what are the principle functions of the kidney
- eliminate waste materials ]
- regulate fluid and electrolyte balance and acid-base balance
- endocrine function (prostaglandins (inflammtion), erythropoietin (growth hormone for RBC), 1,25-(OH)2-D3 (activated vit d3 is formed in kidney), renin)
which part of the kidney do most kidney diseases affect
- most are associated with abnormalities of the GLOMERULAR CAPILLARY or RENAL TUBULE system
which symptoms can suggest renal tract disease
- dysuria
- haematuria
- urinary retention
- alteration of urine volume (either polyuria or oliguria)
- pain along the renal tract
what is the kidney highly sensitive to
- immune reactions
- this is due to IMMUNE COMPLEXES either forming/ being deposited on glomerular epithelial capillary walls
- this can damage the kidney
what is the cause of kidney diseases affecting the glomeruli
- IMMUNOLOGICALLY MEDIATED disease
what is the cause of kidney diseases affecting the tubules
- TOXIC/INFECTIOUS agents
what is the cause of kidney diseases affecting the INTERSTITIUM (intertubular, extraglomerular, extravascular space of the kidney)
- TOXIC/INFECTIOUS agents
what is the cause of kidney diseases affecting the blood vessels
- DECREASED BLOOD SUPPLY which leads to damage
what causes progression to renal failure
- severe damage to all 4 structures (glomeruli, tubules, interstitium and blood vessels) causes CHRONIC RENAL DISEASES which leads to RENAL FAILURE
what is nephritis
inflammation of any part of the kidney
1) glomerulonephritis (GN)
2) interestitial nephritis
3) pyeloneophritis
describe glomerulonephritis
- general term for a GROUP OF DISORDERS: (bilateral, symmetrical (affects both kidneys) immunologically mediated injury to the glomerulus)
- accounts for 1/3 of cases of TERMINAL RENAL FAILURE
- PRIMARY: kidney is the predominant organ involved (e.g. post-streptococcal glomerulonephritis)
- SECONDARY: systemic diseases with glomerular involvement (eg SLE)
what is the pathogenesis of glomerulonephritis
1) in situ fomation of IMMUNE COMPLEX (antibody-antigen complex forms on the glomerulus)
2) or deposition of circulating immune compex (antibody-antigen binding complex is deposited)
3) or the GLOMERULAR basal membrane acts as ANTIGEN O the antibody binds directly to it causing damage
4) OR cell mediated glomerular damage
- these all cause INFLAMMATION which triggers the SECONDARY MECHANISMS
- secondary mechanisms:there is HYPERCEULLULAROTY (inc proliferation of cells), BASEMENT MEMBRANE THICKENING (can cause dysfunciton of kidney), SCLEROSIS and HYALINISATION (loss of structure)
- these can cause: protein leakage O plasma volume is reduced O cardiac output is DECREASES, leads to HYPOVOLAEMIA. This can cause activation on renin-angiotensin-aldosterone system, which causes Na+ sodium and WATER RETENTION and OEDEMA and HIGH BLOOD PRESSURE (hypertension)
MANIFESTS AS:
1) ACUTE NEPHROTIC SYNDROME (classic kidney inflammation)
2) NEPHROTIC SYNDROME ( characterised by increased renal failure)
3) RENAL FAILURE, ACUTE AND CHRONIC
4) ASYMPTOMATIC PROTEINURIA (milder disease, proteins present in urine)
5) MICROSCOPIC HAEMATURIA (blood in urine)
describe the pathogenesis of acute nephritic syndrome
clinical features
management
- exogenous antigen (eg infetcive agents- group A beta-haemolytic Strep.) or endogenous antigen (eg SLE)
- they cause acute nephritic syndrome
Pathology: diffuse (throughout the entire glomerulus) proliferative glomerulonephritis - hypercellular glomeruli
Clinical features:
- Haematuria (due to damage to glomerulus, blood enters urine)
- Proteinuria (protein in urine due to permeability of glomerulus being increased O proteins leak to urine)
- Hypertension (due to sodium and water retention)
- Oedema (periorbital) (due to retention)
- Oliguria (reduced urine due to filtration is damaged O not enough) & uraemia (kidney clearance is reduced)
Management:
- Supportive measures until spontaneous recovery
- Hypertension: salt restriction, diuretics, vasodilators
- Fluid balance monitoring
- In oliguric with fluid overload, fluid restriction
- Management of life-threatening complications
what is nephrotic syndrome
a different type of GN (Glomerulonephritis)
- damage to the BASAL MEMBRANE can cause nephrotic syndrome
- O there is loss of ELECTROSTATIC BARRIER (which repels ions and proteins) and PHYSICAL BARRIERS (due to tissue damage)
- passage of large molecular weight proteins which should be retained into the glomerular filtrate leads to PROTEINURIA
- due to HIGH PROTEIN LOSS, the plasma lacks protien
- O we have HYPOALBUMINAEMIA
- this causes REDUCED ONCOTIC PRESSUE and thus HYPOVOLAEMIA
- O renin-angiotensin-aldosterone is activated and causes Na sodium and water retention which leads to OEDEMA
- hypoalbumibaemia causes INC SYNTHESIS OF PROTEIN in the liver and abnormal transport of circulating lipid and DECREASED CATABOLISM
- excess lipid causes HYPERLIPIDAEMIA
what is classed as proteinuria
> 3.5g/24 h in adults
what is classed as hypoalbuminaemia
serum albumin <30g/L)
how is proteinuria managed/treated
- Steroids, e.g. prednisolone
- Immunosuppressors e.g. cyclophosphamide
how is hyperlipidaemia managed/treated
if oedema:
- bed rest
- dietary salt restriction
- thiazide diuretic
what is renal failure
Failure of renal excretory function due to depression of GFR (Glomerular filtration rate)
- accompanied to a variable extent by failure of:
- Erythropoietin (EPO) production
- Vit D hydroxylation
- Regulation of acid-base balance
- Regulation of salt & water balance, and blood pressure
what is acute renal failure
aetiology
pathogenesis
- Abrupt deterioration in parenchymal renal function;usually (not invariably) reversible over days or wks
causes:
- Pre-renal (~70%): shock, hypovolemia etc
- Intrinsic renal (~25%): acute tubular necrosis etc.
- Post-renal (~5%): obstruction etc
pathogenesis:
Reduced excretion of nitrogenous waste products (urea) causes →uraemia which leads to INC creatinine
what are the clinical features of acute renal failure
- Early stages often asymptomatic
- Symptomatic when plasma urea> 40mmol/L:
−Oliguria, oedema
−Plasma creatinine rises (by ~ 100mol/day)−Hyperkalaemia & metabolic acidosis
−Uraemic syndrome: anorexia, nausea, vomiting, irritability, seizures, coma
what is the treatment for acute renal failure
- Correct reversible underlying factors eg. volume depletion, nephrotoxic drugs
- Treat hyperkalaemia
- Dialysis - Indications: Hyperkalaemia (> 6.5 mmol/L )
Severe metabolic acidosis (pH<7.2)
Pulmonary oedema
Complications of uraemia: encephalopathy, pericarditis, seizures
what s chronic renal failure
long standing and ususally progressive impairment in renal function
causes:
- diabetes
- hypertension
- glomerulonephritis
- pyelonephritis
- cystic (polysystic) renal disease
- nephrotoxins (eg,NSAIDs, esp phenacetin; heavy metals)
what are the clinical features of chronic renal failure
- insidious
- Often asymptomatic until GFR < 15ml/min
- Symptoms common when serum urea > 40mmol/L
- Uraemic syndrome:
- -> Nervous system (malaise, loss of energy, loss of appetite, insomnia)
- -> Gastrointestinal (nausea, vomiting, and diarrhea)
- -> Dermatological (itching)–
- Nocturia and polyuria
- Oedema
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Nomenclature of disease27
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Aetiology22
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Cell injury, apoptosis and death I22
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Cell injury, apoptosis and death II13
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Thrombosis14
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Embolism, infarction, shock22
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Inflammation I30
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Inflammation II16
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Cellular adaptation and tissue regeneration19
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Blood I30
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Blood II29
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Disorder of WBC45
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Disorder of growth, differentiation and tumours24
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Cardiovascular system and diseases I35
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Cardiovascular system and diseases II30
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Disorders of Haemostasis40
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Liver I and II48
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Respiratory system and diseases I and II52
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Kidney diseases25
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Disorders of the CNS46
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UTI I and II37
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GI39
