RENAL FAILURE
AWONIYI O. F.
ACUTE KIDNEY INJURY (ARF)
• Acute renal failure (ARF) is a clinical syndrome in which a sudden
deterioration in renal function results in the inability of the
kidneys(bilateral kidney insult) to maintain fluid and electrolyte
homeostasis.
• In 2002, the Acute dialysis quality initiative(ADQI) was created with
the primary goal of developing a consensus and evidence based
guidelines for the treatment and prevention of AKI, hence the RIFLE
criteria was born.
• Was proposed to stratify the severity of AKI
RIFLE criteria
STAGE GFR criteria UO criteria
RISK SCr Increased 1.5-1.9 times <0.5ml/kg/hr over 6hrs
baseline OR
GFR of less than 25%
INJURY SCr increased 2-3 times of baseline <0.5ml/kg/hr over 12hrs
OR
GFR of less than 50%
FAILURE SCr > 3X of baselin OR <0.3ml/kg/hr over 24hrs
GFR <75% of baseline OR OR
SCr >/= 4mg/dl Anuria(12hrs)
LOSS OF Persistent loss of kidney function >
FUNCTION 4weeks
ESRD Complete loss of kidney function >
3month
THE AKIN CRITERIA
I. Abrupt(within 48 h) reduction of kidney function currently defined
as an absolute increase in serum creatinine of >0.3mg/dl or >100-
200% increase in serum creatinine frome baseline or <0.5ml/kg/hr
for more than 6hrs.
II. A percentage increase in serum creatinine >200-300% or urine
output of <0.5ml/kg/hr for > 12hrs
III. An absolute increase in serum creatinine of at least 4mg/dl or an
increase of > 300% from baseline or a urine output of < 0.3ml/kg/hr
for >24hrs or anuria for 12hrs
• AKI can be community or hospital acquired
• 70% of cases are community acquired
• 30% of cases are hospital acquired
• In temperate region it is mostly hospital acquired
TYPES OF AKI
• Oliguric AKI: urine output is >/= 0.5ml/kg/hr OR <250ml/m2/day
• Non-Oliguric AKI: urine output is > 0.5ml/kg/hr OR > 250ml/m2/day
in the absence of diuretic use
• Anuric AKI The urine output is < 0.39ml/kg/hr OR <20ml/m2/day in
the absence of obstructive uropathy
PATHOGENESIS
• PRE-RENAL
• INTRINSIC RENAL
• POSTRENAL
PRE-RENAL causes
•Prerenal ARF, also called prerenal azotemia, is characterized by
diminished effective circulating arterial volume, which leads to
inadequate renal perfusion and a decreased glomerular filtration rate
(GFR).
• Evidence of kidney damage is absent.
•Common causes of prerenal ARF include:
1. Gastroenteritis
2. Sepsis
3. Severe malaria
4. G6PD
5. Hemorrhage
6. severe hypoalbuminemia
7. cardiac failure
INTRINSIC RENAL
•Includes a variety of disorders characterized by renal parenchymal
damage, including sustained hypoperfusion/ischemia.
Causes include:
1. AGN
2. Renal burkit lymphoma
3. Nephrotic syndrome
4. Haemolytic uremic syndrome/thrombotic thrombocytic purpura
5. Henoch schonlein purpura
6. Nephrotoxin:Tacrolimus, cyclosporine A, NSAIDS, use of mercury containg
cream, consumption of cele water.
7. Tumor lysis syndrome
POST RENAL CAUSES
• Includes a variety of disorders characterized by obstruction of the
urinary tract which may include
1. Posterior urethral valves
2. Ureteropelvic junction obstruction
3. Ureterovesicular junction obstruction
4. Urinary bladder rhabdomyosarcoma
5. Blocked urethral catheter
CLINICAL MANIFESTATION
• A carefully taken history is critical in defining the cause of
ARF
• Some clinical manifestation include
• Malaise
• Anorexia
• Vomiting
• Apathy
• Diminished urine volume
• Early morning facial puffiness that regresses as the day goes by
• Generalized edema and ascities
• Bleeding diathesis(in sever cases)
CLINCAL MANIFESTATION
• Seizure due to uremia
• CCF
• Acidotic breathing
• ON PHYSICAL EXAMINATION
• Tachycardia,
• dry mucous membranes,
• poor peripheral perfusion
• Peripheral edema,
• rales,
• cardiac gallop
OTHERS
• The presence of a rash and arthritis may suggest systemic lupus
erythematosus (SLE) or Henoch-Schönlein purpura nephritis.
• Palpable flank masses may suggest renal vein thrombosis, tumors, cystic
disease, or urinary tract obstruction
• Peripheral edema, rales, and a cardiac gallop suggest volume
overload and the possibility of intrinsic ARF
• ARF from glomerulonephritis or ATN
SOME CLINICAL SCENARIO
• An infant with a 3-day history of vomiting and diarrhea most likely has
prerenal ARF caused by volume depletion
• A 6-yr-old child with a recent pharyngitis who presents with periorbital
edema, hypertension, and gross hematuria most likely has intrinsic ARF
related to ………………………………….
• A critically ill child with a history of protracted hypotension and exposure
to nephrotoxic medications most likely has ………………………………..
• A neonate with a history of hydronephrosis on prenatal ultrasound and a
palpable bladder most likely has congenital urinary tract obstruction,
perhaps related to ……………………………………
INVESTIGATION
A. URINALYSIS
• Will reveal the presence of epithelia cells
• Low specific gravity
• Low urine osmolality (normal value is 800-1300 mOsm of water)
• Protenuria(if the cause is AGN)
• RBCs
B. SERUM CHEMISTRY
• Will reveal
• Hyponatreamia, hyperkalemia, hypocalcemia, hperphosphatemia,
hypermagnesemia
• Uremia, hypercreatinaemia, hyperuricemia,
• Serum protein is normal except in protein loosing nephropathy
• Cholesterol usually normal except in nephrotic syndrome
• GFR is low (normal GFR is 86 – 162ml/min/1.73m2)
C.24hr urine for Na+, Ca+, phosphate, uric acid, urea, creatinine and
protein
D.Random blood and urine collection for FeNa
E.Renal ultrasound will reveal mild to moderate kidney enlargment
F.Micturating cystourethrography is done if it is due to obstructive
uropathy
G.Urine culture for UTI
H.Blood film for malaria parasite
TREATMENT
• Treatment of AKI can be divided into 3
A.Management of Oliguric phase(for 10 days)
• Restrict fluid intake to insensible fluid loss
• 24hr urine + ongoing losses
• Fluid should be salt free and potassium free
• Infection should be treated with antibiotics
• Allopurinol is given to correct hyperuricemia(300mg/m2/day in 3 divided
doses) OR
• Rasburicase to dissolve whatever uric acid that has been produced in the
patient
• Aminophylline infusion- 5mg/kg is added to 10% solution DW infusion and
allow to run slowly for 24hr up to a maxium of 3days
• Salbultamol can be given IV 0.125 – 0.25 to push K+ back into intracellular
compartment
• Calcium lactaate/carbonate
INDICATION FOR DIALYSIS
CLINICAL INDICATION
• Pulmonary edema
• Altered sensorium
• Seizures from uremia/hypertension
• Stage II hypertension not responsive to drug
• Bleeding diathesis
LAB INDICATION
• Hyperkaleamia > 6.5mmol/L
• Urea levels of at least 25mmol/L
• SCr levels of at least 500umol/L
• Serum biocarbonate levels less than 12-15mmol/L
• Serum phosphate level in excess of 1.7mmol/L
B. Management of the recovery phase(for 10 days)
• During this phase px makes improvement in the production of urine
• Clinical sate of patient is better
• There is risk of severe dehydration and electrolyte derangement
from excessive loss in urine
• Routinely Hartmann’s solution is given to run as infusion until px
condition improves
C. Management of Recovery phase(for 10 days)
• All the biochemical derrangement and clinical features resolves and
px returns to normal state of health over the ten day period
COMPLICATIONS
• Aneamia
• Pulmonary oedema
• CCF
• Uremic encephalopathy
• Sepsis
• Bleeding diathesis
PROGNOSIS
• Mortality rate may be as high as 50% in community acquired AKI,
while for hospital acquired mortality rate is 100%
IN OAUTHC
• Community acquired AKI =42%
• Hospital acquired AKI = 30%
• Generally in px that survive the illness condition is reversible
A few px with stage 3 AKI progress to CKD and ESKD
CHRONIC KIDNEY DISEASE
• CKD is a disorder of kidney function and /or proteinuria with or
without urine sediment lasting at least 3month
• It is progressive and irreversible leading to ESKD if untreated
• Stages of CKD are recognized based in the reconmmnedation of the
Kidney disease Outcome Quality initiative guidelines
STAGING OF CKD
STAGING DESCRIPTION GFR
(ml/min/1.73m2)
1. >/= 90 Normal kidney function
2. 60-89 Mild renal insufficiency
3. 30-59 Moderate renal
insufficiency
4. 15-29 Severe reduction in renal
function
5 <15 ESRD
DIAGNOSTIC CRITERIA FOR CKD
1. Presence of bilateral structural kidney anomaly which may be
congenital or acquired in the setting of a normal kidney function
with or without proteinuria
2. Proteinuria of at least 3 month duration with or without sediments
3. A reduction in GFR for at least 3 month with or without proteinuria
CAUSES
• Chronic glomerulonephritis
• PUV
• Bilateral chronic pyelonepritis
• Infantile polycystic kidney disease
• Nephrotic syndrome
• The Pauci Immune vasculitides
• Churg Strauss syndrome
• Wegners granulomatosis
• Microscopic polyangitis
• Lupus nephritis
• HUS
• Duplex kidney with duplex collecting duct
Clinical manifestation
1. Misery
2. Apathy
3. Easy fatiguability
4. Long standing hx of exercise intolerance
5. Long standing hx of bone pain
6. Long standing hx of nausea and vomiting
7. PEM
8. Pruritus
9. Blurring vision
10. Headache
11. Palpitation
12. Pallor
The above symptoms are non-specific. As condition worsens, these
initial features becomes accentuated by
1.Increased vomiting
2.Drowsiness
3.Hiccups
4.Polydipsia initially followed by dehydration
5.Polyuria initially then edema and oliguria
6.CCF
7.HTN
8.Growth retardation
9.Seizures
10.CKD
LAB FEATURES
• Low haematocrit
• Hypocalcaemia, hyponatraemia, hyperphosphatemia, hyperkalemia
• Uremia, protenuria, hypoalbulminaemia
• Increased cholesterol, HDL, LDL and TAG
• Increased GH, Insulin like GH, PTH
• Decreased Vit D.
RADIOLOGICAL FEATURES
• CXR show enlarge heart
• Cardiac echo may reveal LVH
• Carotid or femoral artery echo may reveal hypertrophy of the tunica
media and intima
• X-ray of the hand and wrist revel periosteal erosion and epiphyseal
cupping indicating renal osteodystrophy
• Asymetrical sunken kidney indicate chronic pyelonephritis
TREATMENT
1. Correct aneamia
• Treat mild or moderate anemia with hematinics – folics acid, vit Bco,
elemental iron(6mg/kg/day)
• Vit A should not be given to CKD px
• Give rhuEPO 100-200u/kg/wk in 2 divided doses subcutaneously for 6week
thereafter give monthly
• In severe aneamia trasnfuse px and maintain on heamtinic and EPO regimen
2. Correct malnutrition
• Px is maintained on 400Kcal/m2/day protein intake and intake
should be of high biologic value
3. Treatment of proteinuria
• Proteinuria is nephrotoxic
• It should be treated with ACE/ARB/Aldosterone receptor blocker
4. Treatment of hypertension
• Drug combination include ACEI/AR/spironolactone to control the
blood pressure and to reduce the size of the kidney
• NB: Always monitor the serum creatinine when you give
ACEIs/ARBs because the can cause AKI
5. Anemia: Transfuse if severely anemic
6. Dyslipidemia: HMGCoA reductase inhibitor e.g fluvastatin
7. Hypocalemia and hyperphospatemia : are treated with phospate
binder e.g calcium lactate, calcium acetate and calcium carbonate
8. Growth retardation : correct anemia, correct proteinuria, abort
proteinuria and correct metabolic derrangment(after all thses had
been done with no improvement prescribe recombinant hormone
therapy)
9. Dialysis: Px with stage 5 CKD will need daily hemodailysis until
condition stabilizes and then 3X/week or px can be maintain on
CAPD/CCPD
10. TRANSPLANTATION : The peak of management of CKD stage 5
CONCLUSION
• Kidney failure is mainly determine by decrease in GFR
• AKI is reversible if treated promptly
• AKI can progress to CKI is irreversible but can be managed
• CKI not well managed can progress to ESRD
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