Nephrology

Acute Kidney Injury (AKI) : Causes, Symptoms and Treatment

  • Clinicals
  • Nephrology
  • 2020-12-02 13:13:50
  • 10 minutes, 35 seconds

Acute Kidney Injury (AKI) : Causes, Symptoms and Treatment

Acute kidney injury previously known as acute renal failure is an abrupt reduction in glomerular filtration rate characterized by an increase of blood urea nitrogen (BUN) and serum creatinine with or without a decrement in urine output.

It may result from :

  • Decrease ineffective circulation.
  • Renal cell injury.
  • Arterial or venous obstruction.
  • Obstruction to urine flow.

Effects of Acute kidney injury

  1. The kidneys are unable to perform their major functions of:-
  2. Fluid and electrolyte balance
  3. Blood pressure control
  4. Regulation of acid-base balance
  5. Hormonal control
  6. Excretion of toxic products of metabolism

What are the Causes of Acute Kidney Injury?

 

To function properly, the kidney requires:

  1. Normal blood flow;
  2. Functioning glomeruli and tubules to separate and process an ultrafiltrate containing waste products from the blood; and
  3. Drainage and elimination of formed urine from the body.

The sudden interruption of any of these processes will lead to Acute kidney injury.

Disorders causing AKI are classified on the basis of their primary site of interference with these processes into three large groups.

  • Pre-renal causes,
  • Intrinsic causes and
  • Post renal (obstructive) causes

Conditions that interfere with blood delivery to the kidney are called Prerenal, and are most commonly functional (and potentially reversible) in nature (for example ECF volume contraction, congestive heart failure) but on occasion may be structural (e.g., renal artery stenosis).

Diseases that cause intrinsic injury to the kidney proper (glomeruli, tubules, interstitium, small blood vessels) are grouped under Renal causes or (intrinsic causes) (e.g., acute glomerulonephritis, acute tubular necrosis, acute interstitial nephritis or small vessel vasculitis).

Acute Tubular Necrosis is a distinctive clinicopathological syndrome in which the tubules are the primary site of injury. The terms ARF and ATN should not be used interchangeably.

Finally, conditions that interfere with normal drainage and elimination of formed urine are classified as Postrenal (e.g., prostatic outlet obstruction, bilateral ureteral obstruction).

Pre-renal acute kidney injury (also commonly referred to as “pre-renal azotemia”) and acute tubular necrosis (ATN) are the most common causes of acute kidney injury in hospitalized patients.

Pre-renal Causes

Some combination of hypovolemia, hypotension and diminished renal perfusion is the most common cause of AKI in hospitalized patients. Therefore identification of pre-renal (functional) AKI is important because it the decreased perfusion is reversed promptly, kidney function improves.

Pre-renal ARF may evolve from

  1. Blood loss,
  2. Sodium depletion (due to diarrhea, excessive diuresis or congenital or acquired salt-wasting renal or adrenal disorders),
  3. Burns.
  4. Redistribution of plasma volume to a so-called “third space loses ” (e.g., ascites in patients with hemorrhagic pancreatitis or hepatic cirrhosis), or
  5. Reductions in effective arterial blood volume with consequent renal hypoperfusion (as in congestive heart failure, hepatic cirrhosis or nephrotic syndrome).
  6. Dehydration from other causes.
  7. Gastrointestinal losses
  8. In other situations, especially when for one reason or another renal perfusion is tenuous or already compromised, drugs that affect afferent and/or efferent arteriolar resistance (e.g., NSAIDs, ACE inhibitors) can precipitate pre-renal azotemia.

The kidneys are intrinsically normal, with the restoration of renal perfusion the renal function becomes normal. The diminished intravascular volume leads to a fall in cardiac output decreasing GFR. If reversed within a certain time no renal damage.

 

Pathophysiology of Pre-renal Azotemia

The kidney is able to maintain a relatively constant glomerular filtration rate (GFR) and to a lesser extent renal blood flow (RBF) despite modest reductions in mean arterial pressure. This process, termed renal autoregulation, derives largely from hormonally-mediated adjustments in afferent and efferent arteriolar resistance. By increasing Reff/Raff angiotensin-II and prostaglandin-E maintain PGC and GFR at the expense of RBF.

As a result, filtration fraction (GFR/RBF) and post-glomerular capillary oncotic pressure increase, which facilitates sodium and water reabsorption from the adjacent proximal tubule.

Angiotensin-II also directly increases proximal tubular sodium reabsorption and stimulating aldosterone synthesis and release increases sodium reabsorption in more distal tubular segments as well.

At the same time, volume-related antidiuretic hormone release leads to enhanced water and urea reabsorption in the collecting duct. Urine formed under these conditions is of reduced volume, highly concentrated, and contains scant amounts of sodium.

These characteristics are the basis of tests for distinguishing pre-renal azotemia from acute tubular necrosis. Renal autoregulation breaks down as mean arterial pressure falls below about 80 mm Hg, at which point further adjustments in intra-renal hemodynamics are unable to maintain GFR and RBF in the face of a progressive reduction in renal perfusion pressure.

Causes of intrinsic failure

  • Acute tubular necrosis ATN – may evolve from pre-renal failure
  • Drug nephrotoxicity may be due to acute tubular necrosis.
    • These nephrotoxic drugs are
    • Aminoglycosides, amphotericin B
    • IV radiocontrast peak rise of Cr 3-5 days latter
    • NSAIDs, acetaminophen, cisplatin,
  • Acute cortical necrosis

    Ischemic/hypoxic insults more common in the neonates may have hematuria( gross or   microscopic), HTN, thrombocytopenia, Oliguria, and azotemia

  • Endogenous toxins
  • Glomerulonephritis

-Poststreptococcal
-Lupus erythematosus
-Membranoproliferative
-Idiopathic rapidly progressing GN

  • Vascular Causes

-Hemolytic uremic syndrome (azotemia, thrombocytopenia, anaemia-MAHA) commonest cause of AKI in toddlers. Follows E.coli gastroenteritis.
-Renal vein thrombosis esp in neonates

  • Interstitial Nephritis

-This can be caused by drugs such as Penicillins, Rifampicin, NSAIDs, sulfonamides and present as Rash, fever, eosinophilia, +/-eosinophiluria)

  • Tumors

-Renal parenchymal infiltration
-Uric acid nephropathy especially. Acute lymphoblastic leukemia, B-cell lymphomas)

Post-renal Causes

Post renal kidney injury arises from obstruction of the urinary tract

  • Intra-renal Obstruction
    • Acute uric acid nephropathy
    • Drugs (e.g., acyclovir)
  • Extra-renal Obstruction
    • Renal pelvis or ureter (e.g., stones, clots, tumors, papillary necrosis, retroperitoneal fibrosis)
    • Bladder (e.g., Benign prostate hypertrophy, neuropathic bladder, Neurogenic bladder )
    • Urethra (e.g., urethral stricture)
  • Bilateral ureteral obstruction

The nature of the obstructing lesion, the site of the obstruction, the rapidity of onset, and the magnitude of the obstruction are all important determinants of the presentation of postrenal ARF. Since postrenal ARF is often reversible, it is essential that the clinician quickly recognize and correct the cause of obstruction.

In addition to a careful history and physical examination and examination of the urinary sediment, renal ultrasound and spiral computed tomography are the diagnostic tools most helpful in detecting obstruction.

Because of ‘compensatory’ increases in GFR in the contralateral non-obstructed kidney, unilateral ureteral obstruction does not usually result in a rise in the serum creatinine concentration.

Signs and symptoms

 

Signs and symptoms of the precipitating illness

  • Diarrhea, vomiting, bleeding.
  • Upper respiratory tract infections
  • Systemic lupus erythematosus
  • skin rash, joint pains, fever
  • Drug ingestion (previous 44 days)
  • RVT in neonates
  • Recent urinary tract infection- obstructive uropathy
  • Pain +/-hematuria

Signs and symptoms related to renal failure

  • Patients are usually oliguric (urine volume < 500 mL daily).
  • Pallor
  • Edema
  • Hypertension
  • Clinical features of advancing URAEMIA include anorexia, nausea, and vomiting followed by drowsiness, apathy, confusion, muscle twitching, hiccoughs, fits, and coma. Uremic encephalopathy
  • Anemia is common and is caused by blood loss, hemolysis or decreased erythropoiesis.

Signs and symptoms related to complications

Investigations

A careful microscopic examination of the urine sediment, quantification of the urine volume, determination of urinary electrolytes, and a variety of radiologic studies are the tools the clinician uses in conjunction with a thorough history and physical examination to determine the cause of ARF in any given patient.

  • Urinary sediment
  • Urinary indices
  • Urine volume
  • Kidney function studies: Increased levels of blood urea nitrogen (BUN) and creatinine; the ratio of BUN to creatinine can exceed 20:1
  • Electrolytes (Na, K, Ca, PO, HCO3)
  • Blood gasses analysis if serum HCO3 is less than 20 mEq/l.
  • Uric acid  levels
  • Serum complement C3 levels (decreased in post streptococcus GN, Lupus and membranoproliferative GN)
  • Antistreptolysin O titers
  • HIV, Hep B surface antigen, Heb C antibody
  • Serologic tests may show evidence of conditions, such as in lupus nephritis, ANCA vasculitis or anti-GBM disease or syndrome
  • ANA if positive ds DNA
  • Urine electrolytes (Na, creatinine) to differentiate pre-renal from ITN
  • Urinalysis & microscopy culture and sensitivity
    -Proteinuria, Red blood cell’s WBC's casts suggest intrinsic renal failure
    -RBC casts when present are virtually diagnostic of glomerulonephritis or vasculitis. However, the absence of RBC casts does not exclude glomerulonephritis.
    -Monomorphic (non-dysmorphic) RBC suggests a non-glomerular source of bleeding – i.e., bleeding from the calyces, pelvis, ureter(s), bladder, prostate or urethra. Dysmorphic red blood cells suggest glomerular injury.
  • Complete blood count (can indicate infection; acute blood loss or chronic anemia; thrombotic microangiopathy)
  • Erythrocyte sedimentation rate.↑ ESR will indicate’ myeloma, infection
  • Blood sugar levels may be low due to poor feeding
  • Blood slide for malaria parasite
  • Renal biopsy depending on the cause. Renal biopsy shows a Crescentic type picture in RPGN.
  • ↑ CRP - may be elevated if infection/vasculitis/autoimmune
  • Aortorenal Angiography: Can be helpful in establishing the diagnosis of renal vascular diseases, such as renal artery stenosis, renal atheroembolic disease, atherosclerosis with aortorenal occlusion, and certain cases of necrotizing vasculitis (eg, polyarteritis nodosa),

Imaging
Renal ultrasound should be done urgently for every patient to rule out obstruction.

Principles of management of acute kidney injury

1. Withdraw all nephrotoxic drugs.
2.Deal with emergencies

  • Pulmonary edema
  • Hyperkalemia
  • Metabolic acidosis.

3.Establish Euvolemia

  • Pre-renal-Fluid/blood transfusion.
  • Renal-Diuretics
  • Post renal catheterization.

4.Restriction

  • Fluids-Input output chart with fluid restriction.
  • Previous day output plus 500ml.
  • Salt restriction
  • K+restriction-fruit
  • Protein restricted This balance is achieved best with a protein intake of 0.6 g per kg per day
  • Daily weight

5. Correct electrolytes and acid-base imbalances.

Sodium bicarbonate therapy should be reserved for the treatment of severe metabolic acidosis (i.e., pH below 7.2 or a bicarbonate level below 10 to 15 mEq per dL [10 to 15 mmol per L]) with or without associated hyperkalemia.

It is important to note that sodium bicarbonate and sodium polystyrene sulfonate have a large sodium load and may worsen fluid status in patients with acute renal failure.

6. Dietary considerations-mode of delivery of nutrients.
7. Care for infections.
8.Care for tissue oxygenation
9.Prophylaxis against gastrointestinal bleeding and deep venous thrombosis.
10. Investigate and treat the primary cause.

 

Treatment of acute kidney injury

  • Proper hydration of dehydrated patients
  • Avoidance of nephrotoxic drugs as much as possible
  • Avoid the use of prostaglandin synthetase inhibitor and ACEI in patients with volume depletion and
    renal hypoperfusion
  • Proper hydration when toxic insults are anticipated eg proper hydration in a child receiving chemotherapy, intravascular contrast(1.5 times normal daily fluid requirement)
  • Treatment depends on underlying causes.

If hypovolemic:

-Administer normal saline 20mls/kg-to run in 30 min -1hour
-If no urine output within 2 hours. Reassess patients and catheterize the patient
-Monitor fluid input and output.

Nutritional support

-Prompt and proper nutrition improves the outcome of ARF
-Protein 1-2g/kg (high biological value)
-low potassium
-low phosphate,
-low sodium.

Treat Complications

1.Severe acidosis

Aim at PH - 7.2 and 12mEq/1 of serum HCO3
NaHCO3=0.6 X (kg) X (12- serum HCO3 Give in 30mins. Or 0.5-1 mEq/kg of NaHCO3

If the child’s CNS is intact respiratory compensation will provide partial compensation of acidosis. If obtunded acidosis may be severe.

The remainder to be corrected orally after knowing serum Ca.

The intact respiratory system is necessary

2. Hyperkalemia

Stop any medication, IVF and foods which can cause hyperkalemia
exchange resin 1gm/kg PO 6hourly or PR in sorbitol If >7mEq/l NaHCO3 1mEq/kg over 30 min if there is acidosis

Glucose and insulin (glucose-1ml/kg of 50% dextrose ie 0.5g/kg of glucose + Insulin 0.1 unit/kg over 30 min)

Monitor blood sugar and K may need to repeat infusion 6 hourly until dialysis

Beta-agonists

Hypertension
Severe HTN / hypertensive encephalopathy

-Continuous IV medication
-IV sodium nitroprusside
-IV labetalol

Mild-Moderate HTN
Nifedipine +/- atenolol OR give  Hydralazine (PO) + atenolol

If not able to take PO use IV hydrazine

Hypocalcemia

Dietary restriction and phosphate binders
If severe or bicarbonate therapy is necessary to give 10% calcium gluconate

Avoid calcium supplement if: Ca X P (mmol/l) is over 4.5

Treat gastrointestinal bleeding with anti-acids and Ranitidine.
Adjust Other medication required for the degree of renal failure

Hyperphosphatemia

Dietary restriction and phosphate binders.

Oral calcium carbonate and other calcium compounds bind phosphorus and prevent its absorption. It also provides calcium
Calcium carbonate 30-50mg/kg/dose 6 hourly

Management of post-renal failure

Management is surgical ( NO DIURETICS!!!)

An indwelling urethral catheter should be inserted immediately using a sterile procedure
If the obstruction is relieved to investigate the patient to determine the level of obstruction. –Renal/bladder ultrasound, MCU, DTPA

In most cases, surgical intervention is required
If urine is obtained on catheterization surgical intervention is required immediately. Anticipate post-obstructive diuresis and manage accordingly. May need IVF.

Indications For Renal Replacement Therapy

1.Volume expansion that cannot be managed with diuretics
2. Hyperkalemia >6.5 mmol/L not responding to treatment.
3. Correction of severe acid-base disturbances not responding to treatment.
4.Severe azotemia (BUN >100)
5.Symptoms of uremic pericarditis
6.Uraemic gastritis-N/V, Anorexia, GI Bleeds
7.Uraemic encephalopathy/uremic toxicity
8.Pulmonary edema
9.Intractable hypertension

Prognosis

Mortality is high. 42%
Poor prognosis in HUS and in those with neurological complications.
Infections are an important cause of death.


References:
author

Daniel Ogera

Medical educator, passionate about simplifying difficult medical concepts for easier understanding and mastery by nursing and medical students.

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About this article:
  • Topic:Clinicals
  • Duration:10 minutes, 35 seconds
  • Subtopic:Nephrology

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