2. Acute kidney injury/ acute renal failure
Definition
Significant deterioration
Of kidney function
Occur over hours or days
Manifested as abrupt increased of cr and urea
Important features
Oliguria (<400ml/24h)
Complications
Volume overload
K+ incr
Metabolic acidosis
Problem arised
Isolated problem
OR
More commonly: severe illness, sepsis, trauma, surgery, nephrotic drugs
Epidemiology
Dm, hpt, elderly
3. Causes
1.pre-renal (impaired perfusion HYPOPERFUSION of kidney w blood>autoreg to maintain
gfr>fail to autoreg)
{hypovolemia, hypotension}
-sepsis (systemic vasoD)
-cirrhosis
-congestive cardiac failure
-renal artery stenosis
-limited renal blood flow (impaired cardiac pump efficiency & vascular ds)
-ace & nsaids (impaire autoreg)
2. Intrinsic
Acute tubular necrosis-damage of renal tubular cells dt
-ischaemia (2’ to hypoperfusion)
-vascular problem: vasculitis, cholesterol emboli, hemolytic-uremic synd, thrombotic
thrombocytopenic purpura, GN, interstitial nrphritis, malignant incr bp
-nephrotoxins (drugs like aminoglycosides; amphotericin B; tetracycline, radio contrast agent,
uric acid crystals, hemoglobinuria, myeloma)
3.post-renal
UTI
*hemolytic uremic syndrome: primarily a disease of infancy and early childhood and is
classically characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia,
and acute renal failure.
4. Presentation
• The presentation will depend on the underlying cause and severity of AKI. There may be no symptom
or signs, but oliguria (urine volume less than 0.5 ml/kg/hour) is common. There is an accumulation o
fluid and nitrogenous waste products demonstrated by a rise in blood urea and creatinine.
Symptoms
• Urine output:
– AKI is usually accompanied by oliguria or anuria. However polyuria may occur due to either
reduced fluid reabsorption by damaged renal tubules, or the osmotic effect of accumulated
metabolites.
– Abrupt anuria suggests an acute obstruction, acute and severe glomerulonephritis, or acute ren
artery occlusion.
– Gradual diminution of urine output may indicate a urethral stricture or bladder outlet obstructio
eg, benign prostatic hyperplasia.
• Nausea, vomiting.
• Dehydration.
• Confusion.
Signs
• Hypertension.
• Abdomen: may reveal a large, painless bladder typical of chronic urinary retention.
• Dehydration with postural hypotension and no oedema.
• Fluid overload with raised jugular venous pressure (JVP), pulmonary oedema and peripheral oedema
• Pallor, rash, bruising: petechiae, purpura, and nosebleeds may suggest inflammatory or vascular dise
emboli or disseminated intravascular coagulation.
• Pericardial rub.
5. 1. When to suspect chronic renal failure?
A: -comorbidity (dm, hpt)
-long duration of sx
-abN blood tests
-USS –small kidney (<9cm) w incr echogenicity
(absence of anemia/HYPOca2+/HYPERpo4-acute renal
failure but this may not b true)
2. Why urinary tract obstruction imp to b identified
A: -Uri tract obstr is reversible
-prevent permanent renal damage
6. Chronic renal failure
Definition
Kidney damage for =/> 3 months based on findings of abN structure or function
OR
Gfr <60ml/min/1.73m2 for >3 months w or w/o evidence of kidney damage
Classification (stage)
1(>90) N or high gfr (w evidence of renal damage)
2(60-) slight low gfr (w)
3a(45-) moderate low gfr (w or w/o)
3b(30-)
4(15-) severe low gfr (w or w/o)
5(<15) established renal failure
*end stage renal failure
-gfr<15ml/min/1.73m2
-need for renal replacement therapy (dialysis/transplant)
8. Signs and symptoms
Signs of metabolic acidosis in stage 5 CKD include the following:
• Protein-energy malnutrition (group of related disorders that
include marasmus, kwashiorkor, and intermediate states of
marasmus-kwashiorkor.)
• Loss of lean body mass
• Muscle weakness
Signs of alterations in the way the kidneys are handling salt and water
in stage 5 include the following:
• Peripheral edema
• Pulmonary edema
• Hypertension
(fluid overload cause SOB and ankle swelling)
9. Anemia in CKD is associated with the following:
• Fatigue, Reduced exercise capacity, Reduced quality of life
• Impaired cognitive and immune function
• Development of cardiovascular disease, New onset of heart failure or the
development of more severe heart failure, Increased cardiovascular mortality
Other manifestations of uremia in end-stage renal disease (ESRD), many of which
are more likely in patients who are being inadequately dialyzed, include the
following:
(sx common when urea >40mmol/L, N urea is 2.5-7.5 )
• Encephalopathy: Can progress to coma and death
• Pericarditis: Can be complicated by cardiac tamponade, possibly resulting in
death
• Gastrointestinal symptoms: Anorexia, nausea, vomiting, diarrhea
• Peripheral neuropathy, Restless leg syndrome
• Skin manifestations: Dry skin, pruritus, ecchymosis, Platelet dysfunction with
tendency to bleed
• Fatigue, increased somnolence, failure to thrive, Malnutrition
10. PE
1. Inspect-pallor(anaemia)
-skin: yellow skin pigmentation, purpura, bruising, ecchymoses
(uremia), bleeding(plt)
-nails:brown
-proximal myopathy (dm-peripheral neuropathy)
-incr bp (hpt?)
2. Chest
-apex beat deviate(cardiomegaly)
- Pericardial rub(pericarditis 2’ to uremia)
- Pleural effusion, Pulmonary edema
3. Leg
-Peripheral edema
-hypotonia, weakness, arreflexia, sensory loss in stocking
distribution (peripheral neuropathy dt dm)
11. Nephrotic syndrome
• Pathophysiology
– Damage to the structure of glomerular basement membrane
Increased size or number of pore
Passage of more and large molecule
proteinuria
- Reduction of negatively charged component
Negatively charged protein molecules is not repel
proteinuria
12. • Pathophysiology
– Protein loss in urine> hypoalbuminaemia
– Red in oncotic pressure or retention of Na+>
oedema
– Liver prudce more lipoproteins > hyperlipidaemia
15. Minimal change
disease
• Common in children (76%), adult
(20%) male
• Ix – light microscopy normal, electron
microscopy shows fusion of podocytes
• Association – hodgkin lymphoma,
drugs(NSAIDS)
• Remit with steroids but prone to
relapse. If frequent relapse or steroid
dependence, cyclosporin or
cyclophosphamide
• Prognosis – 1% ESRF
• Pathogenesis
– It is postulated that MCD is a disorder of T cells,
which release a cytokine that injures the
glomerular epithelial foot processes (podocytes).
This, in turn, leads to a decreased synthesis of
polyanions. The polyanions constitute the normal
charge barrier to the filtration of
macromolecules, such as albumin. When the
polyanions are damaged, leakage of albumin
follows.
Focal segmental
glomerulosclerosis
• Ix – light microscopy shows scarring of
certain segment (focal sclerosis),
immunofluroescence showsIgM and c3
deposit in affected areas
• Etiology – primary (idiopathic), secondary
(IgA nephropathy, vesicoureteric reflux,
Heroin, vasculitis, sicke cell)
• Mx – corticosteroids, cyclophosphamide
or cyclosporin if steroid-resistance
• Prognosis – 50% ESRF
• Pathogenesis
• viral- or toxin-mediated damage or
intrarenal hemodynamic changes such as
glomerular hyperperfusion and high
intraglomerular capillary pressure. injury
inherent within or directed to podocytes.
Foot process effacement, proliferation of
mesangial, endothelial, and epithelial
cells in the early stages, followed by
shrinkage/collapse of glomerular
capillaries all lead to scarring
(glomerulosclerosis).
16. Membranous nephropathy
• Epidemiology
– 20-30% of nephrotic in adult
• Association
– Malignancy
– Infection
– Autoimmune
– Drugs
• Prognosis
– Risk of renal vain thrombosis
– 40%(oxford) half(kumar) spontaneous remission
– 40% (kumar) CKD
• Diagnostic test
– Renal biopsy: Light microscopy-thickened glomerular basement membrane
– Immunofluorescent : IgG and c3
• Tx
– Steroids + cyclophosphamide, chlorambucil if deteriorate
17. • MCD – electron microscope shows fusion of
podocytes foot process
• Focal segmental glomerulosclerosis – light
microscope shows scarring of the glomerulus;
electron microscope shows fusion of podocyte
foot process
• Membranous nephropathy – thickening of
glomerular basement membrane
18. Membranous
nephropathy
Cause
• 80% idiopathic
• Secondary
– Malignancy –
lymphoma, ca
– Infection – hep b
hep c, malaria,
syphilis, leprosy
– Autoimmune – SLE
– Toxin - gold
MCD
Cause
• Primary
• Secondary
– Malignacy –
lymphoma, ca
– Infection – HIV
– Drugs – NSAIDs
– Toxin –
mercury/ lead
Focal seg
glomerusclerosis
Cause
• Idiopathic
• Secondary
– Vesicoureteric
reflux
– Single kidney,
aging kidney
– Infection – HIV
– Drug - heroin
19. Diabetic nephropathy
• Clinical diagnosis
– Macroalbuminuria
– Hx of DM >10y
– Microvascular complication : DM retinopathy
• Pathology – accumulation of extracellular matrix
cause expansion of mesangial cell and interstitial
expansion
• Ix – renal biopsy shows nodule and hyaline
deposits in glomerular arterioles. Nodule=
kimmelstiel-wilson lesion
