Acute and reversible deterioration of renal function which develops over a period of days, or rarely weeks and results in uremia is called acute renal failure.
Renal failure may be due to pre-renal, renal or post-renal causes.
The kidneys are inadequately perfused and the GFR is greatly diminished. This may be due to ;
• Decreased cardiac output in cardiac failure.
• Underfilling of the vascular bed due to haemorrhage, severe fluid depletion or vasodilatation resulting from sepsis.
• Diseases of the renal arterioles such as vasculitis or microangiopathic hemolytic states, rapidly progressive (crescentic) glomerulonephritis,
• Injury to tubular cells (acute tubular necrosis) by toxins or ischaemia. Intraluminal obstruction of nephrons from precipitation of crystals or protein.
• Acute intestinal nephritis due to infections or drug reactions.
ARF is caused by obstruction of the urinary tract at any point in its course.
This is also called pre-renal azotemia.
About 70% of cases of acute renal failure (ARF) are due to pre-renal causes.
Pre-renal ARF results from hypoperfusion of kidneys due to a decrease in effective arterial blood volume. lt can immediately be reversed with the restoration of renal blood flow, renal parenchymal damage does not occur. If hypoperfusion persists ischemia can result causing intrinsic renal failure.
• Hemorrhage due to trauma, GI bleed, surgery
• GI loss: vomiting, diarrhoea
• Renal loss: diuresis
• Skin loss: Sweating
Decreased systemic vascular resistance:
Severe liver failure (hepato-renal syndrome)
• Hemorrhages from any cause including complications of pregnancy.
• Gastrointestinal bleeding
• Loss of plasma as in bums and crushing
• From the gastrointestinal tract in severe vomiting, diarrhoea, acute intestinal obstruction, paralytic ileus, pancreatitis, fistulae.
• In urine due to excessive treatment with diuretics, diabetic ketoacidosis
• From the skin due to sweating
• Cardiogenic shock
The diseases which result in renal under perfusion e.g. thrombosis of the Aorta or renal arteries, or aortic aneurysm.
• Identify the cause and treat it
• If hypovolemia or septicaemia – restore circulation by replacing blood, plasma or saline as indicated.
• Maintain scrum electrolytes; especially consider serum potassium level.
• Avoid nephrotoxic drugs.
• Renal function in prerenal failure returns to normal completely once normal renal perfusion has been restored in the early stage.
• If oliguria persists in spite of the restoration of the circulation to normal then acute tubular necrosis is likely to have developed.
Intrinsic diseases of the kidney can cause acute renal failure. These diseases are divided into glomerular, tubular-
interstitial or vascular disease.
1. Primary Glomerulonephritis
2. Secondary Glomerulonephritis
• Diabetic nephropathy
• Systemic vasculitis; SLE. Polyarteritis, Wegener’s granulomatosis
Acute tubular necrosis
• Antibiotics such as aminoglycosides
• Contrast agents
• Heavy metals such as mercury
• Chemical such as carbon tetrachloride
• Hemoglobinuria, myoglobinuria
• Multiple myeloma
• Uric acid (gout)
Acute interstitial nephritis – Usually drug-induced
• Hypertensive nephrosclerosis
• Polyarteritis nodosa
• Atheroma kidney
• ACE inhibitors, NSAIDs
The clinical course of acute renal failure is relatively short-lasting approximately 10-25 days during which time the individual progresses through three phases of the pathophysiological process
L Pre-oliguric phase (0-2 days)
2. Oliguric phase (8-14 days)
3. Diuretic phase (about 10 days)
4. Recovery phase (4-6 months)
• It is the period from the occurrence of the precipitating event until the beginning of the oliguria.
• Symptoms of primary cause are dominant.
• Rapid reversibility if circulation is restored early and completely.
• This period is characterized by oliguria (urine volume less than 400 ml in 24 hours).
• The longer the patient remains in this phase the poorer the prognosis due to the development of complications due to excessive body fluids, electrolyte imbalance and retention of metabolic waste products.
This phase is characterized by an increase in urinary output to about 3-5 litres daily and this may progress to polyuria and dehydration.
Diuresis develops because the damaged tubular epithelium is replaced by an epithelium that has not yet
developed concentrating activity.
This is the period from the stabilization of serum laboratory values until the patient attain either
totally normal or optimal renal function.
1. Fluid overload
5. Metabolic acidosis
8. Bleeding disorders
9. Cardiac arrhythmias
10. Gastrointestinal bleeding
1 1 . Uremic syndrome