Acute kidney injury (AKI), also known as acute renal failure (ARF), is a sudden episode of kidney failure or kidney damage that happens within a few hours CKD is a condition in which the kidneys are damaged and cannot filter blood as well as they should. Because of this, excess fluid and waste from blood remain in the body and may cause other health problems, such as heart disease and stroke.

1. AKI and CKD
Ndlovu

2. Objectives
 Anatomy
 Function
 Acute Kidney Injury (AKI)
 Causes
 Symptoms
 Management
 Chronic Kidney Disease (CKD)
 Causes
 Symptoms
 Dialysis
 Complications

3. Anatomy
 2 Kidneys
 2 Ureters
 Bladder
 Urethra

5. Kidney Function
 Detoxify blood
 Increase calcium absorption
 Calcitriol(1,25 dihydrocholecalciferol)
 Stimulate RBC production
 erythropoietin
 Regulate blood pressure and
electrolyte balance
 renin

8. Classifications
 Acute versus chronic
 Pre-renal, renal, post-renal
 Anuric, oliguric, polyuric

9. Acute Versus Chronic
 Acute
 sudden onset
 rapid reduction in urine output
 Usually reversible
 Tubular cell death and regeneration
 Chronic
 Progressive
 Not reversible
 Nephron loss
 75% of function can be lost before its
noticeable

10. Acute Kidney Injury
 Definition:
– decline in GFR and an inability of the
kidneys to appropriately regulate fluid,
electrolytes, and acid-base homeostasis
– Sudden decline in renal function with
increasing BUN/Cr ratio; with or without
changes in urine output (Johns Hopkins: The Harriet
Lane Handbook, 17th ed. - 2005 )
 Clinical Definition:
– Creatinine > 75 mol/L (0.85 mg/dL)
– Oliguria (<1ml/kg/h) for more than 6 hours
despite aggressive diuretic agent

11. AKI
 Pre-renal = 55%
 Renal parenchymal (intrinsic)= 40%
 Post-renal = 5-15%

13. Causes of AKI
 Pre-renal =
 vomiting, diarrhea, poor fluid intake, fever, use of
diuretics and,
 cardiac failure, liver dysfunction, or septic shock
 Intrinsic
 Interstitial nephritis, acute glomerulonephritis, tubular
necrosis, ischemia, toxins
 Post-renal =
 Congenital Posterior urethral valve
 neurogenic bladder
 bilateral renal calculi

14. STAGING
• KDIGO- RIFLE
• AKIN
• 1. Cr 1.5. UO < 0.5ml/kg/h-
6To12hr.
• 2. Cr 2-2.9 UO < o.5ml/kg/h -
>12hrs
• 3. Cr >3 UO < 0.3ml/kg/h- >24hr

15. Symptoms of AKI
 Decrease urine output (70%)
 Edema, esp. lower extremity
 Mental changes
 Heart failure
 Nausea, vom
 Tachypenic
 Cool, pale, moist skin- Uremic frost

16. AKI Management
 Make/think about the diagnosis
 Treat life threatening conditions
 Identify the cause if possible
 Hypovolemia
 Toxic agents (drugs, myoglobin)
 Obstruction
 Treat reversible elements
 Hydrate
 Remove drug
 Relieve obstruction

17. ARF: Life Threatening
Conditions
 Hyperkalemia
 Volume overload
 Vascular access

18. Hyperkalemia Symptoms
 Weakness
 Lethargy
 Muscle cramps
 Paresthesias
 Dysrhythmias

19. Hyperkalemia & EKG
 K > 5.5 -6
 Tall, peaked T’s
 Wide QRS
 Prolong PR
 Diminished P
 Prolonged QT

21. Hyperkalemia Treatment
 Calcium gluconate (carbonate)
 Sodium Bicarbonate
 Frusemide
 Hemodialysis

22. Take home points
• Acute kidney injury (AKI) describes the situation
where there is a sudden and often reversible loss
of renal function, which develops over days or
weeks and is usually accompanied by a
reduction in urine volume
• Anaemia is common in AKI and may occur as the
result of blood loss, haemolysis or decreased
erythropoiesis.

23. • Biochemical assessment in prerenal AKI usually
reveals evidence of a metabolic acidosis and
hyperkalaemia.
• In established AKI, there is an increased risk of
bleeding and spontaneous gastrointestinal
haemorrhage due to the uraemia

24. Mgt
• Correct hypovolaemia and optimise systemic
haemodynamic status with inotropic drugs if
necessary
• Administer glucose and insulin to correct
hyperkalaemia if K+> 6.5 mmol/L
• Consider administering sodium bicarbonate (100
mmol) to correct acidosis if pH < 7.0 (> 100
nmol/L)
• Administer proton pump antagonists to reduce
the risk of upper gastrointestinal bleeding

25. • Discontinue potentially nephrotoxic drugs and reduce
doses of therapeutic drugs according to level of renal
function
• Match fluid intake to urine output plus an additional 500
mL to cover insensible losses once patient is euvolaemic
• Measure body weight on a regular basis as a guide to fluid
• Requirements
• Ensure adequate nutritional support

26. • Screen for intercurrent infections and treat
promptly if present
• Severe acidosis can be ameliorated with sodium
bicarbonate if volume status allows.
• Restoration of blood volume will correct acidosis
by restoring kidney function.

27. • high protein intake should be avoided.
• This is particularly important in patients with
sepsis and burns who are hypercatabolic
• Typically, the decision to start RRT is driven by
hyperkalaemia, fluid overload or acidosis, uremic
pericarditis/ uremic encephalopathy.

28. • The two main options for RRT in AKI are
haemodialysis and high-volume haemofiltration,
or the hybrid approach of haemodiafiltration.
• Peritoneal dialysis is also an option if
haemodialysis is not available

29. The recovery
• During the recovery phase of AKI, it may be
necessary to provide supplements of
 sodium chloride,
 sodium bicarbonate,
 potassium chloride and
 sometimes phosphate temporarily,
to compensate for increased urinary losses.

30. CKD-
 Definition
is defined as either renal injury
(proteinuria) and/or a glomerular
filtration rate <60 mL/min/1.73 m2
for >3 months

31. CKD
 150–200 cases per million people =
new cases each year
 CKD and ESRD affect more than 2
out of 1,000 people
 Mortality = 20%

32. Causes
 May be acquired or metabolic renal
disease
 Underlying cause correlates closely
with the age of the patient at the
time when the CKD is first detected

33. Causes
 CKD in children younger than 5 yr is most
commonly a result of congenital
abnormalities such as renal hypoplasia,
obstructive uropathy, congenital
nephrotic syndrome, prune belly
syndrome, cortical necrosis, focal
segmental glomerulosclerosis, polycystic
kidney disease, renal vein thrombosis,
and hemolytic uremic syndrome

34. Causes
• After 5 yr of age, acquired diseases (various
forms of glomerulonephritis including lupus
nephritis) and inherited disorders (familial
juvenile nephronophthisis, Alport syndrome)
predominate
• CKD related to metabolic disorders (cystinosis,
hyperoxaluria) and certain inherited disorders
(polycystic kidney disease) may present
throughout the childhood years

35. Generally -causes
• Diabetes mellitus
• Hypertension
• AKI
• Glomerulonephritis
• Infections – HIV
• SLE
• Drugs

36. CKD Symptoms
 Malaise
 Weakness
 Fatigue
 Neuropathy
 CHF
 Anorexia
 Nausea
 Vomiting
Seizure
hiccups
Anemia
Pruritus
Jaundice
Abnormal
heamostasis

37. Acute Problems in CKD
 Relating to underlying disease
 Relating to ESRD
 Dialysis related problems

38. Problems Related to ESRD
 Metabolic – K/Ca
 Volume overload
 Anemia, platelet disorder, GI bleed
 HTN, pericarditis
 Peripheral neuropathy, dialysis
dementia
 Abnormal immune function

39. Dialysis
 ½ of patients with CKD eventually
require dialysis
 Diffuse harmful waste out of body
 Control BP
 Keep safe level of chemicals in body
 2 types
 Hemodialysis
 Peritoneal dialysis

40. Hemodialysis
 3-4 times a week
 Takes 2-4 hours
 Machine filters
blood and
returns it to
body

41. Peritoneal Dialysis
 Abdominal lining filters blood
 3 types
 Continuous ambulatory
 Continuous cyclical
 Intermittent

42. Dialysis Related Problems
 Lightheaded –give fluids
 Hypotension
 Dysrhythmias
 Disequilibration Syndrome
 At end of early sessions
 Confusion, tremor, seizure
 Due to decrease concentration of blood
versus brain leading to cerebral edema

43. Complications of CKD
 Fluid and electrolyte imbalance
(Hyperkalemia, hyponatremia,
hypocalcemia, hyperphosphatemia)
 Metabolic acidosis
 Renal osteodystrophy
 Growth retardation
 Anaemia
 Bleeding tendency and Infection
 Hypertension

44. Take home points
• CKD refers to an irreversible deterioration in
renal function which usually develops over a
period of years
• When death is likely without RRT (CKD stage 5),
it is called end-stage renal disease or failure
(ESRD or ESRF).

45. Disease Proportion Comments
• Congenital and inherited
 5% Polycystic kidney disease,
 Alport’s syndrome
• Renovascular disease
 5% Mostly atheromatous, may be more common

46. • Hypertension 5–20% Causality controversial,
 much may be renal disease
• Glomerular diseases
 10–20% IgA nephropathy is most common

47. • Interstitial diseases 20–30% Often drug-induced
• Systemic inflammatory diseases
 5–10% Systemic lupus erythematosus,
 vasculitis
• Diabetes mellitus 20–40% Large racial and
• geographical differences

48. • Unknown

49. clinic
• Most patients with slowly progressive disease are
asymptomatic until GFR falls below 30 mL/min/1.73 m2
(stage 4 or 5) and some can remain asymptomatic with
much lower GFR values than this.
• An early symptom is nocturia, due to the loss of
concentrating ability and increased osmotic load per
nephron, but this is nonspecific.
• When GFR falls below 15–20 mL/min/1.73 m2, symptoms
and signs are common and can affect almost all body
systems

50. • They typically include
 tiredness or breathlessness, which may, in part, be related
to renal anaemia,
 pruritus,
 anorexia,
 weight loss,
 nausea and vomiting with further deterioration in renal
function
 patients may suffer hiccups

51.  Experience unusually deep respiration related to
metabolic acidosis (Kussmaul’s respiration),
 develop muscular twitching,
 fits,
 drowsiness and coma.
 In both genders, there is loss of libido related,
at least in part, to hypogonadism as a
consequence of hyperprolactinaemia
 Restless leg syndrome

52. • metabolic bone disease may also occur,
including
 osteitis fibrosa cystica,
 osteomalacia and
 osteoporosis

53. Management
• The aims of management in CKD are
 to prevent or slow further renal damage;
 to limit the adverse physiological effects of renal
impairment on the skeleton and on haematopoiesis;
 to treat risk factors for cardiovascular disease;
 to prepare for RRT

54. • Lowering of blood pressure slows the rate at which renal
function declines in CKD, independently of the agent used.
• There is a clear relationship between the degree of
proteinuria and the rate of progression of renal disease,
and strong evidence that reducing proteinuria reduces the
risk of progression.
• Angiotensin-converting enzyme (ACE) inhibitors and
angiotensin II receptor blockers(ARBs) reduce proteinuria
and retard the progression of CKD

55. • There is experimental evidence that restricting
dietary protein can reduce progression of CKD
• Exercise and weight loss may also reduce
proteinuria and have beneficial effects on
cardiovascular risk profile.
• There is some evidence that control of
dyslipidaemia with statins may slow the rate of
progression of renal disease

56. • Recombinant human erythropoietin is effective in
correcting the anaemia of CKD and improving the
associated morbidity- not mortality
• The plasma bicarbonate should be maintained above 22
mmol/L by giving sodium bicarbonate supplements
• Renal replacement therapy (RRT) may be required on a
temporary basis in patients with AKI or on a permanent
basis in CKD
• RENAL TRANSPLANT IS ULTIMATE