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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 :
To function properly, the kidney requires:
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.
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.
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
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.
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.
Ischemic/hypoxic insults more common in the neonates may have hematuria( gross or microscopic), HTN, thrombocytopenia, Oliguria, and azotemia
-Idiopathic rapidly progressing GN
-Hemolytic uremic syndrome (azotemia, thrombocytopenia, anaemia-MAHA) commonest cause of AKI in toddlers. Follows E.coli gastroenteritis.
-Renal vein thrombosis esp in neonates
-This can be caused by drugs such as Penicillins, Rifampicin, NSAIDs, sulfonamides and present as Rash, fever, eosinophilia, +/-eosinophiluria)
-Renal parenchymal infiltration
-Uric acid nephropathy especially. Acute lymphoblastic leukemia, B-cell lymphomas)
Post renal kidney injury arises from obstruction of the urinary tract
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 of the precipitating illness
Signs and symptoms related to complications
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.
Renal ultrasound should be done urgently for every patient to rule out obstruction.
1. Withdraw all nephrotoxic drugs.
2.Deal with emergencies
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.
-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.
-Prompt and proper nutrition improves the outcome of ARF
-Protein 1-2g/kg (high biological value)
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
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
Severe HTN / hypertensive encephalopathy
-Continuous IV medication
-IV sodium nitroprusside
Nifedipine +/- atenolol OR give Hydralazine (PO) + atenolol
If not able to take PO use IV hydrazine
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
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 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.
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
Mortality is high. 42%
Poor prognosis in HUS and in those with neurological complications.
Infections are an important cause of death.