Renal Failure

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The renal failure may be acute or chronic.

Acute renal failure is characterized by widespread abrupt cessation of nephron function
Acute renal failure is a form of total renal failure in which the majority of nephrons suddenly and
simultaneously stop working. Clinically this causes a dramatic fall in urine production (oliguria),
which is often total (anuria). With little opportunity for metabolic compensation, problems
of disturbed fluid and electrolyte balance and failure of elimination develop rapidly.
There is an increase in serum potassium level and metabolic acidosis, and nitrogen retention with uraemia
Several diseases can produce acute renal failure, all of which cause sudden generalized cessation
of nephron activity.

Among the main causes are glomerular diseases; immune-mediated damage to glomeruli is a common
cause of diseases grouped under the term 'glomerulonephritis'. Tubular and interstitial disease
due to hypoxic, toxic or infective damage to tubular epithelial cells may also be responsible,
as may vascular problems leading to failure of perfusion of kidneys, e.g. hypovolaemic shock.
Acute renal failure is often reversible if the damaging stimulus is removed, allowing restoration of normal structure in the kidney through regeneration of damaged elements, particularly tubular epithelial cells.

Where there has been very severe generalized necrosis of the kidney, recovery may not be possible.
Chronic renal failure occurs with slow progressive destruction of individual nephrons over a long period of time.
Chronic renal failure is a form of total renal failure caused by progressive destruction of individual
nephrons over a long period of time. As more and more nephrons are destroyed, renal function becomes
progressively more impaired. However, in contrast to acute renal failure there is opportunity
for metabolic compensation.

Among the main consequences of chronic renal failure are progressive retention of nitrogenous metabolites
(uraemia) and progressive failure of tubular function.

The latter produces early inability to concentrate urine (polyuria) and abnormalities in biochemical
homeostasis (including salt and water retention, compensated metabolic acidosis, and other electrolyte
imbalances, particularly hyperkalaemia). Sodium and fluid retention may cause hypertension.
Failure of renal activation of vitamin D causes secondary hyperparathyroidism and bone disease,
(renal osteodystrophy), and destruction of renal parenchyma leads to reduced
erythropoietin levels which, together with the direct suppressive effect of uraemia on marrow, results
in anaemia. Uraemia also causes defective platelet function and a bleeding tendency.
Several diseases can produce chronic renal failure, all of which cause slow, progressive, irreversible
generalized destruction of nephrons (both glomeruli and tubules).
The main causes of chronic renal failure are vascular disease (long-standing hypertension), disease of glomeruli (glomerulonephritis and diabetic glomerular disease) and disease of tubules and interstitium (infective, toxic and obstructive damage to tubules and renal papillae).

In contrast to many cases of acute renal failure, chronic renal failure is not reversible because
there has been destruction of nephrons. A kidney in which all nephrons have been irreversibly damaged
is macroscopically small and shrivelled and is known as an end-stage kidney.

Diseases affecting pre-glomerular vessels may produce either chronic or acute renal failure
Diseases of pre-glomerular vessels, or central pump failure, have a major impact on the function of the kidney.
In general, slowly progressive disease of the vessels leads to slowly progressive destruction
of nephrons, ischaemic glomerular filtration failure and ischaemic tubular atrophy, culminating
in chronic renal failure and a small, shrunken end-stage kidney.
The initial effect of rapidly progressive disease of vessels or severe central pump
failure is sudden reduction of glomerular filtration, and the development of hypoxic
necrosis of tubular epithelium. This leads to acute renal failure with oliguria or anuria,
and the affected kidney is usually swollen.
In most cases the atherosclerotic occlusion of the renal artery is most severe at its origin
from the aorta; this renal artery stenosis can lead to chronic ischaemia of the affected kidney,
with reduction in function of all nephrons on that side, producing an end-stage shrunken kidney.
The unaffected kidney undergoes compensatory hypertrophy, so renal function is largely unaffected
in most cases. Renal artery stenosis is also caused by arterial fibromuscular dysplasia.
Renal artery stenosis may lead to renovascular hypertension, thought to result from abnormal
activity in the renin-angiotensin system in the chronically ischaemic kidney. It is important in
that it is one of the recognized causes of hypertension that is amenable to surgical correction.
Severe atheroma of the aorta has caused occlusion of the lumen of one of the renal arteries.
This has caused ischaemia to the kidney, which is shrunken. The ischaemic kidney can then precipitate
hypertension by oversecretion of renin.

Benign hypertension produces thickening of the wall of renal vessels, with persistently reduced flow
In long-standing benign hypertension, changes in muscular renal arteries and renal arterioles
lead to reduced flow of blood to glomeruli.

Renal artery branches within the kidney show thickening of the wall due to
a combination of fibroelastic intimal proliferation,elastic lamina reduplication, and muscular
hypertrophy of the media. Afferent arterioles undergo hyalinization, their muscular walls being
replaced by an amorphous material, which is rigid and inelastic.
Chronic and progressive reduction in blood flow to the nephron leads to chronic ischaemia, with
slow conversion of individual glomeruli into a mass of hyaline tissue devoid of capillary lumina.
As the blood supply to the tubule is derived from flow through the glomerulus into the efferent
arteriole and peritubular capillaries, ischaemic destruction of the associated tubule occurs.
This process picks off individual nephrons over a period of many years, with no initial clinical
symptoms. Biochemically a gradual increase in blood levels of urea and a reduction
in creatinine clearance occur.

Eventually, sufficient numbers of nephrons become non-functioning for the patient to develop
manifestations of chronic renal failure.
This sequence of changes, called benign hypertensive nephrosclerosis, is an important
complication of long-standing benign hypertension,chronic renal failure being one of the important
sequelae of benign hypertension.

Renal cortical necrosis
Intravascular coagulation may precipitate renal failure
Large renal infarcts are usually due to thromboemboli in the systemic circulation
The most common cause of renal infarction is the passage of emboli down renal arterial branches.
Typical embolic infarcts in the kidney are usually wedge-shaped subcapsular areas of necrosis, with
the broad base at the capsular surface. Infarcts initially appear red and slightly raised above
the capsular surface, but after 4-5 days they develop a yellowish white centre with a rim of hyperaemia.
Old infarcts appear as narrow, wedge-shaped, depressed scars. The most common causes are emboli
from a mural thrombus formed over a recent myocardial infarct, thrombotic vegetations on mitral and aortic
valves, thrombus on a mitral or aortic valve prosthesis, or thrombus from the left atrium of
patients with atrial fibrillation.
Complete occlusion of a renal artery due to thrombosis leads to infarction of the whole kidney.
However, except as a complication of arterial surgery during renal transplantation, this is a rare occurrence.
Diseases such as microscopic polyarteritis, accelerated hypertension and Henoch-Schnlein purpura
(and other disorders in which there is destruction of small vessel walls) produce microinfarcts, which
are usually multiple ('flea-bitten kidney').
When the disease is limited to very small vessels, the necrosis is confined to segments of the glomerular
capillary tuft (tuft necrosis).
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Revised: 02-11-2014.