It is defined as sudden and usually reversible deterioration of renal functions developing over a period of days or weeks with rapid rise in blood urea. The characteristic features include marked reduction in urine volume (oliguria) , acid- base and electrolyte disturbance. It may be pre-renal, renal or post –renal. Acute deterioration of renal functions i.e., oliguria in a patient with acute on chronic kidney failure.
PRE- RENAL (RENAL HYPOPERFUSION):
Hemorrhage, severe burns, crushing injuries, shock, hypovolemia (loss of fluids i.e., diarrhea, perspiration) ,septicemia, cardiac failure , intravascular hemolysis pancreatitis ,anesthesia and rhabdomyolysis.
INTRA-RENAL (INTRINSIC RENAL DISEASE):
Vasculitis, renovascular obstruction (bilateral or unilateral with one functioning kidney) , microangiopathic hemolytic states, rapidly progressive glomerulonephritis (RPGN) , acute tubulointerstitial nephritis ( or infections –induced) ,acute tubular necrosis due to toxins or ischemia.
OBSTRUCTIVE (POST RENAL):
Urinary tract obstruction (urethral or ureteral or renal pelvis) at any site.
The damage that leads to Acute kidney failure may be caused by:
REDUCED BLOOD FLOW CAN LEAD TO:
Certain diseases can cause clotting within your kidney’s blood vessels, and this can lead to acute kidney failure like:
It aims at keeping the patient alive with the appropriate measures till diuretic phase sets in. It includes:
It is treated by insulin with glucose, calcium gluconate and ion exchange resins to prevent life threatening arrhythmias. Dialysis is reserved for severe hyperkalaemia.
It develops due to fluid overload is treated by salt restriction and diuretics Antihypertensive if required can be given.
Normally, -obligatory water loss of 500 ml/dayoccurs through skin and lungs. There may bean additional loss of water through sweats inthese patients if they develop fever or diarrhoea.Therefore,total loss estimated in these patientsvaries between 800-1000 ml.The fluids to bereplaced is calculated by adding the obligatorylosses to the urine output of the previous day. To be on safer side, one litre of fluid is startedinitially followed by its maintenance by CVP.Noelectrolyte should be given. Hyper calcaemic andhyperphosphataemia can be improved with dietand phosphate binding agents such as aluminium hydroxide or by calcium replacement.
Proteins are given to prevent endogenousbreakdown of proteins. About 20-40g proteinsdaily(0.5 g/kg) is sufficient for this purpose.Theenergy is provided by carbohydrates,hence,liquidglucose preparations or intravenous glucose (10%)may be given in case of vomiting or diarrhoea.
Infection is treated by appropriate antibiotics.Feverand leucocytosis are the signs of infection.Choice of antibiotics depends on the culture and sensitivity.Nephrotoxic antibiotics are to be avoided. There is no role of prophylactic antibiotics in ARF.
Metabolic acidosis is treated as and when it arises. Sodiumbicarbonate (50-100 mEq every 6 hours)employed to keep the bicarbonate levels around18 mmol/dl.
Dialysis (haemodialysis or peritoneal dialysis) or haemoperfusion is employed frequently insituations givenbelow: