This document presents a case of acute kidney injury (AKI) in a 74-year-old male farmer who presented with reduced urine output. It provides details on his medical history, examination, initial workup and assessment of AKI likely due to toxic nephropathy, dehydration and possible sepsis. The document then provides an introduction to AKI including definitions, epidemiology, etiology and pathophysiology involving pre-renal, intrinsic and post-renal causes. It also discusses approaches to assessing patients with AKI including history, physical examination and investigations.
4. HISTORY
Mr. A.F a 74 year old male farmer who presented to the A&E with complaints of
Reduction in urine output x 7 days
insidious in onset with no associated hx of frequency, urgency or hesitancy. No
hx of poor stream or terminal dribbling. No dysuria, no hx of vomiting or
diarrhea.
Patient had a hx of being stung by a swarm of bees 18hrs prior to the onset of
symptoms
No hx of haematuria, however was noticed to have developed bilateral leg
swelling 3 days prior to presentation as well as hiccups
There was associated hx of high grade fever that developed a day prior to
presentation
5. No associated epigastric pain, no hx of irrational talk or excessive somnolence,
no hx of seizures
No hx of ingestion of herbal medications and no NSAID use
A known HTN on medication ?drug name
Not a known diabetic
6. EXAMINATON
An elderly man, not in any obvious distress, multiple maculopapular, dark
coloured skin lesions on head, face, trunk, upper and lower limbs, afebrile, pale,
anicteric, acyanosed, not dehydrated, with bilateral pitting pedal oedema up to
the knee.
Cardiovascular
PR- 68bpm, regularly irregular
BP- 133/72mmHg
HS- S1 & S2 only
Chest
RR- 20cpm; VBS
SpO2- 98%, room air
7. ABDOMEN
Full, MWR, mild epigastric tenderness
No palpable organomegally
CNS
Conscious and alert; oriented in TPP
No asterixis; no focal neurologic deficit
10. Reviewed the following day with result of EUCr. Noted to be anuric
Facial puffiness
Assessment of AKI 20 to AIN
Subsequently scheduled for HD
Amlodopine 5mg dly
Admitted to the ward
NaHCO3 increased to 1g b.d
11. 3 episodes of vomiting and 2
episodes of passage of loose stool
Placed on ORS, Zinc 50mg dly, IV
ondansetron 8mg stat, 4mg b.d
Developed scrotal oedema
Torsemide 100mg dly
Session of HD
Repeat EUCr
K- 4.6
Urea- 16
Creatinine- 866
12. Had a total of 3 sessions of HD, and was discharged home.
To be seen in clinic in one week with results of repeat EUCr, AP-USS,
urinalysis
14. INTRODUCTION
Acute kidney injury (AKI), formerly called acute renal failure, is
commonly considered as an abrupt decline in renal function,
clinically manifesting as a reversible acute increase in nitrogen
waste products—measured by BUN and serum creatinine
levels—over the course of hours to days.
Resultant failure to maintain fluid, electrolyte and acid-base
homeostasis.
15. DEFINING AKI
Despite a relative insensitivity to acute changes in GFR, most
definitions of acute renal dysfunction have been based on serum
Cr, either as an absolute value or as a change from baseline.
Other definitions have incorporated urine output (UO) or the
need for dialysis support.
16. In 2002, the Acute Dialysis Quality Initiative (ADQI) was created to
develop evidence-based guidelines for the treatment and prevention of
AKI, hence the RIFLE criteria was born.
AKI is stratified into 5 stages, based on severity and duration of
renal injury: Risk, Injury, Failure, Loss, and End-stage disease
17.
18. In 2004, the Acute Kidney Injury Network (AKIN) was formed and
modified RIFLE to incorporate small changes in sCRr occurring
within a 48h period and to remove changes in GFR as diagnostic
criteria
Abrupt (within 48hrs) reduction in kidney function currently defined as
an absolute increase in sCr of ≥0.3 mg/dL (≥26.4 μmol/L) or
A percentage increase in sCr of 50% or more (1.5-fold from
baseline) or
A reduction in urine output (oliguria of < 0.5 mL/kg/h for >6 h)
19.
20. The Kidney Disease Improving Global Outcome (KDIGO) defines
AKI as any of the following:
Increase in sCr by 0.3mg/dL or more within 48 hours or
Increase in sCr to 1.5 times baseline or more within the last 7 days or
Urine output less than 0.5 mL/kg/h for 6 hours
21.
22.
23. There are several biomarkers that are being studied and have
shown to exhibit a great sensitivity and specificity in AKI
diagnosis, a good correlation with RRT requirement, as well as
with mortality
Neutrophil gelactinase associated lipocalin (NGAL)
Kidney injury molecule (KIM-1)
Interleukin-6, -8, and -10
Cystatin-C
N-acetyl-β-glucosaminidase (NAG)
Liver fatty acid binding protein
Retinol binding protein
Matrix
metalloproteinase-9
Proatrial natriuretic
peptide
Neutrophil CDIIb
α-Glutathione -S-
transferase (GST)
25. EPIDEMIOLOGY
AKI is common, occurring in up to 18% of hospitalized patients
An independent risk factor for mortality
In a study in Lagos, sepsis was by far the most common cause of AKI
accounting for 50% of all cases followed by obstructive nephropathy and
gastroenteritis.
28. The hydrostatic pressure gradient across the glomerular
capillary wall is the primary driving force for glomerular
filtration
Autoregulation helps protect the glomerular capillary from
sudden changes in systolic pressure
Autoregulation of glomerular filtration is the result of
three major factors that modulate either afferent or
efferent arteriolar tone: these include
myogenic reflex in the afferent arteriole,
tubuloglomerular feedback, and
angiotensin II-mediated vasoconstriction
29. AETIOPATHOGENESIS
The causes of AKI have traditionally been divided into three broad
categories
Pre-renal AKI
Intrinsic renal AKI
Post-renal AKI
31. PRE-RENAL AKI
Pre-renal AKI is the most common form of AKI. It is the designation for a rise
in sCr or BUN concentration due to inadequate renal plasma flow and
intraglomerular hydrostatic pressure to support normal glomerular filtration.
Accounts for about 40 to 70% of AKI
32. By definition, prerenal AKI involves no parenchymal damage to the kidney and
is rapidly reversible once intraglomerular hemodynamics are restored.
It may coexist with other forms of intrinsic AKI associated with processes
acting directly on the renal parenchyma.
Prolonged periods of prerenal azotemia may lead to ischemic injury, often
termed acute tubular necrosis (ATN)
40. HISTORY
AKI has a long differential diagnosis. Adequate hx can help classify the
pathophysiology of AKI as pre-renal, intrinsic, or post-renal failure, and may
suggest some specific aetiologies
Pre-renal AKI
Commonly present with symptoms of hypovolemia; decreased urine output,
thirst, dizziness, orthostatic hypotension
Elicit hx of volume loss from vomiting, diarrhea, polyuria, haemorrhage.
Hx of orthopnoea, PND in advanced cardiac failure
41. Intrinsic renal AKI
Patients can be divided into those with glomerular etiologies and those with
tubular etiologies of AKI
Nephritic syndrome of hematuria, edema, and hypertension indicates a
etiology for AKI (hx of previous sore throat or skin infections)
Acute tubular necrosis (ATN) should be suspected in any patient presenting after
period of hypotension secondary to cardiac arrest, hemorrhage, sepsis, drug
overdose, or surgery.
Elicit hx of exposure to nephrotoxins; current medications and any recent
radiologic examinations
Pigment-induced AKI should be suspected in patients with possible
rhabdomyolysis (muscular pain, seizure, excessive exercise)
Allergic interstitial nephritis should be suspected with fevers, rash, arthralgias,
exposure to certain medications, including NSAIDs and antibiotics.
42. Post-renal AKI
Suspected in older men with symptoms of urgency, frequency, and
hesitancy (prostatic obstruction)
A history of prior gynecologic surgery or abdominopelvic malignancy
Flank pain and hematuria should raise a concern about renal calculi or
papillary necrosis as the source of urinary obstruction.
Certain medications could be pointers of crystal nephropathy causing
tubular obstruction. The use of acyclovir, methotrexate, triamterene,
indinavir, or sulfonamides implies the possibility that crystals of these
medications have caused tubular obstruction.
43. EXAMINATION
Physical examination can give rise to important clues in diagnosing the
aetiology
Skin
Eyes
Cardiovascular system
Abdomen
Pulmonary system
47. INVESTIGATIONS
Urine tests
Urinalysis!! Dipstick can suggest infection (leucocytes + nitrites);
glomerular disease (blood + protein)
Urine microscopy for casts, crystals and cells. Culture for infection
Blood tests
E&U, FBC, LFT, clotting, ESR
Culture blood if signs of infection
48. Imaging
Renal USS; obstruction, hydronephrosis, cysts, small kidneys, masses
Assess corticomedullary differentiation
CXR if signs of fluid overload
Kidney biopsy
If cause of AKI not apparent based on clinical context, physical
examination, lab & radiologic studies and pre-renal, post-renal and
ischemic or nephrotoxic AKI has been deemed unlikely, and other
possibilities are being considered (glomerulonephritis, vasculitis etc.)
49. PRINCIPLES OF MANAGEMENT OF AKI
General measures (fluid & electrolyte balance)
Treat underlying cause
Manage complications
Renal replacement therapy
50. GENERAL MEASURES
Maintain fluid homeostasis and electrolyte balance
Limit fluid intake to insensible loss and ongoing loss if euvolaemic
Avoid K+-containing fluids unless hypokalemic ; supplements and K+
sparing diuretics
Stop nephrotoxic drugs
NSAIDs, gentamicin, nitrofurantoin
Adjust doses of renally excreted drugs
Contrasts; ensure adequate hydration pre and post procedure
51. TREAT UNDERLYING CAUSE
Pre-renal
Correct volume depletion with appropriate fluids
Treat sepsis with appropriate antibiotics
Ionotropic support if signs of shock
Post-renal
Catheterize and consider CT of renal tract
Refer to urologist if obstruction likely cause (consider stent/nephrostomy
insertion)
Intrinsic renal
Evaluate and manage underlying cause as appropriate
55. Hyperkalemia >6mmol/L
BUN >100mg/dl
Severe metabolic acidosis; pH <7.2
Hypermagnesaemia >4.0mmol/L
Biochemical indications
56. PROGNOSIS
The development of AKI is associated with a significantly increased risk of in-
hospital and long-term mortality, longer length of stay, and increased costs.
Pre-renal AKI, with the exception of the cardiorenal and hepatorenal
syndromes, and post-renal azotemia carry a better prognosis than most
cases of intrinsic AKI
The kidneys may recover even after severe, dialysis-requiring AKI. Survivors
of an episode of AKI requiring temporary dialysis, however, are at extremely
high risk for progressive CKD, and up to 10% may develop end-stage renal
disease
57. CONCLUSION
AKI is a syndrome that rarely has a sole and distinct pathophysiology.
Many patients with AKI have a mixed aetiology where the presence of sepsis,
ischaemia and nephrotoxicity often co-exist and complicate recognition and
treatment.
Furthermore the syndrome is quite common amongst patients without
critical illness and it is essential that health care professionals, particularly
those without specialization in renal disorders, detect it easily.
58. …...the ghost of deceased patients that haunt us, do not
ask why we did not employ the latest fad of clinical
investigations. But they ask “Why did you not test my
Urine?”
Sir Robert Hutchinson
(1871- 1960)
59. REFERENCE
Harrison’s principle of Internal Medicine
Oxford handbook of internal medicine
Schrier RW, Wang W, Poole B, Mitra A. Acute renal failure: definitions, diagnosis,
pathogenesis, and therapy. J Clin Invest. 2004 Jul. 114(1):5-14. [QxMD MEDLINE
Link]. [Full Text].
Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, et al. Acute Kidney
Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit
Care. 2007. 11(2):R31. [QxMD MEDLINE Link]. [Full Text].
Ricci Z, Cruz D, Ronco C. The RIFLE criteria and mortality in acute kidney injury: A
systematic review. Kidney Int. 2008 Mar. 73(5):538-46. [QxMD MEDLINE Link].
The RIFLE considered Baseline SCr is necessary to define and classify AKI; this baseline value is frequently unknown in clinical practice.
AKIN classification only relies on SCr and not on GFR changes; baseline SCr is not necessary in the AKIN classification, and it requires at least two values of SCr obtained within a period of 48 h
RIFLE may not detect 10% of AKIN -identified cases, and AKIN may miss ≈25% RIFLE cases
only one criterion needs to be present to fulfill the definition
ATN itself the end product of an ischaemic or a nephrotoxic injury. Accounts for 80-90% of all intrinsic AKI
Pulm edema: oliguric and anuric AKI, due to impaired salt and water excretion.
Bleeding: Direct hematologic effects from AKI-related uremia include decreased erythropoiesis and platelet dysfunction
Malnutrition: AKI is often a severely hypercatabolic state,
Hypovolemia: can be seen during recovery, the polyuric phase , due to osmotic diuresis from retained urea,
if untreated, can lead to significant volume depletion.