)

Causes Goodpasture’s ANCA positive vasculitis – including granulomatosis with polyangiitis Presentation: Haematuria, hypertension, ARF, haemoptysis/SOB, URT involvement (GPA) Histology Glomeruli – epithelial crescents

Goodpasture's Syndrome Pathophysiology IgG anti-GBM antibodies target type 4 collagen within the… Glomerular basement membrane - RPGN – haematuria, hypertension, AKI Lungs - Pulmonary haemorrhage – haemoptysis, hypoxia

Renal biopsy: IgG linear deposits at basement membrane Management Steroids, immunosuppressants Plasma exchange

2. Rapidly Progressive (Crescentic) Glomerulonephritis (RPGN)

2. Rapidly Progressive (Crescentic) Glomerulonephritis (RPGN) Causes Goodpasture’s ANCA positive vasculitis – including granulomatosis with polyangiitis Presentation: Haematuria, hypertension, ARF, haemoptysis/SOB, URT involvement (GPA) Histology Glomeruli – epithelial crescents

Goodpasture's Syndrome

Pathophysiology IgG anti-GBM antibodies target type 4 collagen within the… Glomerular basement membrane - RPGN – haematuria, hypertension, AKI Lungs - Pulmonary haemorrhage – haemoptysis, hypoxia Renal biopsy: IgG linear deposits at basement membrane Management Steroids, immunosuppressants Plasma exchange

Glomerulonephritis with Mixed Nephrotic/Nephritic Picture

A mixed picture (nephritic/nephrotic) can occur with: membranoproliferative glomerulonephritis diffuse proliferative glomerulonephritis (SLE)

Membranoproliferative (mesangiocapillary) Glomerulonephritis Causes: cryoglobulinaemia, Hep C, partial lipodystrophy Bloods: C4 level is low Management: Steroids

Diffuse proliferative glomerulonephritis – Lupus Nephritis A distinct type of glomerulonephritis which is associated with systemic inflammatory diseases, most commonly SLE – LUPUS NEPHRITIS Histology: Immune complex despoition with a wire loop appearance

Renal Tubular Acidosis Renal tubular acidosis (RTA) is a collection of disorders of transport of HCO3 and/or H+ within the renal tubules, resulting in a hyperchloraemic metabolic acidosis (with a normal anion gap). RTA is classified into four main types as below.

Key learning Type 1 - Distal RTA Causes: SLE, rheumatoid arthritis, Sjögren’s Complications: Nephrocalcinosis Type 2 - Proximal RTA Causes: Fanconi syndrome, Wilson’s, cystinosis Complications: Osteomalacia Type 4 - Hyperkalaemic RTA Causes: Hypoaldosteronism Bloods: HypERkalaemia

Back Renal Tubular Acidosis Renal tubular acidosis (RTA) is a collection of disorders of transport of HCO3 and/or H+ within the renal tubules, resulting in a hyperchloraemic metabolic acidosis (with a normal anion gap). RTA is classified into four main types as below. Key learning Type 1 - Distal RTA Causes: SLE, rheumatoid arthritis, Sjögren’s Complications: Nephrocalcinosis Type 2 - Proximal RTA Causes: Fanconi syndrome, Wilson’s, cystinosis Complications: Osteomalacia Type 4 - Hyperkalaemic RTA Causes: Hypoaldosteronism Bloods: HypERkalaemia Anion Gap The anion gap can be calculated with, or without the potassium as follows: Without including potassium: Anion Gap = Sodium − (Chloride + HCO3) The normal range for the anion gap using this formula is approximately 8-12 mmol/L. Alternatively, with the potassium: Anion Gap = (Sodium + Potassium) − (Chloride + HCO3) The normal range for the anion gap using this formula is approximately 10-18 mmol/L.

Pathophysiology The proximal convoluted tubule is responsible for the reabsorption of filtered bicarbonate. The distal tubule is responsible for the excretion of acids. Abnormalities in these processes result in decreased HCO3 reabsorption or impaired H+ excretion, leading to metabolic acidosis.

Type 1 (Distal RTA) Pathophysiology and Causes Pathology: Failure of the distal tubule to excrete H+/acidify urine. Causes: SLE, rheumatoid arthritis, Sjögren’s syndrome. Clinical Features Growth retardation in children. Recurrent kidney stones.

Bloods and Investigation Findings Metabolic acidosis with normal anion gap. Hypokalaemia. Urine pH > 5.5 despite systemic acidosis. Complications Nephrocalcinosis. Management Alkali therapy with sodium bicarbonate or potassium citrate. Potassium supplementation if required.

Type 2 (Proximal RTA) Pathophysiology and Causes Pathology: Failure of the proximal tubule to reabsorb HCO3. Causes: Fanconi syndrome, Wilson’s disease, nephrotic syndrome, cystinosis (most common cause in children). Clinical Features Growth retardation in children. Osteomalacia or rickets. Polyuria and dehydration. Bloods and Investigation Findings Metabolic acidosis with normal anion gap. Hypokalaemia. Generalised aminoaciduria, glycosuria, and phosphaturia.

Complications Osteomalacia - Chronic bicarbonate loss leading to demineralisation of bones. This is often associated with Fanconi syndrome, which involves multiple proximal tubule defects leading to substantial phosphate loss, further contributing to bone demineralisation. Management Large doses of oral bicarbonate. Potassium and phosphate supplements. Treat underlying cause.

Type 4 (Hyperkalaemic RTA) Pathophysiology and Causes Pathology: Hypoaldosteronism resulting in reduced proximal tubule excretion of ammonium, decreasing urine buffering capacity. Causes: Addison’s disease, spironolactone, diabetes mellitus.

Clinical Features Mild to moderate metabolic acidosis. Often asymptomatic until severe. Bloods and Investigation Findings Metabolic acidosis with normal anion gap. Hyperkalaemia. Urine pH < 5.5. Management Dietary potassium restriction. Fludrocortisone in cases of aldosterone deficiency. Sodium bicarbonate if acidosis is severe. Diuretics (e.g., thiazides) to reduce serum potassium.

Type 3 (Combined Proximal and Distal RTA)

Type 3 RTA is now rarely used as a separate classification and is considered a variant of Type 1 or 2. Pathology: Carbonic anhydrase deficiency Bloods: Hypokalaemia

Renal vascular disease Renal artery stenosis encompasses disorders that affect the blood vessels of the kidneys, leading to impaired renal function. Two important causes include atherosclerosis (more common) and fibromuscular dysplasia (FMD).

Atherosclerotic Renal Artery Stenosis Atherosclerosis is a common cause of renal artery disease, characterised by the gradual buildup of plaque within the renal arteries, leading to stenosis and impaired renal perfusion. It accounts for the vast majority of cases (95%). Clinical Features Treatment resistant hypertension Progressive renal impairment Flash pulmonary oedema Creatinine rise > 15% after commencing ACEi Investigation Findings Diagnostic evaluation includes renal artery duplex ultrasound, CT angiography, or MRA to assess the degree of stenosis. Renal arteriography provides definitive confirmation. Management Lifestyle modifications, antihypertensives Revascularisation - balloon angioplasty +/- stenting or surgical bypass

Fibromuscular Dysplasia (FMD) Fibromuscular dysplasia (FMD) is a non-atherosclerotic, non-inflammatory vascular disease that primarily affects medium-sized arteries, including the renal arteries. Pathophysiology FMD involves abnormal cellular growth within the arterial wall, leading to the formation of fibrous tissue and smooth muscle cells. This results in the characteristic "string of beads" appearance on angiography due to alternating stenotic and dilated segments.

Clinical Features Early onset / resistant hypertension Flash pulmonary oedema Progressive renal impairment Creatinine rise > 15% after commencing ACEi Investigation Findings Magnetic resonance angiography - gold standard. "string of beads" appearance Figure 210: Fibromuscular dysplasia "string of beads" appearance on angiography. CC BY 2.0. Management Antihypertensives Endovascular intervention - balloon angioplasty, stenting, surgical revascularisation.

Immunosuppressant medications The advent of effective immunosuppressive agents has significantly reduced the risk of renal transplant rejection. Ciclosporin

Cyclosporine Mechanism of action: Inhibits calcineurin, a phosphatase mediating T cell activation Adverse effects Hypertension Hyperglycaemia Nephrotoxic

Tacrolimus Mechanism of action: Inhibits calcineurin Side effects include: Hypertension Nephrotoxic Hyperglycaemia /Impaired glucose tolerance / diabetes Mycophenolate Mofetil Mechanism: Inhibits inosine monophosphate dehydrogenase, reducing purine synthesis which limits proliferation of B & T lymphocytes Side effects: Marrow suppression Gastrointestinal side effects - diarrhoea, abdominal cramps etc.

Sirolimus Mechanism: Blocks IL-2 receptor inhibiting T cell proliferation Side effects: Hyperlipidaemia Monoclonal antibodies Examples: Daclizumab, Basiliximab Mechanism: Inhibit IL-2 receptors Adverse effects Accelerated cardiovascular disease - hypertension, dyslipidemia and impaired glucose tolerance MALIGNANCY – non-melanoma skin cancer - squamous cell cancer & basal cell cancer. Nephrotoxic – monitor renal function

Other Post Transplant Complications Renal artery thrombosis Features: Sudden, complete loss of urine output Renal artery stenosis Features: Hypertension, peripheral oedema, graft dysfunction Management: Angioplasty of affected vessel Renal vein thrombosis Features: Reduce urine output, haematuria, pain and swelling over the site of the graft

Urinary leak Features: Declining urine output, abdominal pain, fever, declining renal function Investigations: USS shows a perigraft collection Lymphocoele Features: abdominal mass +/- compression of the ureter Very common – 5-10% of transplants Management: percutaneous drainage of lymphocele

Renal Transplant - Complications & Immunosuppression Graft Rejection Rejection occurs when the host’s immune system identifies the allograft as foreign, triggering an immune response. The frequency of this complication has been reduced by the advent of immunosuppressants & accurate HLA matching.

Hyperacute rejection Pathology: Mediated by preformed IgG antibodies vs ABO or HLA antigens from the allograft --> necrosis and thrombosis of vessels. Timeline: Minutes to hours following transplant. Management: Graft removal Acute rejection Pathology: T cell mediated rejection (CD8+) Timeline: Occurs during the first 6 months Causes: HLA mismatch, Cytomegalovirus Management: Steroids, immunosuppression Chronic rejection Pathology: A combination of antibody, and cell mediated responses resulting in allograft fibrosis. Timeline: More than 6 months after transplantation