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Acute Kidney Injury is a rapid loss of renal function due to damage to the kidneys.

Depending on the duration and severity of AKI, a wide range of potentially life
threatening metabolic complications can occur, including metabolic acidosis as well as
fluid and electrolyte imbalances. A widely accepted criterion for AKI is a 50% or greater
increase in serum creatinine above baseline (< 1mg/dL).

More than 90% of the patients recruited in AKI studies using KDIGO-equivalent criteria
originate from North America, Europe, or Ocenia, although these regions represent less
than a fifth of the global population. However, the pooled incidence of AKI in
hospitalized patients reaches 20% globally with moderate variance between
regions.The lower incidence rates onserved in Asian countries (except Japan) may be
due to a poorer recognition rate, for instance because of less systematically performed
serum creatinine tests. AKI patients in South and Southeastern Asia are younger than in
East Asia and Western countries and present with fewer comorbidities. Asian countries
(and to certain extent Latin America) face specific challenges that lead to AKI:
nephrotoxicity of traditional herbal and less strictly regulated nonprescription medicines,
environmental toxins and tropical infectious diseases. (2016 S. Karger AG, Basel)


Etiology Hypoperfusion Parenhymal Obstruction
BUN Value Increased Increased Increased
Creatinine Increased Increased Increased
Urine Output Decreased Varies, often Varies, may be
decreased decreased, or
sudden anuia
Urine Sodium Decreased to <20 Increased to >40 Varies, often
mEq/L mEq/L decreased to
greater or equal to
20 mEq/L
Urinary Sediments Normal, few Abnormal casts Usually normal
hyaline casts and debris
Urine Osmolality Increased to 500 ~350 mOsm, Varies, increased
mOsm similar to serum or equal to serum
Urine Specific Increased Low Normal Varies

Preventing Acute Kidney Injury are as follows:

1. Provide adequate hydration to patients at risk for dehydration, including:

a. Before, during, and after surgery
b. Patients undergoing intensive diagnostic studies requiring fluid restriction
and contrast agents
c. Patients with neoplastic disorders or disorders of metabolism and those
receiving chemotherapy
2. Prevent and treat shock promptly with blood and fluid replacement.
3. Monitor central venous and arterial pressures and hourly urine output of critically
ill patients to detect the onset of renal failure as early as possible.
4. Treat hypotension promptly.
5. Continually assess renal function (urine output, laboratory values) when
6. Take precautions to ensure that the appropriate blood is administered to the
correct patient in order to avoid severe transfusion reactions, which can
precipitate renal failure.
7. Prevent and treat infections promptly. Infection can produce progressive kidney
8. Pay special attention to wounds, burns and other precursor of sepsis.
9. To prevent infections from ascending in the urinary tract, give meticulous care to
patients with indwelling catheters.
10. To prevent toxic drug effects, closely monitor dosage, duration of use, and blood
levels of all medications metabolized or excreted by the kidneys.
Prerenal causes of AKI re factors external to the kidneys. These factors reduce
systemic circulation causing reduction in renal blood flow, and lead to decreased
glomerular perfusion and filtration of the kidneys. Although renal tubular and
glomerular function is preserved, glomerular filtration is reduced as a result of
decreased perfusion. It is important to distinguish prerenal oliguria from the oliguria
of intrarenal AKI. In prerenal oliguria there is no damage to the kidney tissue
(parenchyma). The oliguria is caused by a decrease in circulating blood volume
(severe dehydration, decreased cardiac output, burns) and is usually reversible.
With a decrease in circulating blood volume, autoregulatory mechnisms that
increase angiotensin II, aldosterone, norepinephrine, and antidiuretic hormone
attempt to preserve blood flow to essential of sodium (<20mEq/L), increased salt
and water retention, and decreased urine output.
Prerenal conditions can lead to intrarenal disease if renal ischemia is prolonged.
Prerenal consitions account for many cases of intrarenal AKI. If decreased perfusion
persists for an extended period of time, the kidneys lose their ability to compensate
and damage to renal tissue occurs.

MEDICAL: The objectives of treatment for AKI are to restore normal chemical
balance and prevent complications until repair of renal tissue and restoration of renal
function can occur. Management includes eliminating the underlying cause;
maintaining fluid balance; avoiding fluid excesses; and, when indicated, providing
renal replacement therapy. Prerenal azotemia is treated by optimizing renal
PHARMACOLOGICAL: Hyperkalemia is the most life threatening of the fluid and
electrolyte changes that occur in patients with kidney disorders. Therefore, the
patient is monitored for hyperkalemia through serial serum electrolyte levels
(potassium value greater than 5.0 mEq/L), ECG changes (tall, tented, or peaked T
waves), and changes in clinical status. If the patient is hemodynamically unstable
(low blood pressure, changes in mental status, dysrhythmia) IV dextrose 50%,
insulin, and calcium replacement may be administered to shift potassium back into
the cells.
NUTRITIONAL: AKI causes severe nutritional imbalances (because nausea and
vomiting contribute to inadequate dietary intake), impaired glucose use and protein
synthesis, and increased tissue catabolism. The patient is weighed daily and loses
0.2 to 0.5 kg daily if the nitrogen balance is negative. Foods and fluids containing
potassium or phosphorus are restricted.
NUSING MANAGEMENT: The nurse monitors for complications, participates in
emergency treatment of fluid and electrolyte imbalances, assesses the patient’s

Why did the researcher choose the case?

The researchers chose to present this case because after his successful kidney
transplant last 2004, his new kidney eventually started to malfunction.